the echocardiographers guide

The Echocardiographers’ Guide

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This book is dedicated to Maureen Plappert CVT (dec.) – my wife, friend and partner inechocardiography for 26 years, with all my love.

Ted Plappert

To Ted and the late Maureen Plappert whose dedication and expertise have been invaluableto patients and physicians alike. I have been privileged to work with them for more than25 years at the University of Pennsylvania Medical Center and the Brigham andWomen’s Hospital at Harvard Medical School during which time they have made pivotalcontributions to many ground-breaking national and international clinical trials.

Martin St John Sutton

DEDICATION

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The

Echocardiographers’Guide

Ted Plappert CVT

Martin G St John Sutton MB BS FRCP

Center for Quantitative EchocardiographyHospital of the University of Pennsylvania

Philadelphia, PA USA

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© 2006 Informa UK Limited

First published in the United Kingdom in 2006 by Informa Healthcare, 4 Park Square, Milton Park, Abingdon,Oxon OX14 4RN. Informa Healthcare is a trading division of Informa UK Ltd.Registered office: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales, number 1072954.

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A CIP record for this book is available from the British Library.

Library of Congress Cataloging-in-Publication data available on application

ISBN-13: 978 1 84184 489 3ISBN-10: 1 84184 489 6

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Acknowledgments vi

1 Physics and instrumentation 12 The normal Doppler echocardiographic examination 133 Evaluation of left ventricular systolic function 354 Evaluation of right ventricular function 435 Evaluation of diastolic function 516 Coronary artery disease 617 Valvular heart disease 758 Cardiomyopathies 1179 Diseases of the pericardium 135

10 Diseases of the aorta 14711 Cardiac masses 15512 Congenital cardiac malformations 163

Index 181

v

CONTENTS

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The authors are indebted to the sono-graphers and cardiologists of the echo-cardiography laboratory and Center forQuantitative Echocardiography of theHospital of the University of Pennsylvaniafor their assistance in preparing this text-book. Thanks are due to Silvia Bush, KarenEberman, Toni Emmi, Ginny Englefield,Darryl Fenton, Lise Fishman, Shumin Gao,

Eva Hungler, Monica Pugh, KennethRuddell, and Susan Thomas for their tech-nical expertise, to Drs Hind Rahmoudi,Hirotsugu Hamamoto, and ShinyaKanemoto for assistance with the illustra-tions and to Alan Burgess, Kelly Cornish,and Tim Koder, for editorial assistance.Special thanks to Maureen Plappert.

vi

ACKNOWLEDGMENTS

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1

SOUND

Sound consists of mechanical waves. Unlikeelectromagnetic waves, sound needs amedium through which to propagate.Sound propagates by alternately compress-ing and expanding the particles of themedium. Sound waves can be displayedgraphically as local variations in acousticpressure against time (Figure 1.1). The timefrom the peak of one cycle to the peak ofthe next is the wavelength. Wavelength isrelated to frequency:

Wavelength � propagationvelocity/frequency

The speed at which sound passes througha medium, i.e. its propagation velocity, isrelated to the density of the medium andis greater through dense materials. Soundintensity (power per cross-sectional area) isattenuated as it travels through a medium.Most of the energy loss is through heatresulting from the compression of themedium. Attenuation increases as frequencyincreases. Energy loss is measured in deci-bels per centimeter per megahertz andranges from 0.5 dB/cm to 1.1 dB/cm/MHzin soft tissue. The acoustic impedance of amaterial is the product of its density andpropagation velocity and is measured inrayls (one rayl is equal to one kilogram persquare meter per second).

When a sound wave encounters a bound-ary between two media with differentacoustic impedances, energy is lost as someof the sound wave is redirected. When asound wave strikes a smooth interfacebetween two materials with differentacoustic impedances at a 90� angle, a por-tion of the sound energy will be reflectedback to its source. The magnitude of thereflection will depend on the magnitude ofthe difference in acoustic impedances. If the

PHYSICS AND INSTRUMENTATION

CONTENTS ● Sound ● Transducers ● Two-Dimensional Images ● Doppler● Other Imaging Modalities

1

Pre

ssur

e

Time

Figure 1.1 A sound wave is graphically represented asphasic variations in acoustic pressure (y-axis) against time(x-axis). One wavelength (see double arrow) is measured asthe time from the peak of one cycle to the peak of thenext cycle.

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THE ECHOCARDIOGRAPHERS’ GUIDE

angle of incidence is not 90� sound may notbe reflected back to the source. The angle ofincidence will equal the angle of reflection.When the angle of incidence is not 90� andthe acoustic impedances of two media atthe interface are different, the propagatingsound wave will be refracted, that is, it willchange direction as it passes through theinterface. When the interface between thetwo media is smooth and mirror-like (spec-ular) more sound energy will be reflected,and when the interface is irregular, soundenergy will be reflected in a number ofdirections. If the wavelength is large relativeto the reflector, sound will be scattered inall directions.

TRANSDUCERS

Transducers convert one type of energy toanother. Ultrasound (US) transducers rely onthe piezoelectric properties of certain crys-tals, such as lead zirconate titanate ceramics,to convert electrical activity to mechanicalvibration and mechanical vibrations back toelectrical activity. When a piezoelectric crystalin a transducer is stimulated electricallyit vibrates, producing an acoustic signal.When a piezoelectric crystal is mechanicallydeformed by ultrasound energy returningto the transducer it produces an electricalsignal.

The principal components of a simplesingle-crystal transducer are: a piezoelectriccrystal; damping material behind the crys-tal; a lens; and an impedance matchinglayer in front of the lens (Figure 1.2). Thedamping material limits the vibration of thecrystal, effectively turning it off after a fewcycles and keeping the generated pulse trainshort. A short pulse length improves axialresolution, which is the ability to distinguishindividual structures along the axis of prop-agation of the sound wave. Axial resolutionis equal to one half the pulse length anddoes not change as the sound wave travelsthrough the medium. The pulse length isequal to the product of the frequency andthe number of cycles in the pulse train.Increasing the frequency increases the axial

resolution, but increasing the frequencyalso increases the attenuation. When select-ing a transducer it is therefore necessary tobalance the requirements for penetrationand resolution.

The three-dimensional shape of an unfo-cused US beam resembles a cylinder in thenear field that then diverges in the shape ofa cone. The diameter of the crystal and itsfrequency determine the length of the nearzone. The amount of beam divergence dis-tal to the focal zone is determined by thecrystal diameter. A focused beam is narrowand shaped like an hourglass. The beam canbe focused by using an acoustic lens or acurved crystal. Lateral resolution is the abilityto distinguish individual structures lyingperpendicular to the axis of propagationof the sound wave and is optimal when

Figure 1.2 A simple ultrasound transducer is composedof a piezoelectric crystal (blue), with an acoustic lens (red),and an impedance matching layer (green) in front anddamping material (yellow) behind.

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the beam is at its narrowest. Two adjacentobjects, side by side, will be resolved if theyare farther apart than the width of thebeam.

The acoustic matching layer has an acousticimpedance value that lies between that ofthe crystal and skin. Its purpose is to mini-mize strong reflections at the skin surfaceso that the US beam will penetrate to thetissues.

Part of the transmitted US energy isreflected back to the transducer each timethe beam encounters an interface betweentwo tissues with different acoustic imped-ances while the remainder of the beamcontinues to penetrate. Transducers spendonly a fraction of a percent of the timetransmitting the sound pulse. The rest ofthe time the transducer is in the receivemode ‘listening’ for a reflected signal.When reflected US is received at thetransducer, mechanical deformation of thecrystal results in an oscillating electric orradiofrequency (RF) signal. The distancefrom the transducer to the reflector can becalculated because the speed of sound insoft tissues is a constant (1540 m/s). Whenthe reflected signal (echo) is received by thetransducer it is amplified. Echoes returningto the transducer are differentially ampli-fied as a function of their time of flight, i.e.late returning echoes get more amplifica-tion to compensate for attenuation. Thisdifferential amplification is performedautomatically by the US system and manu-ally by the operator through a time gaincompensation (TGC) control.

The returning signal is complex, consist-ing of oscillating waves with positive andnegative components. The US systemsmoothes the waves and discards the nega-tive components. To shorten the signal andemphasize the leading edge, the first deriv-ative of the signal is calculated and thenegative portion of the signal is again dis-carded. The signal may be amplified or ifthe signal is below a certain threshold deter-mined by the system and the operator itwill be ignored (reject control) (Figure 1.3).

Returning echoes are displayed as dotsalong a line that represents depth in thechest. The brightness of each dot is propor-

tional to the echo intensity, which dependson the amount of reflected US, and is afunction of the difference in acousticimpedances at each interface. This displayof brightness per unit depth along one lineis a B-mode scan line. An M-mode or motionmode display results from graphing return-ing echoes from successive transmittedpulses as a function of time. A sampling rateof 1000 Hz along a scan line can be achievedand provides M-mode with the temporalresolution required to evaluate even thefastest moving cardiac structures.

TWO-DIMENSIONAL IMAGES

For cardiac imaging the US beam is sweptthrough an arc from a point on the chestwall. A single crystal transducer can gener-ate two-dimensional images if the US beamis mechanically oscillated through a plane.The beam is directed in increments throughan arc or sector of 90� and transmits andreceives a B-mode scan line in less than 1�increments. As the angle of the beam foreach scan line is known, a two-dimensionalstill image can be constructed from a seriesof scan lines. The speed of sound in softtissue is 1540 m/s; therefore, it takes anemitted sound train 0.00013 s to travel to adepth of 20 cm. The round trip from the

3

Am

plit

ude

Time

A B C D

E

Figure 1.3 (A) The raw radio-frequency signal returnedto the transducer. (B) The signal is smoothed and thenegative portion discarded. (C) The first derivative of theremaining signal is determined and (D) the negativeportion is again discarded. (E) The signal is amplified.

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transducer to the reflector and back takestwice as long or 0.00026 s. This return tripcan be made 3846 times in one second.Each round trip represents a B-mode scanline, and 120 such scan lines can be made in0.03 s. If one two-dimensional image is con-structed from 120 scan lines derived fromincrementally changing the angle of the USbeam to the transducer face, 32 such imagescan be obtained in one second, i.e. the two-dimensional image can be updated 32 timesin a second and cardiac motion can be seenin real time.

The pulse repetition frequency (PRF) is thenumber of transmit/receive cycles per-formed by the transducer in one second. Inthe example above: 3846 round trips persecond is the PRF, 120 scan lines per imageis the line density, and 32 images per sec-ond is the frame rate. These factors alongwith the depth are all interrelated. If thedepth is decreased the PRF increases, thiscan yield either an increase in the framerate or an increase in the line density. If theline density is increased, then either thedepth or the frame rate must decrease.

Most real-time two-dimensional sectorscans are now made with phased array ratherthan mechanical transducers. A string ofcrystal elements are arranged in a row. All ofthe crystal elements transmit for each scanline. The beam is steered by changing thetiming of the excitation of the crystal ele-ments. The beam can be focused by alteringthe timing of both the excitation (transmitfocus) of the crystals and the receipt ofreturning echoes (Figure 1.4). More than

one focal zone can be employed but eachscan line must be rescanned for each addi-tional focal zone resulting in a decrease inthe number of frames that can be assembledper second.

In the digital scan converter (DSC), B-modescan lines undergo analog to digital conver-sion. Echoes are assigned numerical valuesin increasing order of intensity. The numer-ical value will determine the gray shade of apicture element (pixel) when the digitalinformation from each frame is mapped toa rectangular image. The amplitude range ofreturning echoes is on the order of 100 dB,i.e. the strongest echo is 100 000 timesstronger than the weakest. This range ofecho intensities is compressed by the DSCto fit the 30 dB dynamic range of the display.Operator selectable compression algorithmsmay be linear or logarithmic and determinethe schedule with which incoming echoesare mapped to shades of gray for display(Figure 1.5). For example, a nonlinear algo-rithm might be selected to increase the vis-ibility of weak reflectors while decreasingthe intensity of strong ones to prevent themfrom obscuring adjacent anatomy. The DSCalso fills in missing information betweenscan lines by assigning a numerical valueto what would be a black pixel (no data)based on the average values of neighbor-ing pixels: a process called interpolation.Information from frames adjacent in timecan also be averaged to provide temporalas well as spatial smoothing. The framerate is not reduced but each frame willbe made up of a variable amount of


4

A B C D

Figure 1.4 All elements in a phased array transducer are fired for each scan line. The timing of the excitation of the crystalelements determines the direction of the beam. (A) When elements on the left side of the transducer are fired first the beam isdirected to the right. (B) When fired simultaneously the beam is directed straight ahead. (C) When crystals on the right are firedfirst the beam is angled to the left. (D) Minor variations in the timing of crystal excitation focus the beam.

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information from preceding frames. Theamount of ‘old’ information is determinedby an operator-selected persistence factor.

The digital information must be con-verted back to analog form to be recordedon videotape and this results in a degreeof image degradation. Completely digitalechocardiography labs have been made pos-sible by advances in digital storage mediaand transfer speeds. Images are transferredfrom the US systems to central computers(servers) were they are archived. The imagesare not degraded by digital to analogconversion. Images are easily recalled forviewing, facilitating comparison of serialstudies on a given patient.

DOPPLER

When US strikes a moving target, such asblood moving through the heart, a smallportion of the sound will be reflected backto the transducer. The reflected sound willhave a different frequency than the trans-mitted sound. Subtracting the frequency

that leaves the transducer from the fre-quency that returns to the transducer yieldsa third frequency, a difference frequency,which is in the audible range and is pro-portional to the velocity of the movingtarget. Comparator circuits in the US systemperform these calculations. If the flow istoward the transducer the frequency shift ispositive, and if away from the transducerit is negative. The relation between thedifference frequency and the velocity of thetarget is given by the Doppler equation:

Velocity �

Propagation velocity �Doppler shift________________________

2 � transducer frequency� cos �

The propagation velocity is 1540 m/s; theDoppler shift is the difference frequencyand � (theta) is the angle between theblood flow and the US beam. When � is 0�or 180�, the cosine of � is equal to 1 anddoes not affect the relation but as the beambecomes increasingly less parallel to theflow the angle becomes increasingly impor-tant in the calculation of velocity. At 90�when the cosine of � is 0, no flow can bedetected. The best Doppler velocities areobtained when the flow is parallel to thebeam. The multiple imaging windows avail-able in cardiac scanning allow the beamto be aligned with flow and make anglecorrection for � unnecessary.

Continuous wave Doppler

Continuous wave (CW) Doppler requiresone crystal to transmit sound waves con-stantly and one crystal to receive con-stantly. CW Doppler can measure highvelocities but it samples all of the frequencyshifts along an entire line, which can bepositioned through the region of interest ofthe real-time two-dimensional image. CWDoppler is used when the highest velocitiesare of interest.

Pulsed wave Doppler

In contrast, pulsed-wave (PW) Doppler usesa single crystal, which alternately sends out

5

Compression

Echo intensity

Gra

y sh

ades

Weak Strong

Bla

ckW

hite

Figure 1.5 Echoes returning to the transducer aremapped to gray shades according to their intensities butthe relationship is determined by the operator and neednot be linear.

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US pulses and then listens for their return.The system is gated or set to listen to return-ing signals from a window in time afterthe signal is transmitted. This window oftime corresponds to a window of depth, orsample volume, so that only frequency shiftsthat arise from an operator selected regionof interest along the course of the line willbe received. PW Doppler cannot measurehigh frequency shifts resulting from highvelocity flows without ambiguity as to thedirection of flow. The maximum frequencyshift that can be measured unambiguouslyby PW Doppler is termed the Nyquist limitand is a function of the PRF.

Nyquist limit � PRF/2

Red blood cells within the sample volume(PW) or along the sample line (CW) rarelyhave a uniform velocity or direction ofmotion. Therefore, many frequency shiftsare returned to the transducer. The return-ing signal is complex and is resolved into anumber of single frequency sine waves byfast Fourier transformation (FFT). FFT resolvesthe returning Doppler shifted frequenciesinto their constituent parts and convertsthem to velocity signals that are plottedagainst time. This is known as spectraldisplay or spectral Doppler. Time is on thehorizontal axis and velocity is on thevertical axis with the zero velocity baselinein the center. Flows toward the trans-ducer (positive register) are displayed abovethe baseline and flows away from thetransducer are displayed below the baseline(negative register). Velocities are sampled at5 ms or 10 ms intervals and the resultingvelocity components are assigned to 128locations or bins along the vertical axis, 64for flow toward and 64 for flow away fromthe transducer. Gray shades give the relativeintensity of each velocity within the sam-ple. When red blood cells are moving at arelatively uniform velocity and directionthe resulting graphic (spectral envelope) isthin. Spectral broadening along the velocityaxis represents more disorganized bloodflow. Unwanted low velocity signals orig-inating from the movement of the cardiacstructures lying near the baseline can besuppressed with a high pass ‘wall filter’.

Examination of spectral Doppler waveformsgives the timing, duration, velocity, rate ofchange of velocity, and degree of turbulenceof blood flows (Figure 1.6).

PW Doppler cannot resolve velocitieswhen the Nyquist limit is exceeded. Whenthis occurs, high velocities are shown in theopposite register. An excessively high posi-tive frequency shift reflecting flow towardthe transducer will be displayed graphicallyas negative, moving away from the trans-ducer. This is termed aliasing. As theNyquist limit is equal to half the pulse


6

Figure 1.6 Continuous wave Doppler signal with thesample line through the mitral valve in a patient withmitral stenosis and regurgitation. The vertical distancebetween calibration markers (red dots) is 1 m/s and thehorizontal distance between time markers at the top ofthe spectral display is 200 ms. Velocities above thebaseline represent flow toward the transducer andvelocities below the baseline, flow away from thetransducer. The diastolic velocity signal representsantegrade flow across the mitral valve. The systolic velocitybelow the baseline represents retrograde flow. Note thatboth the systolic and diastolic signals exhibit spectralbroadening indicating turbulent blood flow.

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repetition frequency and the PRF is greaterat shallower depths, aliasing will occur athigher velocities when sampled flows areclose to the transducer. Moving the baselineup or down by assigning more velocity binsto flow toward or away from the transducerwill allow the display of higher velocity sig-nals without aliasing.

High-PRF Doppler

High-PRF Doppler allows higher velocitiesto be assessed at the expense of some ambi-guity as to their point of origin (depth ofsample). PW Doppler signal processingachieves range resolution by processing onlythose signals that return to the transducerwithin a window of time corresponding tothe depth from the transducer of thesample volume. Sound returning from twicethe depth of the sample volume initiated bythe preceding pulse is received within thesame window. If the sample volume is posi-tioned at one half of the distance from thetransducer to the true region of interest,signals from the true region of interest willbe received at double the PRF. In this waysignals from two, three or four times thedistance to the primary sample volume canbe received and analyzed but with a highPRF dependent only on the depth of theproximal sample volume. While high-PRFDoppler is occasionally useful in discrimi-nating velocities at points of interest that

are in close proximity, most flow velocitiesare better assessed using either pure PW orCW Doppler (Figure 1.7).

Blood flow velocity is always related tothe pressure difference between two points,i.e. across a valve, between two chambers oracross an obstruction to flow. Velocity isrelated to the pressure difference by themodified Bernoulli equation:

Pressure difference (mmHg) �4(velocity1

2 � velocity22)

where velocity2 is the proximal velocity andvelocity1 the distal velocity is measured inm/s. When the proximal velocity is 1 orless it can be ignored and the equationsimplifies to:

Pressure difference (mmHg) � 4(velocity2)

Intracardiac pressures can be calculatedfrom Doppler flow velocities. For example,if the peak flow velocity across a stenosedaortic valve is 5 m/s, the pressure differ-ence or gradient between the left ventricleand the aorta will be equal to 4(52) or 100mmHg. The CW Doppler peak velocity ofretrograde flow through the mitral valve insystole, representing mitral regurgitation(MR), must have a velocity that reflects thepressure difference between the left ven-tricle (approximately 100–130 mmHg) andthe left atrium (approximately 5–10 mmHg).A flow velocity of approximately 5 m/s isanticipated for MR (Figure 1.8).

7

CW

LV

LA

High-PRFPWFigure 1.7 In continuous (CW) Dopplerall of the frequency shifts along a scanline are translated into velocities fordisplay. In pulsed-wave (PW) Doppleronly those signals returning from asingle window in time after transmissionof the ultrasound that corresponds to adiscrete distance along the scan line(sample volume) are processed fordisplay. In high pulse repetitionfrequency (PRF) Doppler frequency shiftinformation from multiple samplevolumes equidistant from the transduceris assessed.

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Doppler color flow

Doppler color flow mapping allows bloodflow to be visualized in real time. An array ofhundreds of pulsed wave sample volumesare superimposed over the two-dimensionalimage. Colors are ‘painted’ or mapped intothe sample volumes along each scan lineto represent flow velocities. One standardvelocity map is known by the acronym BART(blue away, red toward) where shades of bluerepresent flow away from the transducer andshades of red represent flow toward thetransducer. Increasing intensities of bluesand reds represent increasing velocities. Ablack band represents zero flow. Turbulencecan be represented by the addition of yel-lows and greens (variance map) (Figure 1.9).

An enormous amount of Doppler infor-mation must be processed for each color-coded frame. Each scan line must besampled (pulsed) from 4 to 20 times to pro-vide color images. Increasing the number ofpulses increases the accuracy of the velocityinformation but decreases the frame rate.The number of scan lines, the depth of thescan, and the width of the color array also

determine the frame rate for Doppler colorflow imaging. Autocorrelation techniquesare used wherein each returning pulse iscompared to the preceding pulse to deter-mine blood movement between pulses.Blood flow direction, mean velocity, andvariance around the mean representingturbulence are captured from each samplevolume.


8

Figure 1.8 Peak systolic velocities of continuous waveDoppler signals through the aortic valve in a patient withaortic stenosis (AS, right panel) and through the mitralvalve in a patient with mitral regurgitation (MR, left panel)are equal at 4.5 m/s. Assuming a normal aortic systolicblood pressure of 120 mmHg systolic and a left atrialpressure of 10 mmHg the left ventricular systolic pressureis 201 mmHg for the patient with AS (120 � 81) and 101mmHg for the patient with MR (10 � 81).

Figure 1.9 A close-up view of a color Doppler variancemap. Shades of red and blue indicate flow toward andaway from the transducer, respectively, becomingprogressively brighter as flow velocity approaches theNyquist limit of 64 cm/s. A black band represents zerovelocity or no flow. Shades of yellow and green (right sideof the map) are added to each color Doppler samplevolume to represent turbulence. When the Nyquist limit isexceeded aliasing occurs. Reds become blues or bluesbecome reds.

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Color Doppler is PW Doppler and willalias when the Nyquist limit is exceeded. Incolor Doppler aliasing is seen by color rever-sal, blues turning to reds and reds turning toblues in keeping with the apparent changein flow direction seen in PW Doppler. As inspectral Doppler, baseline shift and scalecontrols are available. When the scale isreduced, low velocity flow is better appreci-ated. Color Doppler mapping can also besuperimposed on the single scan line of theM-mode display. This format has a hightemporal resolution and is valuable for theprecise timing of flow events.

In color amplitude imaging or powerDoppler the color codes for the intensity ofblood flow, i.e. the density of moving redblood cells in the sample rather than for thevelocity of blood flow. Frequency shiftinformation is not used, amplitude displaysare non-directional and aliasing does notoccur. It is sensitive to motion artifacts andits use in cardiac imaging is limited, but it iswell suited to vascular imaging.

Tissue Doppler imaging

When assessing blood flow, Doppler ultra-sound is optimized for high velocity andlow amplitude signals. To assess myocardialmotion, low velocity, high amplitude sig-nals are given preference. Tissue Dopplerimaging (TDI) measures the velocity oftissue and the timing of its motion. Spectraldisplays (PW), color M-modes and two-dimensional color maps of myocardialvelocity can be generated as well as anumber of derived graphics (Figure 1.10).Motion of the heart in systole is predomi-nantly from the base to the apex so thatvelocity signals are higher at the base andthere is a base to apex velocity gradient. Thedistance traveled by the sampled musclesegment or its displacement is obtained byintegrating the velocity waveform. The termstrain refers to the distance (D) traveledbetween two points (converging in systoleand diverging in diastole) or distancechange normalized to the initial distancebetween the two points. (strain � �D/D). Itis therefore expressed as a percentage ofthe initial distance. Strain rate is the rate of

change of strain or rate of length change.The strain rate can be calculated as:

Strain rate �

Velocity at oneposition � Velocity at a

second position––––––––––––––––––––––

Distance betweenthe two positions

Strain rate is synonymous with myocardialvelocity gradient.

Other imaging modalities

Three-dimensional echocardiographyReal-time transthoracic three-dimensionalimaging has recently emerged. Insteadof acquiring scan plans, entire three-dimensional volumes of reflected US datacan be captured and stored (Figure 1.11).Three-dimensional color Doppler imagescan also be acquired. The three-dimensionalvolumes can be viewed in real time,manipulated on the screen, rotated, slicedalong their x-, y- or z-axis or along anyuser-selected axis and viewed in real time.

Tissue characterizationThe pattern of US reflection from tissuesis a function of their material properties

9

Figure 1.10 The left panel is spectral Tissue Dopplerdisplay with the transducer at the apex. Myocardialvelocities are toward the transducer in systole and awayfrom the transducer in diastole. The right panel is colortissue Doppler imaging. The myocardium is displayed inred indicating motion away from the transducer in thisdiastolic frame.

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including: the spatial distribution of densitywithin them and the number and kind ofinterfaces between tissues with differentdensities. Some tissues have distinct acousticsignatures. Tissue characterization is anattempt to identify different types of tissueby their patterns of reflection. The unpro-cessed radio frequency of the reflected(backscattered) signal is used. The integratedbackscatter varies cyclically between systoleand diastole in normal myocardium. Thiscyclic variation is lost or muted in themuscle tissue in some disease processes.

Contrast echocardiographyThe blood pools can be opacified by theinjection of a contrast agent. Microbubbleswill form in a saline solution agitated with asmall amount of air. These microbubbles arestrong reflectors of ultrasound. When thissolution is injected into a peripheral veinduring an ultrasound examination it opaci-

fies the right heart chambers with echoes.This technique is often used to identifyintracardiac shunts (Figure 1.12). It can alsoaid in the CW Doppler interrogation oftricuspid regurgitation, enhancing signalsfrom small regurgitant jets. Microbubblesmanufactured with human serum albuminor perfluorocarbons are available that aresmall enough to transit the pulmonarycapillaries. A peripheral injection of theseagents will cause first the right heart cham-bers and then the left heart chambers tobe opacified (Figure 1.13). These contrastagents improve LV endocardial definition.Myocardial opacification can be achievedwith these agents when either injected intoa peripheral vein or directly into a coro-nary artery to assess myocardial perfusion(Figure 1.14).

Modern transducers transmit a broadrange of frequencies. The operator canimage at 2.25 MHz for a large patient or


10

Figure 1.11 An apical four-chamber slice through athree-dimensional volume. The three-dimensional volumecan be sliced along the x-, y- or z-axis or any user selectedaxis and viewed in real time. There is a catheter (arrow) inthe left ventricle (LV) (RV, right ventricle; RA, right atrium;LA, left atrium).

Figure 1.12 An intravenous contrast injection has causedopacification of the right heart chambers and somecontrast material is seen in the left atrium and ventricle.The immediate appearance of ‘bubbles’ on the left side ofthe heart indicates an intracardiac shunt (RV, rightventricle; RA, right atrium).

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3.5 MHz for a smaller patient with the sametransducer. These broadband transducershave led to the introduction of harmonicimaging. For example, a transmitted fre-quency of 2 MHz would cause a harmonicfrequency of 4 MHz to be received. Byimaging with a low transmitted frequencyand receiving at double the transmittedfrequency, penetration is enhanced andnoise is reduced. Harmonic imaging isprincipally a noise reduction technique andmay result in loss of signal and shadowingin the periphery of the image.

11

Figure 1.13 Manufactured microbubbles when injected into a peripheral vein opacify the right heart chambers and thentransit the pulmonary circulation to opacify the left heart (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, leftatrium).

Figure 1.14 A modified four-chamber view in an ovinemyocardial infarction model. Contrast material wasinjected directly into the left main coronary artery. Thereflectivity of normally perfused myocardium (circled inyellow) is enhanced. Non-perfused muscle (circled in red)is not (LV, left ventricle; LA, left atrium; AO, aorta).

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This chapter will describe a method of per-forming a complete tranthoracic echocar-diographic examination, which integratesM-mode, two-dimensional imaging, andDoppler for each acoustic window. Alltechnologists should follow a systematicprotocol so that no important informationis omitted. After the patient is greeted andthe test explained, a brief history should beobtained before beginning the examina-tion. This will help keep the examinationfocused on relevant clinical issues.

ANATOMY

The acoustic windows through whichsound can propagate are located along theleft sternal edge (parasternal), at the apex,inferior and lateral to the point of maxi-mum impulse (PMI), inferior to the xiphoidprocess (subcostal), at the supersternalnotch, and at the upper right sternal edge.The left supraclavicular fossa is also usefulfor imaging the superior vena cava and adja-cent structures. The tomographic anatomyand Doppler flow signals that can beobtained from each window are describedin detail below. Thorough knowledge of theinstrumentation of the ultrasound systemused is required but careful attention mustbe paid to patient positioning to optimizeimaging and Doppler signals.

The heart, including the proximal greatvessels, is almost completely surrounded bythe bones of the thoracic cage and thelungs. Ultrasound is absorbed by bone andscattered by the air in the lungs. It is moretechnically difficult to obtain optimalimages in elderly patients with calcificationof the costochondral junctions, and inpatients with obstructive pulmonary dis-ease and hyperinflated lungs. In thinpatients the heart may be retrosternal anddifficult to image.

The long axis of the heart extends fromthe PMI (which can be palpated at the fifthor sixth left intercostal space between themidclavicular and anterior axillary line) toa point on the middle of the right clavicle,so that the interatrial and interventricu-lar septa are oriented along a line that isapproximately 30–45� from the sagittalplane. The right ventricle (RV) is anterior tothe left ventricle (LV) and the right atrium(RA) and RV inflow tract are predominantlyretrosternal.

THE PARASTERNAL WINDOW

For parasternal imaging the recumbentpatient is placed in the full left lateral decu-bitus position to allow the heart to hangdown from behind the sternum as much aspossible, bring the apex closer to the chest

THE NORMAL DOPPLERECHOCARDIOGRAPHIC EXAMINATION

CONTENTS ● Anatomy ● The Parasternal Window ● The Apical Window ● The SubcostalWindow ● The Suprasternal Notch Views ● The Right Parasternal Transducer Position

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wall, and increase the size of the window.The head is elevated 30� to lower thediaphragm. Patients are instructed to placetheir left arm above the head and put theirshoulders back to open up the intercostalspaces. Electrocardiographic (EKG) leads areattached and the signal is adjusted to obtainan upright QRS complex. A pillow for thepatient’s head is essential.

The long axis view

The transducer is oriented along the longaxis of the heart from the right shoulder tothe left flank. The transducer is in approxi-mately the third or fourth intercostal spaceclose to the left sternal edge. Held expira-tion enlarges the size of the parasternalwindow. The long axis (LAX) image is opti-mized so that the interventricular septum(IVS) is horizontal on the screen with theapex at the left (Figure 2.1). If the IVS anglesup from the right of the screen to the left,then a higher intercostal space should besought. Moving the transducer closer to thesternum and turning the patient to a morelateral position helps display the IVS in ahorizontal orientation.

Both leaflets of the mitral valve (MV) andtwo cusps of the aortic valve (AOV) are dis-

played. The right coronary cusp of the AOVis seen in the anterior aortic root and it isusually the noncoronary cusp that is seen inthe posterior aortic root. The left ventricularwalls seen in this view are the posterior walland the anterior IVS. The RV outflow tractcrosses the LV outflow tract anteriorly.

The coronary sinus is often visualized as asmall circular structure in the posterior atrio-ventricular sulcus. The sinuses of Valsalvain the aortic root and their terminationat the sinotubular junction can be seen.The descending thoracic aorta is locatedbehind the left atrium (LA), superior to theatrioventricular (AV) groove (Figure 2.2).

M-mode anatomy

The M-mode cursor is first positionedthrough the aorta and LA (Figure 2.3). M-modes are a graphic representation indepth of penetration versus time of thestructures sampled along the scan line. Theanterior and posterior walls of the aortamove anteriorly in systole as the LA fills.The AOV cusps separate in early systole,stay apart through ejection and come backtogether forming a box within the aorta.When closed, the AOV leaflets are visual-ized as a line in the middle of the aorta.

Figure 2.1 Parasternal long axis view from a normal subject (RVOT, right ventricular outflow tract; AO, aorta; LV, leftventricle; LA, left atrium).

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THE NORMAL DOPPLER ECHOCARDIOGRAPHIC EXAMINATION

The aortic root diameter is measured at theAOV opening and the LA size is measuredat its maximum (late systole).

The M-mode cursor is next directedthrough the MV leaflets (Figure 2.4). At theD point the anterior and posterior leafletsseparate. They are farthest apart at the Epoint and partially closed at the F point.The MV leaflets separate again with atrialcontraction. The A point is the second pos-itive peak. At the C point the MV is closed.

The M-mode cursor is then directedthrough the LV just below (apical to) thetips of the MV leaflets (Figure 2.5). Thebeam first passes through the RV outflowtract then the IVS, LV cavity, and thenLV posterior wall. RV free wall thicknessusually cannot be measured, as the RV epi-cardium is too close to the transducer. TheLV posterior wall endocardial reflection isidentified as the line with the most rapidrise in systole, and usually shows a presys-tolic dip caused by atrial contraction. Theposterior wall epicardial interface can beidentified in systole when there is normally

a slight separation between the visceral andparietal layers of the pericardium. The peri-cardium is a good reflector of ultrasound andwill be the last remaining echo when thegain is decreased. Measurements are made atend-diastole, which is defined as the peak ofthe QRS complex and at end-systole definedas the point of maximum posterior excur-sion of the left side of the IVS. By conven-tion, measurements of the LV cavity aremade from the leading edge of the leftseptal endocardial reflection to the leadingedge of the posterior LV wall endocardium(Table 2.1).

The RA/RV view or RV inflow tract view

The anterior tricuspid valve leaflet is thelargest and most excursive and divides the

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Figure 2.2 Parasternal long axis view in early diastole.The black arrow indicates the coronary sinus (RV, rightventricle; AO, aorta; LV, left ventricle; LA, left atrium; Dao,descending aorta).

Figure 2.3 M-mode echocardiogram showing the aortaand left atrium. Separation of the right and noncoronarycusps of the aortic valve forms the box-like pattern withinthe aorta in systole. The aortic valve closure line is seen asa horizontal stripe in the center of the aorta. The verticaldistance between depth markers (red dots) is 1 cm anddepth markers are generated at 1 s intervals (RVOT, rightventricular outflow tract; AO, aorta; AOV, aortic valve; LA,left atrium).

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RV into inflow and outflow tracts. Twoleaflets of the tricuspid valve (TV), the RA,and a variable amount of the RV are visual-ized in the RA/RV view or RV inflow tractview (Figure 2.6). This is the only view thatroutinely shows the posterior leaflet of theTV. The coronary sinus can often be seenentering the RA in this view. From the LAXplane the transducer is rotated 10–15� coun-terclockwise and angled inferiorly andmedially to show the RV inflow tract. It is

often helpful to move the transducer to alower intercostal space to obtain this view.This positions the RV inflow nearly parallelto the beam and is especially useful forevaluating tricuspid regurgitation (TR). TRappears as a color Doppler flow disturbancein the RA in systole (Figure 2.7). The sever-ity of the TR is approximately proportionalto the spatial extent of the color distur-bance. If TR is seen with color Doppler, thecontinuous wave (CW) Doppler sample lineis aligned through the direction of flow ofthe color signal (Figure 2.8). The maximumvelocity of the TR signal on the CW spectraldisplay is related to the maximum pressuredifference between the RV and the RA insystole by the modified Bernoulli formula:

Pressure difference � 4 � (peak velocity2)

For example, a velocity of 2.5 m/s representsa pressure difference of 25 mmHg betweenthe RV and the RA in systole.

Normal antegrade flow through the TV indiastole is biphasic, low velocity, and oftenrespiro-phasic. Early diastolic filling velocityrises to an E point, filling slows in mid-diastole and then reaches a second peak, theA point caused by atrial contraction. The Ewave is always higher in normal subjects.

The long axis of the RV outflow tractand pulmonary artery can be visualized byrotating the transducer about 20� clockwise


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Left ventricular internal end-diastolicdimension (LVIDd) 4.8 � 0.4

Left ventricular internal end-systolicdimension (LVIDs) 3.0 � 0.4

Interventricular septal thickness atend-diastole (IVSTd) 0.9 � 0.2

Interventricular septal thickness atend-systole (IVSTs) 1.3 � 0.2

Posterior wall thickness at end-diastole(PWTd) 0.8 � 0.1

Posterior wall thickness at end-systole(PWTs) 1.3 � 0.2

Left atrium (LA) 3.3 � 0.5Aorta (AO) 2.9 � 0.4

The normal range for the percent change in LV diameter is

28–41%.

Table 2.1 Normal M-mode values in cm (mean � SD)

Figure 2.4 M-mode echocardiogram of the mitral valve.Mitral valve D, E, F, A, and C points are labeled on thesecond cycle (see text) (RV, right ventricle; LV, left ventricle;MV, mitral valve).

Figure 2.5 M-mode echocardiogram of the left ventricleat the tips of the mitral valve (RV, right ventricle; LV leftventricle).

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Figure 2.6 Right ventricular inflow tract or RA/RV view. The anterior and posterior tricuspid valve leaflets are visualized. Theupward pointing arrow indicates a Chiari network, the downward pointing arrow indicates the thebesian valve, which is rarelyseen, at the mouth of the coronary sinus (RV, right ventricle; RA, right atrium; CS, coronary sinus).

Figure 2.7 Right ventricular inflow tract or RA/RV viewwith color flow Doppler mapping in systole demonstratingmild tricuspid regurgitation as a blue signal in the rightatrium. Mild tricuspid regurgitation is often seen innormal subjects (RV, right ventricle; LV, left ventricle; RA,right atrium).

Figure 2.8 Continuous wave Doppler signal of tricuspidregurgitation with a peak velocity of 3 m/s representinga right ventricle to right atrial pressure gradient of36 mmHg. The vertical distance between calibrationmarkers is 1 m/s.

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from the parasternal LAX of the LV andangling superiorly and to the left (Figure2.9).

The short axis view

From the LAX the transducer is next turned90� clockwise into short axis (SAX) orienta-tion. The plane extends from the patient’sright flank to the left shoulder. Transducer

position and angulation are kept constantwhile the transducer is rotated. If the LAXview displayed the IVS as horizontal then inthe SAX view it will be round. SAX imagingis begun in the intercostal space in whichthe MV is seen with the transducer mostperpendicular to the chest wall (Figure 2.10).In SAX the LV cavity is round and the walls,which are uniformly thick, move inward asthey thicken symmetrically in systole. The


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Figure 2.9 A parasternal long axis view of the right ventricular outflow tract (RVOT) and pulmonary artery (PA). The pulmonicvalve is indicated by an arrow (LV, left ventricle).

Figure 2.10 A parasternal short axis view at the level of the mitral valve. The mitral valve is open in the early diastolic panelon the right taken at the time of the E point of the mitral valve M-mode and closed in the systolic panel on the right (RV, rightventricle; LV, left ventricle).

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beam must not be allowed to wander superi-orly into the left atrium in systole. This cancause the false appearance of a posterior wallmotion abnormality. The anterior MV leafletopens toward the anterior IVS and dividesthe LV into inflow and outflow portions.

The anterior and posterior IV sulci arelocated where the RV free wall meets the LVfree wall. The transducer is angled slightlyand slowly to the apex. SAX images at thelevel of the high papillary muscles (Figure2.11) and then the low papillary muscles arerecorded. The papillary muscles should bepositioned symmetrically within the circularLV cavity, the posteromedial papillary mus-cle is at about 8 o’clock and the anterolateralpapillary muscle at 4 o’clock. LV wall motionand thickening should be uniform. The wallsegments are in clockwise order from theanterior IV sulcus, designated as: anterior,lateral, posterior, inferior, posterior septal,and anterior septal (Figure 2.12).

The transducer is now angled backthrough the SAX of the MV and upward tothe right shoulder to obtain a SAX at thebase of the heart showing the aorta in circu-lar cross-section with the LA posterior(Figure 2.13). Slight clockwise rotation ofthe transducer frequently brings the wing-shaped left atrial appendage (LAA) into view.From the SAX at AOV level, moving thetransducer 1 cm lateral and angling medially

helps to visualize the AOV leaflets. The rightcoronary cusp is anterior, the left coronarycusp is posterior and to the right of theimage and the noncoronary cusp is posteriorand to the left. The commissure betweenthe right and left coronary cusps marks the

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Figure 2.11 A parasternal short axis view at the high papillary muscle level (RV, right ventricle; LV, left ventricle).

Figure 2.12 Anatomic preparation sliced in short axis atthe level of the papillary muscles. Color coded wallsegments are in clockwise order from the anteriorinterventricular sulcus (the junction of the right ventricularand left ventricular free walls anteriorly): anterior (Ant.),lateral (Lat.), posterior (Post.), inferior (Inf.), posteriorseptal (PS), and anterior septal (AS).

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insertion point of the right pulmonic valvecusp and the commissure between theright and noncoronary cusps marks theinsertion of the septal leaflet of the tri-cuspid valve. The intra-atrial septum arisesfrom the midpoint of the noncoronarycusp.

The transducer often fits into the inter-costal spaces in short axis better than inlong axis because of its shape. If so, it can bemanipulated closer to the sternum, allowingfor a better M-mode sweep.

Angling the transducer up and to the leftshoulder slightly from the SAX of the AO


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Figure 2.13 A parasternal short axis view at the level of the aortic valve (AOV) and left atrium (LA). The three leaflets of theaortic valve, the right (R), left (L) and noncoronary (N) are seen. The left atrial appendage (LAA) is a wing-like extension of theleft atrium (LA) (RV, right ventricle; RA, right atrium; PA, pulmonary artery).

Figure 2.14 A parasternal short axis view at the base of the heart demonstrating the pulmonary artery from the pulmonicvalve (arrow) to the bifurcation (RV, right ventricle; AO, aorta; PA, pulmonary artery; Dao, descending aorta).

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and LA, with an approximate 5–10� clock-wise rotation optimizes the pulmonaryartery, which can often be visualizedbeyond its bifurcation into right and leftbranches (Figure 2.14). The PW Dopplersample volume is positioned just proximal

to the pulmonic valve and the spectral dis-play is obtained. A thin envelope indicatinglaminar flow is displayed (Figure 2.15).Normal transpulmonic maximum systolicflow velocity is between 0.5 m/s and 0.9 m/s.RV stroke volume can be estimated usingthe diameter of the RV outflow tract andthe flow velocity integral (FVI) of the RVoutflow tract systolic flow taken at the samespot. The area under the curve of the RVoutflow tract systolic flow (FVI) is multi-plied by the cross-sectional area of thevessel obtained using the formula:

Area � p (diameter/2)2

A minor amount of pulmonary insuffi-ciency (PI) is often present in normal sub-jects and can be seen by color Doppler as asmall candle flame in the RV outflow tractin diastole. When PI is detected by colorflow mapping a pulsed-wave (PW) Dopplersample is positioned within the color dis-turbance and a spectral display is obtained(Figure 2.16). The velocity of the spectralsignal of PI reflects the pressure differencebetween the PA and the RV in diastole. CWDoppler is rarely required to visualize the

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Figure 2.15 Pulsed-wave Doppler signal with the samplevolume positioned in the right ventricular outflow tractjust proximal to the pulmonic valve. The vertical distancebetween the calibration markers is 0.2 m/s.

Figure 2.16 (A) A parasternal short axis view at the level of the aortic valve (AOV) and left atrium (LA) with color flow Dopplerdemonstrating mild pulmonic insufficiency (PI) as a small color signal in the right ventricular outflow tract in diastole (RV, rightventricle; RA, right atrium; PA, pulmonary artery). (B) Pulsed-wave Doppler signal demonstrating systolic forward flow (downfrom the baseline) and PI (up from the baseline).

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peak flow velocity of PI even in the pres-ence of pulmonary hypertension becausethis signal is close to the transducer, thepulse repetition frequency (PRF) is high andaliasing only occurs at high velocity.

The M-mode cursor can be positionedthrough the right cusp of the pulmonicvalve, systolic opening is away from thetransducer. A presystolic dip caused by atrialcontraction is seen in normal subjects.

THE APICAL WINDOW

From a SAX parasternal position the trans-ducer is moved inferiorly and laterally tobeyond the point of maximal impulseand angled to the patient’s right shoulderto obtain an apical four-chamber view(Figure 2.17).

The left heart chambers are on the rightof the screen and the right heart chambersare on the left. The atria are in the far field.The patient is in full left lateral decubitusposition but may be turned back to theright slightly to accommodate the trans-

ducer between the patient and the bed. Ifthe four-chamber image appears to be tooround then the transducer should be movedlower on the chest. If the ventricles are fore-shortened, the apical myocardium will notbe seen and wall motion at the apex will beoverestimated. If the IVS angles up to theright of the screen then the transducershould be moved laterally until the IVS isvertically oriented in the middle of thesector. It is often desirable to move thetransducer even lower and more lateralthan the perceived apical window andhave the patient hold their breath at end-inspiration. This lowers the diaphragm andbrings the heart into the ultrasound beamallowing visualization of the full length ofthe ventricles.

The RV is more heavily trabeculated thanthe LV and a prominent linear structure, themoderator band, is seen angling across theRV cavity from a point on the right side ofthe IVS one-third of the distance from theapex to the apical RV free wall. Three of thefour pulmonary veins are often seen enter-ing the LA. They are in counterclockwiseorder from the lower left: the right superior,


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Figure 2.17 Apical four-chamber view. The posterior interventricular septum and lateral wall of the left ventricle (LV) areseen in this view (RV, right ventricle; RA, right atrium; LA, left atrium).

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the left superior, and the left inferior pul-monary veins (Figure 2.18). Slight anteriorangulation (elevation) of the transducer(about 5�) shows the aorta exiting the LV.This is termed the five-chamber view(Figure 2.19). Occasionally, even more ante-rior angulation will demonstrate the PAleaving the RV. Posterior angulation oftenshows the coronary sinus in the posterioratrioventricular sulcus.

The LV lateral wall and posterior septumare seen in the four-chamber view with theanterolateral papillary muscle within theLV cavity. Segmental wall motion can beassessed and should appear symmetrical.The insertion of the TV into the IVS isslightly more apical than that of the MV.The chordae tendinea originate from the

tips of each papillary muscle and insert intothe overlying commissure and into bothleaflets of the MV. No chordae originatefrom the septum and connect to the MVbut the septal leaflet of the TV has chordalconnections to the right IVS.

The ultrasound beam is parallel to bloodflow entering the LV and RV, and also theLA. The apical four-chamber view is idealfor Doppler interrogation of the mitral andtricuspid valves. Color flow mapping of theatria is used to detect and semiquantify MRand TR in systole, the spatial extent of theturbulent color disturbance approximatesthe severity of regurgitation (Figure 2.20).The transducer must be swept through theorthogonal plane not to miss or underesti-mate these flow disturbances. When MR or

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Figure 2.18 Apical four-chamber view in systole showingthe entrance of three of the four pulmonary veins into theleft atrium (LA). They are: 1, the right superior vein, 2, theleft superior vein, and 3, the left inferior pulmonary vein(RV, right ventricle; LV, left ventricle; RA, right atrium; LA,left atrium).

Figure 2.19 The apical five-chamber view is obtained byangling the scan plane anteriorly from the apical four-chamber view (RV, right ventricle; LV, left ventricle; RA,right atrium; LA, left atrium; AO, aorta).

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TR is present CW Doppler is used to obtainspectral waveforms of these signals (Figure2.21). The maximum velocity of the CW TRsignal reflects the pressure differencebetween the RV and RA in systole. RA pres-sure can be estimated and when added tothe RV � RA pressure difference gives theRV pressure in systole. In the absence ofpulmonic stenosis, the RV systolic pressureis equal to the pulmonary artery systolicpressure (PASP). The peak velocity of theMR tracing gives the LV � LA pressuregradient in systole.

If the CW signal of TR is obtained fromboth the RA/RV view and the apical four-chamber view the highest velocity is used toestimate PASP. Flow velocity can be under-estimated if the beam is not parallel to theflow but it cannot be overestimated.

Diastolic transmitral flow is easily assessedfrom the apical four-chamber view andreflects the biphasic nature of LV filling.

When LA pressure exceeds LV pressure, theMV opens and early blood flow velocityreaches a peak at the E point. In mid-diastoleflow and flow velocity approach zero innormal subjects with slow heart rates. Thesecond peak of the LV filling waveform iscaused by atrial contraction and is maxi-mum at the A point. The E wave is higherthan the A wave in young to middle agednormal subjects (Figure 2.22).

Flow from the pulmonary veins to the LAoccurs in systole when the base of the heartcontracts toward the apex and in diastolewith MV opening. The PW spectral Doppler


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Figure 2.20 An apical four-chamber view demonstratingthe approximate spatial extent of color disturbances ofmitral and tricuspid regurgitation for each grade ofseverity (RV, right ventricle; LV, left ventricle).

Figure 2.21 Continuous wave Doppler signal of mitralregurgitation with a peak velocity of approximately 4.5 m/sindicating a peak systolic left ventricular/left atrialpressure gradient of 81 mmHg.

Figure 2.22 Pulsed-wave Doppler with the samplevolume positioned at the tips of the mitral valve leaflets.The vertical distance between calibration markers is0.5 m/s.

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display of flow in the pulmonary veinstherefore shows two principal waves (Figure2.23). The systolic wave is often biphasicand its two peaks are designated S1 and S2.The systole peak flow is normally higherthan the diastolic. Atrial contraction causesa small retrograde flow.

With the transducer angled up to thefive-chamber view the PW Doppler samplevolume is positioned just proximal to theaortic cusps and a thin systolic envelope

representing laminar flow out of the LV isobtained (Figure 2.24). The maximal flowvelocity and especially the area under the LVoutflow tract flow tracing are proportionalto the LV stroke volume. The area under thecurve is the FVI or stroke distance and ismeasured in centimeters. Stroke volume isestimated by multiplying the FVI by thecross-sectional area of the LV outflow tract.The cross-sectional area is obtained frommeasuring the LV outflow tract diameter in

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Figure 2.23 Pulsed-wave Doppler signal obtained withthe sample volume positioned within the right superiorpulmonary vein. S (systolic), D (diastolic) and A (atrialcontraction) waves are labeled. The vertical distancebetween calibration markers is 0.2 m/s.

Figure 2.24 Pulsed-wave Doppler signal with the samplevolume in the left ventricular outflow tract approximately0.5 cm proximal to the aortic valve. The vertical distancebetween the calibration markers is 0.2 m/s.

IVCT

LVET

LVOT

MR

AO

LV

LA

DFT

IVRT

1

2

3

4

5

120

80

Pre

ssur

e (m

mH

g)Ve

loci

ty (m

/s)

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Figure 2.25 A graphic representation of the temporalrelation between mitral regurgitation (MR) and leftventricular outflow (LVOT). The MR signal exists when LVpressure exceeds left atrial (LA) pressure while LV forwardflow occurs when LV pressure exceeds aortic pressure. Thedifference is the isovolumic contraction time (IVCT) as LVpressure rises and the isovolumic relaxation time (IVRT) asLV pressure falls (LVET, left ventricular ejection time; DFT,diastolic filling time).

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the parasternal LAX and assuming a circularcross-section using the formula:

Area � p (diameter/2)2

The LV outflow tract diameter is measuredby two-dimensional echo in the parasternalLAX as the length of a line drawn betweenthe insertion points of the right and non-coronary cusps of the aortic valve in earlysystole. Note that any errors made in meas-uring the outflow tract diameters aresquared in the area formula.

The isovolumic contraction (IVCT) andrelaxation times (IVRT) can be estimated bycomparing MR duration with LV outflowtract flow duration. MR begins when LVpressure exceeds LA pressure but LV forwardflow cannot begin until LV pressure exceedsaortic pressure. The difference is the IVCTperiod. Similarly, LV forward flow ends ataortic valve closure when aortic pressureexceeds LV pressure but MR does not end

until LA pressure exceeds LV pressure at thetime of MV opening. The difference in timebetween the two events is the IVRT (Figure2.25). IVCT and IVRT can be directly meas-ured when the PW sample volume is posi-tioned between the LV inflow and outflowtracts so that the signals of each can be seen.

The apical long axis view

The apical LAX view is obtained with90–120� counterclockwise rotation from theapical four-chamber view. Transducer posi-tion and angulation are held constant. Theanatomy visualized in this plane is identicalto that seen in parasternal LAX (Figure 2.26).The posterior wall of the LV and the anteriorIVS are seen in this view. The aortic valveand RV outflow tract are also seen. Theirpresence indicates that this plane encoun-ters the SAX plane along its 12 o’clock to6 o’clock axis.


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Figure 2.26 Apical long axis or apical three-chambered view. The anterior septum and posterior left ventricular (LV) walls areseen in this view. This plane is identical to the parasternal long axis view (LV, left ventricle; LA, left atrium; AO, aorta).

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The apical two-chamber view

This view is obtained with clockwise rota-tion from the apical LAX or counterclock-wise rotation from the apical four-chamberview (Figure 2.27). The anterior and inferiorLV walls are seen in this view. This view isdistinguished from the apical LAX in thatno part of the RV or IVS is visualized. Theapical two-chamber view intersects theclock face of the SAX at about 2 o’clock and8 o’clock (Figure 2.28). A portion of thedescending thoracic aorta can be seen withmedial and inferior angulation of thetransducer from this view (Figure 2.29).

The apical short axis view

This is a SAX view of the tip of the LV (i.e.below the papillary muscles). It is obtainedby bringing the transducer to the SAX orien-tation while at the apical imaging windowand then moving up an intercostal space ortwo. The LV appears circular and a smallcrescent of the RV cavity may also be seen

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Figure 2.27 Apical two-chamber view. The anterior and inferior left ventricular (LV) walls are seen in this view (LA, leftatrium).

Apical

MiddlePS

PS

AS

AS

AS

P

P

P

I

I

A

A

L

L

Basal

Figure 2.28 Diagrammatic representation of the relationof the parasternal and apical scan planes. The apical longaxis plane intersects the parasternal short axis plane at the12 o’clock and 6 o’clock positions, the apical two-chamberplane at the 2 o’clock and 8 o’clock position and the apicalfour-chamber plane at the 4 o’clock and 10 o’clockpositions (A, anterior; L, lateral; P, posterior; I, inferior; PS,posteroseptal; AS, anteroseptal).

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(Figure 2.30). The depth, focus, and gainshould be adjusted to optimize the nearfield of the image and a higher transducerfrequency can be used.

THE SUBCOSTAL WINDOW

The patient is turned to the supine positionand asked to bend the knees to help to relaxthe abdominal muscles. The head of thebed is lowered so that the patient maylie flat. The subcostal four-chamber view isobtained with the transducer at either theright or left subcostal margin immediatelybelow the xiphoid process and angled par-allel to the sternum. The depth may haveto be increased. Held inspiration usuallyhelps the image quality by lowering thediaphragm and bringing the heart closer tothe transducer. The plane of the subcostalfour-chamber view is identical to the apicalfour-chamber view except that the fulllength of the ventricles is not usually appre-ciated. The apex points to the right of thescreen. The RV free wall, IVS and inter-atrial septum (IAS) are now nearly perpen-dicular to the beam. The thickness of the RVfree wall is best evaluated from this view(Figure 2.31). Angling the transducer to thepatient’s right and somewhat posteriorlywill show the IVC and middle hepatic vein(MHV) (Figure 2.32). The MHV is verticallyoriented and well situated for PW Dopplerinterrogation (Figure 2.33). Systolic flowinto the RA is predominant as the base ofthe heart moves toward the apex. A second


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Figure 2.29 Inferior and medial angulation of thetransducer from the apical two-chamber viewdemonstrates a portion of the descending thoracic aorta(Dao) (LV, left ventricle; LA, left atrium).

Figure 2.30 A short axis near the cardiac apex. The arrow indicates a trabeculation crossing the LV cavity (LV, left ventricle;RV, right ventricle).

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Figure 2.31 Subcostal four-chamber view. The anatomy sampled in this view is identical to that seen in the apical four-chamber view except that the apex is generally not seen in the subcostal four-chamber view (RV, right ventricle; LV, leftventricle; RA, right atrium; LA, left atrium).

Figure 2.32 On angling the transducer to the patient’sright from a subcostal four-chamber view the inferior venacava (IVC) and middle hepatic vein (MHV) are visualized(RA, right atrium).

Figure 2.33 Pulsed-wave Doppler signal with the samplevolume positioned in the middle hepatic vein. Flow intothe inferior vena cava and right atrium is biphasic with apredominant systolic wave and a diastolic wave. There is asmall retrograde wave caused by atrial contraction. Thevertical distance between the calibration markers is 0.2 m/s.

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wave during diastole occurs with tricuspidvalve opening. Flow ceases or is reversedwith atrial contraction. Severe TR causessystolic flow reversal. RA pressure can beestimated by examining the IVC (Table 2.2).

The transducer is then rotated 90� coun-terclockwise and angled laterally to obtainSAX images of the LV (Figure 2.34). As thetransducer is angled toward the midline,

the SAX of first the MV and then the basalstructures is brought into view (Figure 2.35).The AOV can often be visualized in SAX.The subcostal sweep is identical to theparasternal SAX sweep except that theimages are rotated about 30� clockwise inthe subcostal window. Flow across the pul-monic valve into the main PA is parallel tothe beam, so this imaging plane is good forthe Doppler evaluation of pulmonary valvu-lar stenosis and regurgitation (Figure 2.36).The infundibulum is at a better angle to thebeam than it is in the parasternal projectionmaking this view ideal for the detectionand evaluation of pulmonic subvalvularobstruction. Directing the transducer to thepatient’s left permits visualization of thedistal descending thoracic and proximalabdominal aorta.

Caudal angulation of the transducershows the IVC and aorta in cross-section.The aorta is to the right of the screen (thepatient’s left) and is usually rounder thenthe IVC (Figure 2.37). When in doubt, theycan be distinguished by their Doppler flowpatterns.


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RAP

Small IVC (�1.5 cm) with �50%inspiratory collapse 0–5 mmHg

Nl IVC size (1.5–2.5 cm) with �50%inspiratory collapse 5–10 mmHg

Nl IVC size (1.5–2.5 cm) with �50%inspiratory collapse 10–15 mmHg

IVC is dilated (�2.5 cm) with noinspiratory collapse 15–20 mmHg

Table 2.2 Right-atrial pressure (RAP) estimated byinspection of the inferior vena cava (IVC)

Figure 2.34 Subcostal short axis at the level of the papillary muscles (RV, right ventricle; LV, left ventricle).

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THE SUPRASTERNAL NOTCH VIEWS

Still remaining in the supine position, thepatient is asked to hyperextend their neck.A pillow under the shoulders may facilitatethis. The transducer is positioned in thesuprasternal notch and angled caudally. Thebeam is angled at 50–60� to the coronalplane to show the aorta in its long axis(Figure 2.38). The ascending aorta is on theleft of the screen, transverse aorta is in thenear field and the proximal descendingaorta is on the right. The origins of thebrachiocephalic vessels are also seen arisingfrom the superior aspect of the transverseaorta. They are from proximal to distal: theinnominate, the left common carotid, andleft subclavian arteries. The ascending aortais anterior to the descending aorta and is onthe right of the spine and the descendingaorta is to the left of the spine. Flow towardthe transducer in the ascending aorta andflow away from the transducer in thedescending aorta can be assessed by PW, CW,and color Doppler. Color Doppler shows redflow in the ascending aorta and the blueflow in the descending aorta. These flowsare separated by a band without color at

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Figure 2.35 (A) Subcostal short axis at the base of the heart. (B) The inferior vena cava (IVC) and superior vena cava (SVC) areseen entering the right atrium (RA). The SVC is not routinely seen from the subcostal view (RV, right ventricle; LA, left atrium;AO, aorta; PA, pulmonary artery).

Figure 2.36 Subcostal short axis view at the base of theheart. The bifurcation of the pulmonary artery (PA) is seen(RV, right ventricle; LA, left atrium; RA, right atrium;R, right pulmonary artery; L, left pulmonary artery).

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12 o’clock where the flow is perpendicularto the transducer. The aorta arches over theright PA whereas the brachiocephalic orinnominate vein is anterior to the aorticarch. Inferior to the right PA in this projec-tion is the LA. Posterior angulation of thetransducer in a more coronal orientationcan sometimes, more often in children,allow visualization of the pulmonary veinsentering the LA transversely, one at eachcorner. The left pulmonary veins are on theleft and the superior pulmonary veins arecloser to the right PA. This projection isknown as the ‘crab’ view.

The suprasternal notch view is useful forCW evaluation of transaortic flow in aorticstenosis and is the only view that permitsDoppler evaluation of flow across a coarcta-tion of the aorta. Coarctation of the aortausually occurs distal to the origin of the leftsubclavian artery at the site of the ligmen-tum arteriosum. A 90� counterclockwiserotation of the transducer displays thetransverse aorta in circular section with theright PA beneath its long axis. In somepatients, particularly in those with congen-ital abnormalities, the ascending aorta is tothe left of the spine and the descendingaorta is on the right. This is a right aorticarch. The technologist must be aware of


32

Figure 2.37 (A) The abdominal aorta (Dao) is seen in its long axis. Two arteries are seen arising from the anterior surface ofthe Dao. They are the celiac trunk (1) and the superior mesenteric artery (2). (B) The abdominal aorta and inferior vena cava(IVC) are seen in short axis.

Figure 2.38 Suprasternal notch view with the aorta inlong axis. The brachiocephalic vessels arising from thesuperior aspect of the transverse aorta (Tao) are fromproximal to distal: the innominate (a), the left commoncarotid (b), and the left subclavian (c). The ascending aortais not well seen (Dao, descending aorta).

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the transducer orientation and note thiscondition, as it will not be revealed by therecorded images.

Placing the transducer in the left supra-clavicular fossa and angling the beam paral-lel to the spine shows the superior venacava in its long axis (Figure 2.39). It cansometimes be followed to its junction withthe RA. The PW Doppler flow pattern issimilar to that seen when the sample volumeis in the MHV.

THE RIGHT PARASTERNAL TRANSDUCERPOSITION

This window is important in the evaluationof the aortic valve and ascending aorta. It isfrequently advantageous in evaluating the

Interatrial Septum (IAS) and should be con-sidered in all patients when left parasternalimages are suboptimal. The patient isdirected to turn into a full right lateral decu-bitus position with the right arm placedabove the head and the head of the examtable elevated 30�. With the transducer atthe upper right sternal edge, a LAX view ofthe ascending aorta from the AOV to theright PA is obtained (Figure 2.40). This is anextension of the left parasternal LAX view.The higher the intercostal space the morevertically oriented is the ascending aorta.Flow through the AOV can be aligned withthe beam and this view is indispensable inthe Doppler evaluation of aortic stenosisespecially in elderly patients in whom theaorta is unfolded.

Rotation of the transducer 90� clockwisegives a SAX through the base of the heart. Itis occasionally possible to obtain a wholeSAX sweep from this window especiallywhen the heart is malpositioned. Rightparasternal SAX imaging offers specialadvantages for the evaluation of the IAS. Inthis view the IAS is more perpendicular tothe beam than it is in the left parasternalwindow and it is closer to the transducerthan in the subcostal four-chambered view.

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Figure 2.39 The superior vena cava (SVC) is seen in itslong axis with the transducer positioned in the leftsupraclavicular fossa and angled parallel to the spine.

Figure 2.40 Right parasternal long axis view of theascending aorta (AO) (LV, left ventricle; LA, left atrium).

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‘PARASPINAL’ IMAGING

In the presence of a large left pleural effu-sion the transducer can be moved laterallyfrom an apical four-chambered view to theleft subscapular region. As the transducer ismoved, the apex angles more and more tothe left of the screen assuming a horizontalorientation with the LV lateral wall closestto the transducer (Figure 2.41). Rotating thetransducer 90� allows SAX imaging with theRV free wall in the far field.


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Figure 2.41 Paraspinal four-chamber view. The presenceof a large left pleural effusion (PL) enables visualization ofthe heart from the patient’s left midscapular area (LV, leftventricle; LA, left atrium; RV, right ventricle; RA, rightatrium).

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35

Evaluation of left ventricular (LV) systolicfunction is a critically important applica-tion of Doppler echocardiography. LV ejec-tion fraction and other ejection phasemeasures of ventricular function guidetherapy and provide prognostic informa-tion but are load dependent. The evaluationof ventricular systolic function must takeinto account the loading conditions.

Afterload is the resistance the ventriculemust overcome to eject blood. Afterloadmay be defined as end-systolic wall stress,the pressure within the muscle, that is pro-portional to systolic cavity pressure andcavity radius, and inversely proportional towall thickness. When afterload increases,ejection fraction decreases. Increased peaksystolic wall stress is a powerful stimulus forpressure overload hypertrophy as in chronichypertension and aortic stenosis, in whichsarcomeres are replicated in parallel. Thisincreases wall thickness, LV mass, and LVmass to volume ratio, and normalizes wallstress.

Preload is the distending force on theventricle prior to contraction. Increasingpreload within a physiologic range increasesmyocardial fiber stretch, which resultsin enhanced contraction (Frank–Starlingmechanism) (Figure 3.1). Preload can be esti-mated as end-diastolic pressure, volume orwall stress, and it is influenced by a numberof factors including intravascular volume,atrial contraction, and ventricular chamber

stiffness. Elevated end-diastolic wall stressis the stimulus for volume overload hyper-trophy as in aortic and mitral regurgitation,in which sarcomeres are replicated in seriesresulting in a ventricle with increased cavityvolume and normal wall thickness.

The ratios of LV wall thickness to cavityradius, mass to volume, and major to minoraxis diameter are almost constant in allmammalian hearts. Deviations from normalin any of these parameters are mediatedthrough global or regional alterations inload. The extent of ventricular remodelingcan be assessed echocardiographically by

EVALUATION OF LEFT VENTRICULARSYSTOLIC FUNCTION

CONTENTS ● M-mode ● Two Dimensional ● Doppler ● Tissue Doppler● Strain and Strain Rate

3

LV end-diastolic volume

Str

oke

volu

me

Figure 3.1 The Frank–Starling relationship. As preloadincreases, stroke volume increases but a point is ultimatelyreached when further increase in preload does not affectoutput (LV, left ventricle).

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the quantitation of ventricular cavity size,mass, shape, and function.

M-MODE

LV size can be assessed from M-mode meas-urements of the LV internal diameter(LVID). Fractional shortening, the percent-age change in LVID from diastole to systole(% delta D), provides an approximationof global LV systolic function when theventricle contracts symmetrically. The %delta D divided by the LV ejection time isthe mean velocity of circumferential fibershortening (VcF) measured in ventricularcircumferences per second.

If the ventricle is assumed to have theshape of a prolate ellipse with two equalshort axis diameters and a long axis lengthequal to twice the short axis diameter,ventricular volumes can be calculated bythe formulae:

Volume � 4/3 � � LVID � LVID/2 �LVID/2

This equation simplifies to:

Volume � �/3 � LVID3 orapproximately LVID3

This cube formula for LV volumes can beused for normal ventricles. However, as theventricle enlarges it becomes more spheri-cal, i.e. the increase in short axis diameteris greater than the increase in cavity length.The cube formula overestimates the volumesin dilated ventricles. The formula:

Volume � (7.0/(2.4 � LVID) � (LVID3))

includes the correction factor developed byTeicholz et al, which better reflects the axisratio of the enlarged ventricle.

Wall thickness and left ventricular mass

The relative wall thickness (H/r ratio) isdefined as twice the posterior wall thicknessdivided by the LVID in diastole. An H/r ratioof greater than 0.42 is diagnostic of pressureoverload hypertrophy.

LV mass (LVM) can be calculated byM-mode using the cube or the Teicholzformulae for volumes. The volume of the LVcavity is subtracted from the volume of thecavity plus the LV muscle and is multipliedby the density of muscle (1.055 g/cm3) toyield muscle mass in grams.

LVM � 1.055 � ((PWT � LVID � IVST)3 �(LVID)3)

where PWT is posterior wall thickness andIVST is interventricular septal thickness.

Two-dimensional echo

A trained echocardiographer can visuallyestimate systolic function accurately andreproducibly by observing the differencebetween LV diastolic and systolic cavityareas from multiple scan planes. The visualassessment is generally expressed as ejec-tion fraction. A normal LV ejects �55%of its end-diastolic volume in systole.Mildly depressed systolic function is gradedas between 40% and 50%, moderatelydepressed from 30% to 40% and severelydepressed as less than 30%. Quantitativeevaluation of LV volumes and ejectionfraction is more time consuming and relieson good image quality and conventionalscan plane orientation.

LV cavity volume A number of algorithms are available toconvert measured LV cavity areas to vol-umes (Figure 3.2, Table 3.1). The 5/6 area� length algorithm uses the cavity areafrom the short axis at the high papillarymuscle level. The apical cavity length ismeasured from the midpoint of a line con-necting the insertion points of the mitralvalve leaflets in the apical four-chamberview to the apical endocardial border. Shortaxis cavity area multiplied by the apicallength would be the cavity volume if it wasshaped like a cylinder. Multiplying this by5/6 gives the volume of a bullet-shapedventricle. The normal LV is roughly bullet-shaped, but with ventricular enlargementthe ventricle becomes increasingly spheri-cal. As the LV dilates the 5/6 area � length

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EVALUATION OF LEFT VENTRICULAR SYSTOLIC FUNCTION

algorithm will increasingly overestimatetrue volume.

The apical area/length formula Volume � 0.85 (area1 � area2/length), whichassumes that the ventricle is a prolateellipse of revolution, uses the apical four-chamber cavity area and either the apicallong axis or two-chamber area together withthe apical length. A single plane versionuses the apical four-chamber area andlength alone: volume � 0.85 (area2/length).This method, like the bullet formula,becomes less reliable when there are regionsof akinesis or dyskinesis.

The Simpson rule method This method does not make assumptionsabout ventricular shape and is the preferredmethod for LV volume calculation. Oncethe endocardial silhouette is traced, thebase to apex length is automatically deter-mined. This length (L) is divided into anumber of segments of equal height (L/n)and lines perpendicular to it are drawn con-

necting the opposing walls. The lengths ofthese lines are the diameters of cylinderswith height L/n. The LV volume is calcu-lated by summing the volumes of all thecylinders (Figure 3.3).

R L/n � (p (d/2)2)

If biplane tracings are made, two diame-ters from orthogonal apical views are usedto calculate the area of an ellipse, which ismultiplied by L/n, and all of the volumes ofthe stack are summed, i.e:

Volume (biplane) � R p � (D1/2) �(D2/2) � L/n

Both apical four-chamber and two-chambersingle plane volumes correlate closely withbiplane volumes. Apical lengths measuredfrom the two-chamber view are consistentlyslightly longer than apical four-chamberlengths because the mitral annulus, thebase from which the lengths are measured,is not planar. The annulus is farther fromthe apex in the two-chamber view.

LV shape

LV shape can be assessed as the ratio of cav-ity diameter and cavity length or as theratio of the short axis cavity area to theapical cavity area. LV cavity volume can bedivided by the volume of a sphere whosediameter is equal to the apical cavity length.

LV shape � LV volume / 4/3p((LAX length/2)3)

All methods provide an index of spheri-city, the ventricle is more spherical as theratios approach unity.

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5/6 Area length Simpson rule (MOD)(0.85 Area2/length)

Figure 3.2 The 5/6 area � lengthalgorithm assumes that the left ventricle(LV) is bullet-shaped. The 0.85(area2/length) algorithm assumes that theLV has the shape of a prolate ellipse. TheSimpson rule method of disks (MOD) makesno assumptions about LV shape.

Bullet � 5/6 SAX cavity area � LAX lengthProlate ellipse � 0.85 � LAX area1 �

LAX area2 /LAX lengthSimpson rule (single plane) � R L/n � (p d/2)2

Simpson rule (biplane) � p �(D1/2) �(D2/2) � L/n

LAX, long axis.

Table 3.1 Two-dimensional methods for quantitationof left ventricular volume

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LV mass/hypertrophy

LV mass is calculated from two-dimensionalecho images as the difference between LVcavity volume and LV muscle plus cavityvolume multiplied by the density of muscle(1.055 g/cm3). The LV epicardial border isonly rarely clearly visualized in the apicalimages so the 5/6 area � length methodis the only two-dimensional method ingeneral use for LV mass estimation (Figure3.4). The LV cavity area is planimetered atend-diastole in the short axis view at thepapillary muscle level; the papillary musclesand trabecular structures are generallyincluded with the cavity. LV cavity area ismultiplied by the LV cavity length from theMV annulus to the apical endocardiumfrom an apical four-chamber view at end-diastole and by the constant 5/6 to yieldcavity volume. The area surrounded by theright septal edge and LV epicardium fromthe same short axis image is planimeteredand this is multiplied by the LV cavity lengthfrom the MV annulus to the apical epi-cardium and by the constant 5/6. When thelength to the epicardium cannot be deter-mined, 1.0 cm is added to the length of theepicardium to represent the thickness of the

myocardium at the apex. The cavity volumeis subtracted from the cavity plus musclevolume and the difference is multiplied bythe density of muscle to yield LV mass.

2-D LVM �5/6 �{[(SAX total area � (LAX cavitylength �1.0 cm)]� (SAX cavity area

� LAX cavity length)}


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Figure 3.3 Simpson rule left ventricular (LV) cavity volumes are calculated by summing the volumes of disks whose diameteris the distance between apposing LV walls and whose height is equal to the cavity length divided by the number of disks (L/n).

Leng

th

Area

Figure 3.4 Left ventricular (LV) mass is calculated usingareas from the parasternal short axis view and LV lengthfrom the apical four-chamber view. The LV lengths inFigures 3.4(A) and 3.4(B) are equal but Figure 3.4(B) hasa more spherical shape.

A B

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Three-dimensional echocardiographyThree-dimensional volumetric data can beacquired in real time or with electrocardio-graphic (EKG) gating, using matrix arraytransducers or reconstructed from two-dimensional images when their properspatial and temporal orientation is known.Analysis of three-dimensional echocardio-graphic images for LV volumes showscloser agreement with magnetic resonanceimaging (MRI) than two-dimensionalechocardiograms with lower interobservervariability.

DOPPLER

Doppler echocardiography is essential for anunderstanding of valvular heart disease andthe evaluation of LV systolic and diastolicfunction.

The Tei index

This is a Doppler method for assessing com-bined systolic and diastolic ventricular per-formance that relies on the measurement oftemporal intervals. The Tei index is calcu-

lated as isovolumic contraction time (IVCT)plus the isovolumic relaxation time (IVRT)divided by the LV ejection time (LVET)(Figure 3.5).

TEI index � (IVRT � IVCT)/LVET

The isovolumic intervals need not be meas-ured separately as cycle length minus thesum of LVET and the diastolic filling timewill equal the sum of IVRT and IVCT. Thisratio has proved to be useful in the serialassessment of patients taking cardiotoxicchemotherapy, patients with cardiomy-opathies, congenital heart disease, andfollowing cardiac transplantation.

Force and acceleration

The peak velocity of the LV outflow tractflow velocity signal divided by the timefrom the onset of flow to peak velocity (theacceleration time) is the acceleration (cm/s/s)(Figure 3.6). It is a reflection of the rate ofincrease of LV pressure (�dP/dT) in earlysystole.

Acceleration decreases when systolicfunction is impaired. The force of systolicejection is equal to the product of accelera-tion of blood and the mass of blood being

39

IVCT

LVET

LVOT

MV

DFT

IVRT

Figure 3.5 A graphic representation of the timing of LVinflow (MV) and outflow (LVOT). The Tei index is equal toisovolumic contraction time (IVCT) plus isovolumicrelaxation time (IVRT) divided by LV ejection time (LVET). Itis also equal to cycle length minus the sum of diastolicfilling time (DFT) and LVET divided by LVET.

Figure 3.6 Force is equal to mass multiplied byacceleration. Acceleration is equal to the peak velocityattained divided by the acceleration time (At) and isrepresented by the arrow on the second cycle. The shadedarea in the first cycle is the flow velocity integral (FVI)during the acceleration time. This FVI multiplied by thecross-sectional area of the left ventricular outflow tractand by the density of blood (1.055 g/cm3) is the mass ofblood ejected during the acceleration interval.

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accelerated. The mass of the blood is thestroke volume during the acceleration timewhich is equal to the product of the cross-sectional area (CSA) of the LV outflow tractand the flow velocity integral from onset ofejection to peak velocity and the density ofblood.

Force � (1.055 � CSA � FVIAT) �(peak velocity/acceleration time)

Mitral regurgitation dP/dT

The rate of rise of pressure in the LV(�dP/dT) can be calculated from the slopeof the continuous wave Doppler signal ofmitral regurgitation (�dV/dT) as pressureis related to velocity by the modifiedBournoulli equation where delta pressure �4 � (velocity2). As left atrial pressure isassumed to be constant during systole, thetime required for the ventricle to increasethe mitral regurgitant velocity from 1 m/s to3 m/s is the time required to increase LVpressure by 32 mmHg. The normal value for�dP/dT is approximately 800 mmHg/s.

4 � (32) � 4 � (12)dP/dT � –––––––––––––––––––––––––

Time from 1 m/s to 3 m/s

This measurement is made prior to aorticvalve opening and is therefore independentof afterload but it is sensitive to changes inpreload (Figure 3.7).


Tissue Doppler imaging (TDI) informationcan be displayed as a spectral signal froma single pulsed-wave sample volume, acolor encoded M-mode tracing or as two-dimensional real time color Doppler (Figure3.9). Pulsed wave (spectral) TDI measuresmyocardial peak velocity and color-codedTDI gives mean myocardial velocities.Various color maps can be used; one colorrepresents movement away from the trans-ducer and another color represents move-ment toward the transducer, with brightercolors reflecting higher velocities. Usingparallel digital processing and high pulserepetition frequency, frame rates of greaterthan 200 Hz can be achieved. Myocardialvelocities are low relative to blood flow,rarely exceeding 20 cm/s so that aliasing isnot encountered. TDI signals depend on thefrequency shift information of the reflectedultrasound and not its amplitude and TDI isapplicable even when two-dimensionalimages are of poor quality.

Frequency shift information from TDI isangle dependent so that only motion par-allel to the beam can be measured accu-rately. Contraction toward the center ofthe LV cavity or radial shortening can beevaluated from the parasternal LAX andSAX views. The myocardial velocities ofcircumferentially oriented muscle fiberscan be sampled from small segments of thelateral wall and septum from the paraster-nal SAX. Longitudinal contraction, whichis primarily due to subendocardial musclefiber shortening, can be assessed from api-cal views. Myocardial velocity gradientscan be shown; velocities increase from theepicardium to the endocardium and fromthe apex to the base.

Displayed velocities are the sum of localmuscle contraction along the axis of thebeam and motion of the entire heart. In sys-tole the walls of the LV move toward thecenter of the chamber while the whole


40

Figure 3.7 The continuous wave Doppler signal of mitralregurgitation (MR) can be used to calculate left ventricular(LV) dP/dT. In this example the time for the MR velocity torise from 1 m/s to 3 m/s is approximately 70 ms. dP/dT �32/0.070 � 457 mmHg/s indicating moderately impairedLV systolic function.

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heart moves toward the anterior chest wall.From the parasternal window, whole heartmotion exaggerates posterior wall velocitiesbut diminishes septal velocities.

Longitudinal tissue velocities are sampledat the base from the apical window. Aninitial positive systolic wave ‘S1’ associatedwith isovolumic contraction can often beappreciated. S1 is followed by a larger posi-tive S2 wave reflecting the descent of thebase of the heart during LV ejection. After adiscernible isovolumic relaxation interval,the motion of the base of the heart reversesin diastole, which is marked by two consec-utive negative deflections caused by earlyventricular filling (E�) and atrial contraction(A�).

When peak S2 waves from several wallsare averaged, excellent correlations withradionuclide and contrast ventriculographicejection fractions are demonstrated even inpatients with wall motion abnormalities.Wall motion abnormalities subjacent toindividual annular sampling sites arereflected on TDI by decreased peak veloci-ties, decreased systolic time velocity inte-grals, and increased time to peak velocity inthe spectral tracing (Figure 3.8).

Digitally stored color TDI images can beanalyzed off-line to yield velocity-codedcolor M-modes from straight or curved linesamples and velocity versus time graphsfrom any individual point. The spatial reso-lution of color TDI is sufficiently good sothat velocity signals from the endocardium,

mid-wall and epicardium of the same wallsegment can be differentiated.

Wall motion velocities are higher and lessheterogeneous in the lateral and posteriorwalls compared with the septum, and lowerandmoreheterogeneous inthemid-ventriclecompared with the base. The reproducibil-ity of velocities in myocardium at the apexis low because the myocardial velocities arelow and the direction of fiber shortening isnot parallel to the beam.

41

Figure 3.8 TDI spectral waveforms from anormal subject and a patient with a restrictivecardiomyopathy (RCM). Both systolic anddiastolic velocities are markedly reduced inthe patient with RCM. The vertical distancebetween calibration markers is 5 cm/s.

Figure 3.9 Color TDI from the apical four-chamber view.The left panel was taken in early systole and the rightpanel in late systole. The interventricular septum is blue inthe early systolic frame indicating early systoliccontraction. The lateral wall is blue in the late systolicpanel indicating late and dyssynchronous contraction ofthe lateral wall.

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Strain and strain rateStrain is the deformation of a materialcaused by an applied stress. Regional strainin the heart is an important determinant ofcardiac remodeling. TDI can measure strainand the rate of change of strain noninva-sively. Strain rate is the difference in veloc-ity between two points divided by thedistance between the points. In TDI it is themyocardial velocity gradient. Integratingstrain rate over time gives the strain, whichis equal to the change in the distancebetween two points divided by the originaldistance between the two points. Strain andstrain rate imaging are accomplished byassessing the velocity differences and theirintegrals between very small distancesthroughout the two-dimensional myocar-dial velocity field, color coding the resultsand superimposing them on the anatomicimage. Because the distances betweensamples are small the effects of motionimparted on the sample from adjacentmyocardial segments and the effects ofwhole heart motion are minimized. As withtwo-dimensional velocity color images, two-dimensional strain and strain rate imagescan be analyzed off-line to obtain straightor curved line color M-mode displays ordepict strain versus time and strain rateversus time from any point within themyocardium (Figure 3.10). Strain correlatesclosely with peak �dP/dT and strain rateimaging can clearly distinguish regions ofhypokinesis and akinesis from normal.

Other techniques are available for display-ing TDI information including a mapping

technique, which codes wall segments withvelocities within normal ranges with onecolor and slower moving segments withanother color to focus attention on areas ofmyocardium that become hypokinetic dur-ing stress testing. The same technology cancolor code for the time to peak velocitywith normal wall segments in one color andregions with delayed peak velocities inanother color. This technique is an effort toquickly identify patients with dyssynergiccontraction patterns who would benefitfrom cardiac resynchronization therapy.


42

9.2

Strain rate

Strain

150 300 450 600 750 900 1050 1200

7.35.5

Velo

city

(cm

/s)

3.71.80.0

�1.8�3.7�5.5�7.3�9.2

2.19

150

0

0 300 450 600 750 900 1050 1200

1.751.31

Str

ain

rate

(1/S

)

Str

ain

(%)0.87

0.440.00

�0.44�0.87�1.31�1.75

12.09.06.03.00.0�3.0�6.0�9.0�12.0

�2.19

Figure 3.10 TDI signals analyzed off-line to obtain avelocity versus time plot (top panel) and strain (red) andstrain rate (blue) versus time graphs (bottom panel).

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43

Right ventricular (RV) inflow and outflowtracts are separated by the crista supraven-tricularis, which is a ridge of tissue com-posed of three prominent muscle bundles:● the parietal band – situated between the

pulmonic valve (PV) and tricuspid valve(TV) annuli and makes up the lateral andposterior RV outflow tracts

● the infundibular septum – between theright and left ventricular outflow tracts

● the septal band – travels down the inter-ventricular septum and bifurcates intoinferior and anterosuperior limbs.

The moderator band, which carries fibers ofthe right bundle branch, arises from theapical termination of the septal band andcrosses the RV cavity to insert into the RVfree wall close to the anterior papillarymuscle of the TV.

The shape of the TV annulus resemblesthe letter ‘D’ turned 90� clockwise. The sep-tal leaflet is parallel to the septum and theposterior leaflet is parallel to the posterioror diaphragmatic RV free wall. The anteriorleaflet is the largest and most excursive andforms a curtain between the RV inflow andoutflow tracts.

The right and left ventricles have similarvolumes and ejection fractions but thethickness of the LV free wall is two to threetimes greater than that of the RV, while RVmass is normally one-sixth that of the leftventricle (LV). The shape of the RV is com-

plex, being triangular in its base to apexdimension and crescentic in cross-section.The normal septal curvature is convex tothe RV and concave to the LV. Because ofits complex shape there are no simple geo-metric models for calculating RV volumeand ejection fraction by two-dimensionalecho. However, three-dimensional echo-cardiography can accurately measure RVvolumes.

RV systolic function is generally assessedqualitatively from apical and subcostal four-chambered views and RV size is assessedboth in absolute terms and with referenceto left ventricular size. The normal area andtransverse diameter of the RV from theapical four-chamber view are approxi-mately two-thirds of the LV and the majorlength of the RV from the TV annulus tothe apex is 1–2 cm less than the LV length.Shortening of the RV from base to apex insystole can be measured by directing theM-mode cursor from the apex to the medialtricuspid annulus. This method is knownas TAPSE (Tricuspid Annular Plane SystolicExcursion) and it correlates well withradionuclide angiography RV ejectionfractions (Figure 4.1). Tissue Doppler meas-urements of RV long axis contractionvelocity measured from the RV free wallnear the TV annulus can characterize RVsystolic function.

The pulmonary circulation is character-ized by low pressure and low resistance.

EVALUATION OF RIGHT VENTRICULARFUNCTION

CONTENTS ● Right Ventricular Volume Overload ● Right Ventricular Pressure Overload● Acute Pulmonary Embolism

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Normal pulmonary artery pressure (PAP) insystole ranges from 15 mmHg to 30 mmHgand in diastole from 4 mmHg to 12 mmHg.Mean PAP is between 9 mmHg and 19mmHg. There is normally an increase inright heart flow with inspiration as RVafterload is decreased and systemic venousreturn is augmented.

RIGHT VENTRICULAR VOLUME OVERLOAD

RV volume overload is caused by left-to-right shunt or tricuspid insufficiency.The right ventricle remodels in response topreload excess by cavity dilatation (Figure4.2). RV dilatation is associated with a morespherical cavity shape and paradoxical sep-tal motion (Figure 4.3), which when severeresults in a circular RV and crescentic LV inshort axis and can cause LV outflow tractobstruction. As the RV dilates it forms theapex and the moderator band is nearly per-pendicular to the interventricular septum(Figure 4.4).

Paradoxical septal motion decreases theLV diameter and the LV becomes ‘D’ shapedin diastole (Figure 4.5). The altered LVgeometry together with reduced LV preloadmay decrease LV ejection fraction. The TVpapillary muscles are displaced (Figure 4.6)with RV enlargement causing tricuspidregurgitation (TR). TV annular dilatationoccurs with increasing severity of TR as aconsequence of RV enlargement. RA andinferior vena cava (IVC) enlargement resultfrom severe TR (Figure 4.7) and the IVC nolonger reduces its diameter with inspiration(Figure 4.8). TR results in retrograde systolicflow in the IVC and middle hepatic vein,which can be detected by pulsed and colorDoppler (Figure 4.9).

RIGHT VENTRICULAR PRESSUREOVERLOAD

The RV responds to afterload excess with RVhypertrophy, increased RV wall thicknessand RV muscle mass (Figure 4.10). The RVbecomes more spherical in shape with pres-sure overload. The normal septal curvatureis reversed in both diastole and systole. LVpreload is diminished, and there is prolon-gation of the LV isovolumic relaxation timeand decreased E wave and increased A wavepeak velocities on the transmitral Dopplersignal. RV pressure overload may be acute(pulmonary embolism) or chronic from pul-monary disease, mitral valve disease ormore frequently from LV dysfunction. The

Figure 4.1 Tricuspid Annular Plane Systolic Excursion(TAPSE) is an M-mode measure (arrow) obtained from theapical four-chamber view that reflects global rightventricular systolic function.

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EVALUATION OF RIGHT VENTRICULAR FUNCTION

RV can generate suprasystemic pressureswhen the onset of the pressure overload isgradual.

The term ‘cor pulmonale’ describeschronic right heart dysfunction caused by

abnormalities of the vessels of the lungs andapplies to a diverse group of conditions,which elevate the pulmonary vascularresistance causing pulmonary hypertension(Figure 4.11). Pulmonary hypertension isalso caused by cardiac disease associatedwith increased left atrial pressure as in mitralstenosis, left heart failure, and chronicallyelevated pulmonary flow due to shuntssuch as atrial or ventricular septal defects orpatent ductus arteriosus. Eisenmenger syn-drome refers to left-to-right shunts thatreverse direction due to the development ofsevere irreversible pulmonary hypertension.

In pulmonary hypertension the pul-monary artery dilates and the plane of thepulmonic valve is displaced anteriorly andto the right. In severe pulmonary hyperten-sion the pulmonic valve can be anteriorto the aortic valve. When this occurs thepulmonary valve can sometimes be imagedin short axis. RV wall thickness can bemeasured from the subcostal or parasternalwindows and RV hypertrophy is presentwhen the RV wall thickness is �0.5 cm(Figure 4.12). RV systolic pressure can beestimated with continuous wave Dopplerfrom the sum of the maximum velocity ofthe TR jet (Figure 4.13) and an estimate ofthe RA pressure. RV systolic pressure is equalto pulmonary artery systolic pressure whenthere is no RV outflow tract obstruction. The

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Figure 4.2 Parasternal long axis view. The right ventricle (RV) is markedly enlarged (LV, left ventricle; LA, left atrium; AO, aorta).

Figure 4.3 M-mode of the right and left ventricles. TheRV is markedly enlarged and the interventricular septalmotion is paradoxical. Septal motion is toward the RV insystole and toward the LV in diastole.

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Figure 4.4 Apical four-chamber view in a patient with severe right ventricular (RV) volume overload. The RV forms theapex and the moderator band (arrow) is perpendicular to the interventricular septum (LV, left ventricle; LA, left atrium;RA, right atrium).

Figure 4.5 Parasternal short axis image of a patient withright ventricular (RV) volume overload. The RV is enlargedand the interventricular septum (arrow) exhibitsparadoxical motion (LV, left ventricle).

Figure 4.6 Parasternal short axis view of the base of theheart in a patient with right ventricular (RV) enlargement.RV papillary muscles (arrow) are not normally seen in thisplane. RV enlargement displaces the TV papillary musclesand causes TR (RA, right atrium; RV, right ventricle; LA, leftatrium; PA, pulmonary artery).

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Figure 4.7 RA/RV view in a patient with markedly dilated right heart chambers. The papillary muscle is prominent in thediastolic frame. Moderately severe tricuspid regurgitation is seen in the systolic frame with color Doppler (RA, right atrium;RV, right ventricle).

Figure 4.8 Subcostal view of a markedly enlargedinferior vena cava (IVC) resulting from severe TR. A smallpericardial effusion (PE) is seen adjacent to the right atrialfree wall.

Figure 4.9 Pulsed wave Doppler signal with the samplevolume in the middle hepatic vein. There is markedsystolic flow reversal caused by severe tricuspidregurgitation.

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pulsed wave Doppler signal of systolicvelocity in the pulmonary artery normallypeaks later than the systolic velocity in theLV outflow tract. Time to peak velocity(acceleration time) shortens with increasingpulmonary artery systolic pressure. A pul-monary artery acceleration time of � 100 msis associated with pulmonary hypertension.Mid-systolic notching of the pulmonary

artery flow profile is a specific but insensi-tive sign of pulmonary hypertension as ismid-systolic notching of the pulmonic valveM-mode (Figure 4.14). Pulmonary arterydiastolic pressures can be estimated fromthe pulsed or continuous wave signal ofpulmonary valve insufficiency. Peak orend-diastolic pressure gradients retrogradeacross the pulmonic valve are calculatedfrom the Bernoulli equation and added to anestimated RV diastolic pressure, which isroughly equivalent to mean RA pressure.

The RV remodels in response to alter-ations in preload and afterload. The RVhypertrophies in response to increasedafterload but unlike the LV in pressureoverload hypertrophy, RV dilatation almostinvariably follows RV hypertrophy. This isdue to superimposition of volume overloadfrom tricuspid regurgitation on RV pres-sure overload. Pure RV pressure overloadhypertrophy is rare.

ACUTE PULMONARY EMBOLISM

Most pulmonary emboli originate fromdeep vein thrombi in the pelvis or legs.


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Figure 4.10 Parasternal short axis view showing hypertrophy of the right ventricular (RV) free wall and trabeculations. Thereis also a small pericardial effusion (*) (LV, left ventricle).

Figure 4.11 A giant pulmonary artery (PA) in a patientwith severe chronic pulmonary emboli. There is a largelaminated thrombus (*) and ‘smoke’ (AO, aorta).

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Figure 4.12 Right ventricular (RV) free wall thickness is greater than 1 cm in the diastolic subcostal short axis view indicatingsevere RVH.

Figure 4.13 Continuous wave Doppler of tricuspidregurgitation with a peak velocity of 3.7 m/s indicating anRV/RA pressure gradient of 55 mmHg.

Figure 4.14 An M-mode of the pulmonic valve showingmid-systolic partial closure or the ‘W’ sign. This is a specificbut insensitive sign of pulmonary hypertension.

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When a pulmonary embolus obstructs lessthan 25% of the pulmonary vasculaturethere is little increase in RV afterload andheart rate and blood pressure will remainnormal. Approximately 50% of patients

with documented pulmonary emboli havenormal echocardiograms. Larger embolipresent an acute afterload excess to the RV.A normal RV is unable to generate pressuresgreater than 40–45 mmHg acutely and ifPAP exceeds this level, the RV dilates andfails. When the RV is able to generatepressures in excess of 50 mmHg, there isRV hypertrophy indicating a chronic oracute-on-chronic disease process.

In acute severe pulmonary embolism theRV dilates and RV systolic function is strik-ingly diminished. Septal motion is paradoxi-cal and the LV is under filled and decreased insize. The ratio of RV to LV size predicts thedegree of obstruction. Doppler signals of TRand pulmonary insufficiency show moderatepulmonary hypertension. Visualization ofthrombus in the pulmonary artery (Figure4.15) or elongated, hypermobile, serpiginousclot (thrombus in transit) in the RA are spe-cific but insensitive markers of pulmonaryembolism (Figure 4.16).

A distinct regional pattern of RV systolicdysfunction in which the mid-wall of the RVis akinetic but the apical motion is normal(McConnell sign) has been used to identifypatients with pulmonary embolism. RVinfarction may show a similar pattern ofRV wall motion but in RV infarction PAP islow and there is usually evidence of an LVinferior wall motion abnormality.


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Figure 4.15 A thrombus is identified (arrow) at thepulmonary artery (PA) bifurcation in this parasternal shortaxis view (AO, aorta; RVOT, right ventricle outflow tract).

Figure 4.16 A mobile right atrial (RA) thrombus (arrow) is identified in a patient with suspected pulmonary embolism (LV, leftventricle, RV, right ventricle).

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Diastolic dysfunction can be defined as aninability of the left ventricle (LV) to attain anormal end-diastolic volume without aninappropriate increase in LV end-diastolicpressure (LVEDP). Increased resistance tofilling causes elevated filling pressures,which result in heart failure symptoms ofpulmonary congestion and dyspnea. Thelevel of LVEDP is closely correlated withexercise limitation in patients with heartfailure. Diastolic dysfunction is more com-mon in women and is largely a disease ofelderly people. Diastolic dysfunction isoften attributable to changes within themyocardium that accompany the hyper-trophic response to chronic pressure over-load. In addition to myocyte hypertrophy,increased systolic wall stress stimulates thesynthesis of interstitial and perivascular fib-rillar collagen in the extracellular matrix,which increases chamber stiffness. Chamberstiffness and myocardial relaxation are themain determinants of diastolic function.

STIFFNESS AND RELAXATION

Stiffness can be defined as the force (thechange in pressure) required to produce achange in volume (dP/dV). Its reciprocal(dV/dP) is termed compliance. The diastolicpressure–volume relation is nonlinear. Inearly diastole, when volume is low, a

change in pressure results in a much greaterchange in volume than at end-diastolewhen pressure is high, i.e. as volumeincreases, the slope of the pressure–volumerelation increases (Figure 5.1). Chamberstiffness (dP/dV) at any point on the dias-tolic pressure–volume curve is defined as the

EVALUATION OF DIASTOLIC FUNCTION

CONTENTS ● Stiffness and Relaxation ● M-Mode and Two-Dimensional Imaging● Spectral Doppler

5

Pre

ssur

e

Volume

Figure 5.1 A graphic representation of the diastolicpressure–volume relation. A given change in pressureresults in a much greater change in volume when volumeis low (red) than when it is high (blue). Chamber stiffness isdefined as the slope of the tangent to any point on thepressure–volume curve.

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slope of a tangent to the curve. Chamberstiffness is linearly related to pressure, andits reciprocal is chamber compliance.Compliance is a passive property of themyocardium that is also determined by

preload. Increases in preload move thepressure/volume intercept point upward onthe curve, while changes in the materialproperties of the myocardium, due to fibro-sis or post-infarction scarring, move thepressure/volume intercept upward andto the left. In both cases, stiffness isincreased. An elevated LVEDP causes anincrease in calculated stiffness even withouta change of the end-diastolic pressure/volume relation (Figure 5.2).

Another important determinant of dias-tolic function is myocardial relaxation, aprocess requiring energy. Myocardial relax-ation occurs principally during the isovolu-mic relaxation time (IVRT) between aorticvalve closure and mitral valve opening. Tau,the time constant of relaxation thatdescribes the decay in LV diastolic pressure,is a measure of relaxation that requirescardiac catheterization. LV pressures fromthe point of peak negative dP/dT, whichapproximates aortic valve closure, to apoint 5 mmHg greater than end-diastolicpressure, approximating the time of mitralvalve opening, are logarithmically trans-formed and plotted against time. Thedecrease in LV pressure is assumed to bemono-exponential and the pressures aretransformed to a logarithmic scale so thattheir relation with time is linear (Figure5.3). Tau is the reciprocal of the slope of the

AO

LV

LA

120

80

Pre

ssur

e (m

mH

g)

Log

pre

ssur

e

Time

40

Figure 5.3 (A) Tau, the time constant of relaxation is calculated from diastolic pressures measured at cardiac catheterization(red arrow). (B) These pressures are log transformed and plotted against time so that the relationship is linear (LV, left ventricle;LA, left atrium; AO, aorta).

LV volume (mL)

LV p

ress

ure

(mm

Hg)

50

50

100

100

Figure 5.2 Three pressure–volume loops are shown:green is normal, black represents diastolic dysfunction,and blue represents systolic dysfunction. Systolicdysfunction causes an elevation in left ventricular (LV) end-diastolic pressure and an increase in stiffness, but there isno change in the pressure–volume relation. It is shiftedupward and to the right but lies on the same normalcurve. Diastolic dysfunction with a change in the materialproperties of the myocardium displaces thepressure–volume relation upward and to the left.

A B

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log pressure versus time relation and isnormally 30–40 ms.

At end-systole muscle fibers are shorterthan they are at rest and systolic compres-sion of connective tissues stores potentialenergy which is released with LV relaxation.This elastic recoil causes a ‘suction’ thatfacilitates LV pressure decline during theisovolumic interval. Suction is strongest atthe apex. LV pressure continues to declineeven after mitral valve (MV) opening as vol-ume rises, thus, systolic function is a major

determinant of relaxation. The contribu-tion of elastic recoil to diastolic filling is lostwhen systolic function is poor. Increased LVafterload delays relaxation and dyssynchro-nous contraction, usually caused by leftbundle branch block (LBBB), delays theonset of contraction causing shorteningto persist beyond ejection. This results indyssynchronous and prolonged relaxation.

The relative contributions of the separatephases of diastole to LV filling can be seenwhen LV volume is plotted against time(Figure 5.4). The rapid filling phase ofdiastole begins when left atrial (LA) pressureexceeds LV pressure and the MV opens. Thepeak rate of filling is directly related to theLA/LV pressure gradient. Increasing LVvolume causes LV pressure to rise and therate of filling to slow. Diastasis follows rapidfilling when LA and LV pressures approxi-mate but this phase of diastole is absentat high heart rates. Atrial contraction thenrenews the LA/LV pressure gradient. Atrialcontraction contributes about 15–20% ofLV end-diastolic volume in normal subjects,but the added fiber stretch supplied by atrialcontraction is an important determinantof systolic function via the Frank–Starlingmechanism.

M-MODE AND TWO-DIMENSIONALIMAGING

Evaluation of LV diastolic function beginswith a visual assessment of LV filling withM-mode and two-dimensional imaging.The excellent temporal resolution of M-mode echocardiography allows a qualitativeassessment of the rate of increase in cavitysize and rate of LV wall thinning. Flatteningof the E–F slope on the MV M-mode in theabsence of mitral stenosis or aortic insuffi-ciency is associated with decreased LVcompliance. Prolongation of the finalclosing slope (A–C) of the MV M-mode isassociated with an increased LVEDP in theabsence of first degree atrioventricularblock. If the P–R interval minus the A–Cinterval is greater than 60 ms the LVEDP isusually greater than 20 mmHg.

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LV volume

Pressure

TransmitralDoppler

Pulmonaryvein Doppler

RF

SF

AF

AO

LV

LA

E

S1S2 D

A

A

Figure 5.4 Left ventricular (LV) volume, LV, left atrial (LA)and aortic (AO) pressure, Transmitral and pulmonaryvenous Doppler velocity waveforms plotted against time(RF, rapid filling; SF, slow filling; AF, filling provided byatrial contraction).

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Careful observation of two-dimensionalecho images, particularly short axis imagesof the LV, will often reveal slow and pro-longed filling associated with diastolicdysfunction but this assessment is difficultwhen the heart rate is elevated. The pres-ence of left ventricular hypertrophy (LVH)or regional heterogeneity of contractionsuggests the presence of diastolic dysfunc-tion. LA enlargement is associated withelevated LVEDP.

SPECTRAL DOPPLER

Spectral Doppler is the tool of choice for theevaluation of diastolic function. When LVinflow and outflow signals are sampledsimultaneously by either pulsed or continu-ous wave Doppler, the isovolumic relaxationtime (IVRT) can be measured directly as thetime from the end of LV outflow tract flow tothe beginning of transmitral flow. IVRT isprolonged when LV relaxation is impairedbut it is load dependent. Hypovolemia oruse of venodilators such as nitroglycerinlower LA pressure thereby delaying MVopening (the time at which LA pressureexceeds LV pressure) and prolonging IVRT.The IVRT is not a true measure of relaxation,but a shortened IVRT indicates elevated LApressure, whereas a long IVRT in combina-tion with systolic dysfunction indicates anormal or near-normal filling pressure.

The slope of the continuous wave Dopplersignal of mitral regurgitation is a surrogatefor LV �dP/dT (rise in pressure) and indica-tor of LV systolic function (see Chapter3); similarly negative dP/dT accuratelycharacterizes LV relaxation and correlateswith tau.

Transmitral Doppler

Spectral Doppler of transmitral flow revealsthe instantaneous pressure gradient betweenthe LA and LV throughout diastole and thissignal has long had a role in assessingdiastolic function. The MV opens when LApressure exceeds LV pressure and transvalvu-lar velocity reaches a peak at the E point

which ranges from 70 cm/s to 100 cm/s innormal subjects. LA and LV pressures thenequilibrate; the rate of equilibration is pro-vided by the down slope from the E peak.Mitral deceleration time is measured as a lin-ear approximation of the time that it takesfor velocity to return to the baseline fromthe peak of the E wave. Diastasis follows andis marked by low or absent flow velocitiesalthough flow may continue due to inertialforces. The duration of diastasis is deter-mined by the heart rate. Atrial contractioncauses a second spike in the LA/LV pressuregradient. It reaches a peak at between45 cm/s and 70 cm/s in normal subjects. Thenormal ratio of E wave to A wave velocity is1.0–1.5.

There are many factors that affect thetransmitral velocity waveform; amongthem are heart rate and rhythm, aging, andpreload. As the heart rate increases, time fordiastasis is reduced, the A wave occurs ear-lier and its maximum velocity is increased.At rates of greater than 100 beats/minfusion of the E wave and A waves occursresulting in monophasic diastolic filling. Inatrial fibrillation the A wave is lost andthe height of the E wave is determined bythe length of the preceding cardiac cycle.Increasing age is associated with decreased Ewave velocities, increased A wave velocities,and prolongation of both the IVRT anddeceleration times. These are ‘normal’ find-ings in elderly people due to age-relatedchanges in the myocardial extracellularmatrix that slow diastolic relaxation.

Abnormal transmitral flow patterns havebeen described. Impaired relaxation pro-longs IVRT as LV pressure falls slowly. Theearly LA/LV pressure gradient is thereforerelatively low and this is reflected in adiminished E wave maximal velocity. Asearly filling is decreased, LA volume is largerat the time of atrial contraction and thisresults in a higher A wave. There is reversalof the normal E/A ratio and decelerationtime is prolonged. These findings are associ-ated with a low pulmonary capillary wedgepressure (�15 mmHg).

A restrictive filling pattern occurs whenthere is a high LA pressure and a non-distensible ventricle. It is marked by a


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shortened IVRT, a high E wave, a shortdeceleration time and a small A wave. Thesefindings reflect a high LA pressure at MVopening, and rapid filling of the LV that ter-minates rapidly. The A wave is low velocitydue to either atrial dysfunction or a highLVEDP. Although this pattern is abnormaland associated with a poor prognosis inpatients with infiltrative and dilated cardio-myopathies, it is often a marker of increasedLV filling pressures secondary to systolicdysfunction alone and does not always indi-cate an intrinsic alteration of myocardialdiastolic properties.

As LV filling pressures rise and the LVinflow Doppler pattern transitions fromimpaired relaxation to restrictive filling, apattern mimicking normal occurs. This‘pseudonormal’ pattern results from acombination of impaired relaxation andelevated filling pressures. In this pattern Ewave and A wave velocities and their ratioare approximately normal, the IVRT isneither shortened nor prolonged and decel-eration time is within the normal range.Thus classification of diastolic function asnormal based only on the transmitral flowvelocity pattern will often be erroneous.Patients with decreased systolic functionand a normal appearing transmitral flowvelocity profile should be considered to bepseudonormal with moderately elevated LApressures (Figure 5.5).

Changes in preload affect the E wavevelocity. As previously noted, hypovolemiaand venodilators lower LA pressure. Thisdecreases the E wave maximal velocity.Mitral regurgitation increases preload andE wave amplitude. A patient with a pseudo-normal pattern of transmitral flow mayconvert to a restrictive pattern with volumeinfusion, the development of mitral regurgi-tation or worsening diastolic function.Worsening systolic function with an ele-vated LV diastolic pressure is reflected bya change in the transmitral Doppler flowpattern from delayed relaxation to pseudo-normal or from pseudonormal to restrictive.

E wave deceleration time correlatesclosely with LV filling pressure in the pres-ence of systolic dysfunction but whenpatients with normal ejection fractions are

55

Figure 5.5 Three pulsed wave Doppler transmitral flowvelocity waveforms are presented. The top paneldemonstrates the pattern of impaired relaxation with alow velocity E wave, a high A velocity wave, and aprolonged deceleration time. The middle panel shows apseudonormal pattern and the bottom panel is anexample of the restrictive pattern with a high velocityE wave, low velocity A wave, and short deceleration time.

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included, the relation becomes nonsignifi-cant. This illustrates the fact that a rapid Ewave deceleration time may occur not onlywhen diastolic function is severely impaired(high LA pressures with an abrupt termina-tion of filling), but also when it is optimal(rapid relaxation).

The Valsalva maneuver can be used todistinguish patients with a normal patternof transmitral flow from a pseudonormalpattern. By causing intrathoracic pressure toexceed the pressure in the great veins venousreturn and preload is decreased. The reduc-tion in preload from this maneuver causes apseudonormal pattern of transmitral flow torevert to a pattern of impaired relaxation.Patients with normal filling will have ahypovolemic response; their E and A waveswill both decrease. The Valsalva maneuvercauses a restrictive pattern to revert to apseudonormal pattern in some patients.Patients with a restrictive pattern that can bereversed by the Valsalva maneuver or bydrug therapy have a better prognosis thanpatients with a fixed restrictive pattern.

Pulmonary vein Doppler

The pulmonary veins are visualized fromthe apical four-chamber view, less fre-quently from high parasternal short axisviews and the suprasternal notch. In theapical four-chamber view the right upperpulmonary vein is oriented so that flowinto the LA is nearly parallel with the ultra-sound beam. It is helpful to identify pul-monary venous flow in this vessel by colorDoppler and then to position the pulsedwave sample volume in the vein 1–2 cmaway from the LA (Figure 5.6).

Normal pulmonary venous flow consistsof a forward S wave in systole, a D wave indiastole, and a retrograde Ar wave causedby atrial contraction. The S wave may bebiphasic, the early phase (Se) attributed toLA relaxation and the later (Sl) associatedwith apical displacement of the MV annu-lus. The D wave is associated with MV open-ing and LV filling prior to atrial contraction.Atrial contraction forces blood into theLV but also retrograde into the pulmonaryveins. When LV compliance is reduced,

resistance to forward flow into the ventricleis increased and the retrograde Ar wave willbe enhanced in velocity and duration. TheS wave is higher in normal subjects than theD wave and when it is biphasic Sl will behigher than Se. In mitral regurgitation theS wave may be blunted. Reversal of theS wave is a mark of severe mitral regurgita-tion. The ratio of S velocity to D velocity isapproximately 1.3–1.5 in normals with theS flow velocity integral occupying 60–68%of the total flow velocity integral. As withthe transmitral E and A waves, pulmonaryvein S and D waves may fuse at high heartrates, and as with the transmitral flow, age-related changes have been described. TheD wave decreases and the Ar and S waveincrease with advancing age.

Pulmonary venous Doppler waveformscan be obtained in between 60% and 90%


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Figure 5.6 Apical four-chamber view with color Dopplerdemonstrating flow in the pulmonary veins (RV, rightventricle; LV, left ventricle; LA, left atrium; RA, right atrium).

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of patients with transthoracic echo but it isoften difficult to obtain an A wave fromwhich amplitude and duration can bemeasured. In patients with the pattern ofimpaired relaxation on the transmitralDoppler waveform, the D wave of thepulmonary venous signal may be bluntedcorresponding to a low velocity transmitralE wave (Figure 5.7). The amplitude andduration of the Ar wave will be increased ifLV compliance is reduced and atrial func-tion is preserved. As LA pressure rises itscompliance is diminished. The size of theAr wave depends on LV compliance and LAfunction. During the pseudonormal phasethe Ar may be enhanced due to poor LVcompliance, but worsening LV diastolicfunction can result in LA enlargement,mechanical failure of atrial contraction anda reduced Ar.

The magnitude of the S wave is primarilyrelated to LA compliance and therefore thepulmonary vein systolic fraction (the pro-portion of the total pulmonary venous flowvelocity integral contributed by the S wave)is inversely related to mean LA pressure

57

Figure 5.7 Pulmonary venous pulsed wave Dopplersignal. The velocity of the D wave is reduced. Thiscorresponds to a low velocity E wave on the transmitralDoppler waveform and typifies the pattern of impairedrelaxation.

Figure 5.8 Three patterns of pulmonary venous flow arepresented: (A) the pattern of impaired relaxation with alow velocity D wave; (B) this is pseudonormal; and (C) is anexample of the restrictive pattern with a high velocity Dwave and low velocity S wave.

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(LAP) or LVEDP. Transition from pseudonor-mal to reversibly restrictive and fixedrestrictive physiology is marked by progres-sively lower S waves, a predominant D waveand an S/D ratio falling to below �1.0(Figure 5.8). Several studies have showngood correlations between pulmonary cap-illary wedge pressure or LVEDP and systolicfraction. As LVEDP increases, the resistanceto blood flow into the LV during atrial con-traction increases. This shortens the dura-tion of the transmitral A wave but prolongsthe duration of the pulmonary venous Arwave. An Ar �A duration predicts an LVEDP�15 mmHg and this relation is maintainedirrespective of systolic function.

Propagation velocity

Blood flow entering the LV reaches its max-imum velocity progressively later as thewave of filling propagates from the MVannulus to apex. This can be demonstratedby comparing a pulsed wave spectralDoppler tracing of LV inflow taken with thesample volume at the annulus with onetaken at the midcavity level. The timefrom maximum velocity at the annulus tomaximum velocity at a given point withinthe LV is prolonged in the presence of dias-tolic dysfunction. Color Doppler M-modewith the cursor directed through LV inflowdisplays a map of velocity against time andpermits measurement of this time delay(TD) and the propagation velocity (Vp),which is the slope of any isovelocity lineon this display. Adjustment of the scaleand baseline shift functions of the color

M-mode display will demonstrate an iso-velocity line at the aliasing velocity. Vp ismeasured as the slope of this line from theannulus to a point approximately 4 cm intothe LV, and it gives the rate of propagationof peak velocity of the early diastolic wavefrom base to apex. Vp ranges from 45 cm/s


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Figure 5.10 Tissue Doppler imaging with the samplevolume near the mitral valve annulus adjacent to the LVlateral wall. The E� velocity is reduced but the transmitralDoppler flow appeared normal. This indicates that thetransmitral Doppler was pseudonormal. The verticaldistance between calibration markers is 5 cm/s.

Figure 5.9 The color Doppler M-mode propagation velocity (Vp) is the slope of any isovelocity line (arrows). Three examplesare shown: (A) is from a normal subject and the Vp is �50 cm/s; (B) is from a patient with a pseudonormal transmitral Dopplerflow pattern; and (C) is from a patient with a restrictive transmitral Doppler flow pattern.

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to 55 cm/s in normal subjects and decreaseswith age. Vp is reduced equally in patientsexhibiting a pattern of impaired relaxationon the transmitral spectral Doppler tracingand patients with a pseudonormal pattern.Vp is further reduced in patients with therestrictive pattern of transmitral flowdemonstrating that the driving force of thehigh early transmitral pressure gradient israpidly attenuated (Figure 5.9). Vp is inde-pendent of the preload and correlates wellwith tau and peak negative dP/dT, indicat-ing that it is principally determined byrelaxation. Vp also varies with systolicfunction, cavity shape, and the extent ofsegmental wall dysfunction, emphasizingthe interrelation of systolic and diastolicfunction.

The ratio of the transmitral E wavevelocity and Vp is related to pulmonaryartery capillary wedge pressures. The E wavevelocity is determined by relaxation andLA pressure, while Vp is determined solelyby relaxation. Dividing E by Vp controlsfor the effects of relaxation and provides abetter estimate of filling pressures thaneither variable alone. The relation betweenE/Vp and filling pressure is maintained inpatients with atrial fibrillation.


The normal pattern of diastolic myocardialvelocity is biphasic with an early negativepeak designated E� and a later negative peakcaused by atrial contraction termed A�.Normal values for E� at the medial mitralannulus are from 10 cm/s to 15 cm/s andthose at the lateral annulus are from15 cm/s to 20 cm/s. The E� peak velocity ishigher than the A� velocity in normals andlike the transmitral E wave, E� decreaseswith age. E� velocity is reduced in diastolicdysfunction but does not change with vari-ations in preload. Maneuvers that increasepreload such as volume infusion or leg lift-ing will cause a pattern of impaired relax-ation on the transmitral flow to change to apseudonormal pattern with no change inE�. Reduced E� velocity with a normal trans-mitral flow profile indicates pseudonormal-ization (Figure 5.10). Normal transmitral

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Figure 5.11 (A) Transmitral PW Doppler demonstratingthe restrictive filling pattern. The vertical distance betweencalibration markers is 20 cm/s; (B) PW TDI with a lowvelocity E� wave. The vertical distance between calibrationmarkers is 5 cm/s. The E/E� ratio (115/3 � 38) indicates anelevated LVEDP.

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flow can be distinguished from pseudonor-mal by a combination of a tissue Dopplerimaging E� of �8.5 cm/s and an E�/A� ratioof �1.0. A normal ratio of E/E� is �8. Theratio does not change with impairedrelaxation as both E and E� are reduced. Asdiastolic function deteriorates, the LA pres-sure rises causing an increase in E but nochange in E� (Figure 5.11). The E/E� ratiocontinues to increase with the appearanceof a restrictive pattern of transmitral flowcaused by further increases in LA pressure.The E/E� ratio has also been used to predictLV filling pressure. An E/E� ratio �8accurately predicts a normal mean LV end-diastolic pressure (LVEDP) and an E/E� ratioof �15 accurately predicts a mean LVEDP of�15 mmHg. However, intermediate valuesof E/E� are associated with a wide variationin mean LVEDP.

Abnormal tissue Doppler imaging veloci-ties have been used to differentiate physio-logic hypertrophy in athletes’ hearts fromthat in pressure overload hypertrophy.Doppler findings in diastolic dysfunctionare summarized in Table 5.1 and Figure 5.12.


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Normal Delayed relaxation Pseudo normal Restrictive

E High Low HighE/A �1 �1 �1.0 �2.0Isovolumetric relaxation

time �100 ms �100 ms �60 msDT �220 ms �220 ms �220 ms �150 msS wave �D Higher Lower BluntedD wave �S Lower HigherA rev Low (up with age) Prominent �35 unless Prominent unless

atrial failure atrial failurePropagation velocity �55 (45 in elderly) �45 cm/s �45 cm/s LowerE� �10 (8 in elderly) �8 cm/s �8 cm/s LowerE/E� �8 �8 Higher HigherLA pressure Normal Normal Moderately elevated High

Table 5.1 Summary of diastolic function

MVDoppler

Pulmonaryvein Doppler TDI Vp

Impairedrelaxation

Diastolicdysfunction(reversible)

Diastolicdysfunction

(fixed)

Normal

Pseudonormal

Figure 5.12 Transmitral Doppler waveforms, pulmonaryvenous Doppler waveforms, tissue Doppler imaging (TDI)waveforms and propagation velocity slopes are sketchedfor normal, impaired relaxation, pseudonormal, andirreversible and fixed diastolic dysfunction patterns. Asdiastolic dysfunction progresses from impaired relaxationthrough to irreversible diastolic dysfunction, transmitral Ewave velocities increase, while pulmonary venous S wavevelocities, pulsed wave TDI E� velocities and propagationvelocity (Vp) are increasingly reduced.

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The successful use of Doppler/echocardiog-raphy in the evaluation of patients withknown or suspected coronary artery disease(CAD) requires: the technical expertise toobtain high quality images; experience inrecognizing and semi-quantifying varia-tions in regional function; and a detailedknowledge of coronary anatomy and itsrelations with the regional blood supply.

CORONARY ANATOMY

The ostia of the main right and left coro-nary arteries arise from their respectivesinuses of Valsalva approximately two-thirds of the way from the aortic annulus tothe sinotubular junction. In the short axisview of the aortic valve the proximal 1–2 cmof the right coronary artery (RCA) may bevisualized at the 12 o’clock position (Figure6.1). The RCA travels medially and inferi-orly in the right atrioventricular sulcusbeneath the right atrial appendage. TheRCA has a variable number of branches thattravel from base to apex and supply theanterior and lateral aspects of the right ven-tricle, the most prominent of which is theacute marginal branch. In 90% of subjects,the RCA continues as the posterior descend-ing coronary artery (PDA) in the posteriorinterventricular sulcus. The coronary arterythat continues as the PDA is termed the

dominant artery. The RCA supplies thebasal and mid-thirds of the inferior andposterior left and right ventricular walls, theposterior one-third of the interventricularseptum, the posteromedial papillary mus-cle, the right bundle branch, and the poste-rior left bundle branch. Posterolateralbranches of the RCA continue beyond thePDA in the atrioventricular sulcus and giveoff a branch that loops back to supply theatrioventricular node. In two-thirds of sub-jects the RCA also supplies the sinoatrialnode.

The left main coronary artery can oftenbe seen in a short axis view of the aorta atthe 3 o’clock position. It is usually between5 mm and 20 mm long. In two-thirds ofcases the left main bifurcates into the leftanterior descending (LAD) coronary artery,which lies in the anterior interventricularsulcus, and the circumflex coronary artery,which travels under the left atrialappendage to the left atrioventricular sul-cus. Here the circumflex artery gives off oneto three obtuse marginal branches thattravel from base to apex and nourish theleft ventricular (LV) lateral wall and antero-lateral papillary muscle, which is also sup-plied by the LAD. The terminal branches ofthe circumflex anastomose with the PDAand posterolateral branches of the RCA.Anastomoses are present from birth andbecome collateral sources of blood flowwhen a stenosis limits competing flow into

CORONARY ARTERY DISEASE

CONTENTS ● Coronary Anatomy ● Wall Motion Abnormalities ● EchocardiographicEvaluation of the Patient with Acute Chest Pain ● Complications of Acute Infarction

6

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a vessel. In one-third of cases, the left maintrifurcates into the LAD, circumflex, and anintermediate vessel that parallels the obtusemarginal vessels.

When the circumflex becomes the PDA(10% of subjects) the left coronary arteryis dominant, and the circumflex suppliesthe basal, mid and often apical thirds ofthe posterior LV wall. The length of theRCA is reciprocally related to that of thecircumflex.

The LAD descends in the anterior inter-ventricular sulcus from base to apex andascends in the posterior interventricular sul-cus for a variable distance where its termi-nal branches anastomose with the PDA. TheLAD gives off septal perforators that supplythe anterior two-thirds of the interventricu-lar septum and the entire apical septum anddiagonal vessels (usually two but there maybe more smaller vessels) that supply the LVfree wall. The LAD may also supply the rightventricular (RV) anterior free wall andusually supplies the RV apex (Figure 6.2).

Critical stenoses tend to occur at bendsand branch points of the coronary arteriesand occur mostly in the proximal half ofthe LAD, the distal half of the RCA, and the

mid-portion of the circumflex. Regionalwall motion abnormalities (WMAs) result-ing from myocardial ischemia or infarctiondue to coronary artery occlusion occur inregions of myocardium in the distributionof the occluded coronary artery. Althoughcoronary artery flow distribution varies, it isusually possible to identify the culprit vesselfrom the location of a WMA. Occlusion ofthe LAD results in akinesis of the anteriorwall and anterior septum beginning at thelevel of obstruction and continuing apicallyalong the course of the vessel (Figure 6.3).The apical third of the LV and often avariable amount of the RV apex becomesakinetic in the majority (�80%) of LADinfarctions. Occlusion of the RCA causesWMAs of the basal and middle thirds of theRV posterior wall, the posterior interven-tricular septum and the LV posterior andinferior walls when there is right coronaryartery dominance. A similar pattern ofWMA is observed in occlusion of the cir-cumflex occlusion in left coronary arterydominance. A WMA resulting from anocclusion of the circumflex when there isright dominance usually extends to the lat-eral wall and not inferiorly. Extension of an

Figure 6.1 The left main (LM) coronary artery is seen in the left panel (arrow) and the origin of the right coronary artery(RCA) is shown in the right panel (arrow). With the aortic valve in short axis, slight clockwise rotation facilitates visualization ofthe LM, while slight counter-clockwise rotation with superior angulation helps to show the RCA (R, right coronary cusp; L, leftcoronary cusp; N, noncoronary cusp; LA, left atrium; PA, pulmonary artery; AO, aorta).

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63

PDA

LMCIRCLADRCA

�

�

�

�

AO

Figure 6.2 Diagram of the coronary arteries.The left anterior descending coronary artery (LAD)travels in the anterior interventricular sulcus andwraps around the apex ascending for a variabledistance in the posterior interventricular sulcus.The right coronary artery (RCA) usually gives offthe posterior descending artery (PDA) (LM, leftmain; CIRC, circumflex; AO, aorta).

Figure 6.3 Parasternal long axis view. The interventricular septum is thin and akinetic resulting from occlusion of theproximal left anterior descending coronary artery (LV, left ventricle; LA, left atrium).

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inferior WMA to any apical wall segment isinfrequent (�40%). WMAs involving thebasal and mid LV lateral wall from stenoticlesions of the circumflex are rare (�5%)(Figure 6.4). Thus, infarction of the antero-lateral papillary muscle is much lesscommon than infarction of the postero-

medial papillary muscle. Patients may haveeither inferior (IMIs) or anterior (AMIs)infarctions. Those with IMIs have a propen-sity for dysrhythmias and mitral regurgita-tion due to posteromedial papillary muscledysfunction (Figure 6.5). Patients with AMIsare more likely to undergo LV remodeling


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Figure 6.4 Apical four-chamber view. The basal and mid-portions of the lateral wall are akinetic resulting from occlusion ofthe circumflex coronary. A mitral valve annuloplasty ring is also demonstrated (arrow) (RV, right ventricle; LV, left ventricle; RA,right atrium; LA, left atrium).

Figure 6.5 Parasternal short axis view showing posterior and inferior wall akinesis as a consequence of occlusion of theposterior descending artery (LV, left ventricle).

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and to form aneurysms with increased riskfor mural thrombus (Figure 6.6).

WALL MOTION ABNORMALITIES

The principal goal of echocardiography inpatients with CAD is the evaluation ofregional variations in systolic function.Images adequate for the analysis of regionalvariations in systolic function can beobtained in approximately 95% of allpatients by skilled and experienced sonog-raphers but interpretation is complicated bya number of factors. WMAs may be difficultto recognize in subendocardial infarctswhen less than 20% of the transmuralthickness is affected. In such cases wallmotion may be normal or only mildlyhypokinetic. LV dyssynchrony caused bypacing or native delays in electrical conduc-tion may be difficult to distinguish fromregional akinesis or hypokinesis.

The size of a WMA does not correlateexactly with infarct size. Infarct size is over-estimated when the normally perfused

borderzone myocardium is tethered by theinfarcted muscle. This tethering affectsendocardial excursion and wall thickening.Similarly, infarcted muscle can be pulledalong by the vigorous contraction of adja-cent segments but this does not affect itswall thickening. There may be discordancebetween the size of a wall motion abnor-mality and regional myocardial perfusionfor a variable time after successful reperfu-sion. The presence of an old infarction mayconfound the detection of a new WMA, buta wall segment that is thin and highlyreflective of ultrasound (echo bright), indi-cating scar tissue, can be considered old.

Size of WMAs/quantitation of regionaldysfunction

WMAs are scored using a 16-segment modelof the LV; six segments from the basal thirdof the heart, six from the middle third, andfour from the apex, because there is lessmuscle mass at the apex. The LV is dividedinto thirds using the papillary muscles’tips and bases as lines of demarcation (Figure6.7). Each wall segment, visualized from a

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Figure 6.6 Apical three-chamber view. There is extensive posterior wall and apical akinesis. A large mobile thrombus (arrow)is seen at the apex. There is also extensive calcification of the aortic valve and mitral annulus (LV, left ventricle; LA, left atrium).

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combination of parasternal and apical imag-ing views, is graded based on endocardialexcursion and wall thickening:

1 – wall motion is normal or hyperdynamic2 – the wall is hypokinetic3 – the wall is akinetic4 – the wall is dyskinetic (i.e. moves para-

doxically with systole).

The scores for all 16 segments are thensummed to give a global assessment of LVsystolic function. Higher wall motion scores(WMS) are associated with worse clinicaloutcomes after an infarction predicting anincreased risk of death, development ofcongestive heart failure and malignantarrhythmias.

Quantitative analysis of LV WMAs can beachieved by comparison of diastolic and

systolic endocardial silhouettes. This ispossible from the apical imaging planesbecause as the ventricle contracts the mitralannulus moves toward the apex with negli-gible translational or rotational motion.Comparison of the two silhouettes revealsthe endocardial excursion of each wall seg-ment toward the centroid (center of gravity)of the LV. For an akinetic segment the twosilhouettes are superimposable (Figure 6.8).The length of the akinetic segment can bemeasured and indexed to the percentage ofthe total endocardial perimeter or cavitylength.

In Sheehan’s centerline method, regionalendocardial excursion is quantified by iden-tifying the diastolic and systolic endocardialboundaries. A line intermediate betweenthe two boundaries, the centerline, is deter-mined and 100 equidistant chords aredrawn perpendicular to it. The endocardialexcursion from diastole to systole is meas-ured along each chord. The resulting linearmeasurements can be displayed graphicallyoverlying a range of normal values for eachchord.

ECHOCARDIOGRAPHIC EVALUATION OFTHE PATIENT WITH ACUTE CHEST PAIN

The absence of a regional WMA at rest doesnot exclude the diagnosis of severe epicar-dial CAD or even total coronary arteryocclusion in the presence of collateral ves-sels. Between 20% and 40% of patientswith non-Q wave infarctions do not have adetectable WMA, but patients withoutWMAs typically have small infarctions anda favorable prognosis. Echocardiographycan identify other causes of chest pain,such as pericarditis with pericardial effu-sion, aortic stenosis, pulmonary embolismor aortic dissection (although the diagnosisof aortic dissection cannot be excluded bytransthoracic echocardiography alone).

Regional function can be assessed com-pletely from the apical window alone orfrom a combination of apical and paraster-nal images. The motion pattern of each leftand right ventricular wall segment can be


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Apical

Middle

Basal

PS

PS4 CH

3 CH

2 CH

L

L

AS

LA LA AO RA

RV

LA

AS

P

P

I

I

A

A

Figure 6.7 Relation between the apical scan planes andthe short axis plane. The apical four-chamber (4 CH) viewintersects the clock face of the short axis at approximately4 o’clock and 10 o’clock and shows the lateral wall (L)and posterior interventricular septum (PS). The apicalthree-chamber (3 CH) or apical long axis view intersects theclock face of the short axis at approximately 12 o’clock and6 o’clock and shows the anterior interventricular septum(AS) and posterior wall (P). The apical two-chamber (2 CH)view intersects the clock face of the short axis atapproximately 2 o’clock and 8 o’clock and shows theinferior and anterior walls (RV, right ventricle; LV, leftventricle; RA, right atrium; LA, left atrium).

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carefully evaluated. Ejection fraction andLV end-systolic volume are major determi-nants of survival after an infarction. Thepresence and severity of mitral regurgita-tion should always be assessed by colorDoppler post-infarction because even mildregurgitation is associated with increased1-year mortality, development of congestiveheart failure and recurrent MI. Doppler alsoprovides important homodynamic informa-tion. Pulmonary artery (PA) pressure canbe estimated when tricuspid regurgitation(TR) is present. Left atrial or pulmonary cap-illary wedge pressure can be estimated usingone of several Doppler or tissue Dopplertechniques (see Chapter 4). Pseudonormaland restrictive patterns of transmitral flowearly after an AMI predict progressive LVenlargement and a greatly increased 1-yearmortality.

Obtaining high-quality images is oftentechnically challenging in patients in car-diogenic shock who are being mechani-cally ventilated and cannot be positionedoptimally for the exam. Parasternal imagesare often obscured. Rolling the patient totheir left side even a small amount andpropping them up with pillows will greatly

increase the yield from the apical imagingwindow. Off axis images (intermediatebetween the parasternal and apical win-dows) are often obtainable and providesubstantial information. Images from thesubcostal window are frequently fully diag-nostic and should always be attempted inthis setting.

COMPLICATIONS OF ACUTE INFARCTION

Aneurysms

LV aneurysms are regional dilatations/deformations of the infarcted myocardiumthat bulge in systole but also have an abnor-mal contour in diastole (Figures 6.9, 6.10).They are more commonly associated withAMIs than IMIs and 90% involve the apex.The walls of an aneurysm are thin, fibrosedand highly reflective of ultrasound (‘echobright’). Aneurysms usually develop withindays to weeks of a transmural infarction.Early aneurysm formation, within 5 days ofinfarction, is associated with an 80% 1-yearmortality. Systolic bulging is mechanically

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Figure 6.8 (A) From a patient with a large anterior infarction, and (B) from a patient with a large inferior wall infarction thatextends to the apex. Endocardial boundaries are traced in diastole (red) and systole (blue). In the panels on the right, systolicendocardial excursion is the difference between the diastolic and systolic silhouettes. The akinetic wall segments do not move,their diastolic and systolic endocardial tracings are superimposed (LV, left ventricle; LA, left atrium).

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Figure 6.9 Apical four-chamber view demonstrating a left ventricular (LV) apical aneurysm. The aneurysm has an abnormalcontour in diastole and expands slightly in systole (RV, right ventricle; RA, right atrium; LA, left atrium).

Figure 6.10 Apical two-chamber view demonstrating a left ventricular (LV) apical aneurysm. The apex has an abnormalcontour in diastole and the aneurysm expands in systole (LA, left atrium).

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disadvantageous and the aneurysm andadjacent tissue is a substrate for ventriculararrhythmias.

Thrombus

WMAs, whether aneurysmal or akinetic, arecommonly the nidus for mural thrombusformation and associated systemic emboli.Thrombus is less frequent following IMIthan AMI (Figure 6.11). Mural thrombus isidentified echocardiographically as a mass,attached to but distinct from the endo-cardium, which protrudes into the cavity. Itis necessary to differentiate intracavitaryclot, which is visible in orthogonal imagingplanes and moves with the cardiac cycle,from trabeculations, which are linear andoften reticulated (Figure 6.12), and fromartifacts, which can extend outside of thecavity, and do not move with the cardiaccycle. Visualization of thrombus from atleast two echocardiographic imaging planesis mandatory for diagnosis. Suspectedthrombus must be distinguished from falsechords and trabeculations, and apical shortaxis views of the LV are particularly usefulfor this. Thrombi may have a broad (sessile)

(Figure 6.13) or narrow (pedunculated) baseof attachment and may be highly mobile.The appearance of a mural thrombus varies,becoming more echo-dense as it ages. Thecenter of a thrombus may liquefy andbecome echolucent. The risk of systemic orcerebral emboli is increased in patients withapical aneurysms and poor systolic functioneven without echocardiographic documen-tation of thrombus. The risk for systemiccardioembolism increases when the throm-bus protrudes into the LV cavity and whenthe thrombus is mobile.

Cardiac rupture

Rupture of the LV free wall is a leading causeof death following an acute infarction,occurring in 3% of cases and accounting for10–15% of in hospital deaths post infarc-tion. Cardiac rupture usually occurs in thefirst week after a transmural infarction ina myocardial segment that was previouslyhealthy, having neither fibrosis nor collater-als. It is more common in females, elderlypeople and hypertensive patients. Cardiacrupture is rarely witnessed echocardio-graphically because it results in tamponade,

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Figure 6.11 Apical four-chamber view from a patient with a large apical aneurysm. A large laminated mural thrombus (*)lines the aneurysm (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

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Figure 6.12 An apical short axis view of the left ventricle (LV) demonstrating a mobile, protuberant thrombus (*) with ahypoechoic center that represents liquefaction of the core of the thrombus. From the apical four-chamber view the transduceris brought to a parasternal short axis orientation and moved one or two intercostal spaces higher on the chest to acquireapical short axis images. The focal zone should be brought to the near field and a higher transducer frequency can beemployed (RV, right ventricle).

Figure 6.13 Apical four-chamber view in a patient with a large laminated apical mural thrombus. A right ventricular (RV)pacing wire is also seen (arrow) (LV, left ventricle; RA, right atrium; LA, left atrium).

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shock, and rapid demise. Occasionally,small subacute ruptures may be detected.Pericardial clot and an effusion thatincreases in size over time may signalimpending complete cardiac rupture andthe need for emergent surgical repair.

Pseudoaneurysm

Myocardial rupture may be contained bypreexisting pericardial adhesions resultingin a pseudoaneurysm (Figure 6.14). The LVcavity is in direct communion with thepericardial space causing a localized out-pouching, which is usually lined withthrombus (Figures 6.15, 6.16). The point ofentry or neck of a pseudoaneurysm is nar-row relative to its size and this usuallyallows it to be distinguished from a trueaneurysm, which is contained by scarredmyocardium rather than the parietal peri-cardium. Color Doppler flow mappingoften reveals a characteristic pattern of flow

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Figure 6.14 Apical two-chamber view of an apicalpseudoaneurysm (P) lined with thrombus (*) (LV, leftventricle; LA, left atrium).

Figure 6.15 Parasternal long axis view. Medial angulation of the transducer demonstrates an inferior wall pseudoaneurysmlined with thrombus (*) (RV, right ventricle; LV, left ventricle; LA, left atrium; AO, aorta).

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into the pseudoaneurysm in systole andback into the ventricle in diastole and canestablish the presence of a communicationwhen it cannot be visualized with two-dimensional imaging. Pseudoaneurysmscan be small or large (several hundredmilliliters) and deprive the systemic circula-tion of a significant amount of the strokevolume. They usually contain thrombus,which can embolize and also rupturecausing sudden death. Prompt surgicalrepair is mandated in almost all cases.

Ventricular septal rupture

Rupture of the interventricular septum ispredisposed by the same factors as free wallrupture and also usually occurs in the firstweek after an infarction. The mortality rateis high (95–100%) without surgical repair.When ventricular septal rupture accompa-nies an anterior infarction, the site of septalrupture (VSD) is in the apical third of theventricle, usually in close proximity to themoderator band (Figure 6.17). VSDs in thislocation are imaged best from the apical


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Figure 6.16 Parasternal short axis views. A large inferior wall pseudoaneurysm that expands in systole is shown. ‘Smoke’ isseen in the pseudoaneurysm (RV, right ventricle; LVOT, left ventricular outflow tract; Dao, descending thoracic aorta).

Figure 6.17 Apical four-chamber view with color Dopplerdemonstrating systolic flow at the apex from LV to RVthrough a post-infarction ventricular septal defect (RV,right ventricle; LV, left ventricle; RA, right atrium; LA, leftatrium).

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four-chamber, apical short axis, and sub-costal four-chamber views. VSDs in associa-tion with inferior wall infarctions occur atthe base of the heart beneath the postero-medial papillary muscle near the junctionof the septum with the RV free wall andmay have a serpiginous course. VSDs in theinferior wall are best seen from the paraster-

nal (Figure 6.18) and subcostal short axisviews (Figure 6.19) but may be difficult tovisualize with two-dimensional echo andare often first recognized with color flowDoppler. Continuous wave Doppler of theflow across a VSD can be used to obtain theinterventricular pressure gradient. Off axisimaging is often necessary to align the

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Figure 6.18 Parasternal short axis view at the level of the papillary muscles. The diastolic frame shows a very thin inferiorwall. The systolic frame demonstrates an interventricular communication (arrow) associated with inferior left ventricular (LV)wall and right ventricular (RV) free wall akinesis.

Figure 6.19 Subcostal four-chamber view. There is a large defect in the basal posterior septum in the left panel. Color flowDoppler demonstrates a large left-to-right shunt through the ventricular septal defect in systole (RV, right ventricle; LV, leftventricle; RA, right atrium; LA, left atrium).

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beam with the flow. The magnitude of theleft-to-right shunt (Qp/Qs) can be calcu-lated by Doppler echocardiography. A stepup in the oxygen saturation of blood in theRV found at cardiac catheterization in apatient with an acute MI is strongly sugges-tive of a VSD but if color Doppler doesnot reveal flow across the interventricularseptum, the interatrial septum should becarefully examined. Elevated LV diastolicpressures caused by the infarction mayincrease left-to-right shunting across apreviously unsuspected small atrial septaldefect or patent foramen ovale.

Papillary muscle rupture

Papillary muscle rupture occurs in approxi-mately 1% of myocardial infarctions andusually affects the posteromedial papillarymuscle. It results in acute severe mitralregurgitation and pulmonary edema that isusually fatal if the entire trunk of the pap-illary muscle is ruptured. In acute mitralregurgitation the force of the regurgitantjet is not blunted by a large compliant LAas in chronic mitral regurgitation but istransmitted to the pulmonary vasculature.

The affected papillary muscle and usuallythe underlying myocardium are thin andecho-dense on two-dimensional echo. Oneof the mitral leaflets is often flail and rup-tured chords attached to the leaflets exhibita chaotic motion pattern. The rupturedhead of the papillary muscle is often visibleas a mobile mass attached to the leaflet thatprolapses into the LA in systole and maymimic a valvular vegetation. The jet ofmitral regurgitation is often eccentric andthe severity of the regurgitation can beunderestimated by color Doppler. The con-tinuous wave Doppler signal may demon-strate a steep slope from early to late systolereflecting rapid equilibration of LA and LV

pressures. Systolic flow reversal in the pul-monary veins and a heightened E wave onthe transmitral diastolic waveform shouldalso raise the suspicion of acute severe mitralregurgitation. TEE may be necessary fordiagnosis as patients are often tachycardic,in cardiogenic shock, and mechanicallyventilated.

Right ventricular infarction

Right ventricular infarction complicatesbetween one-third to one-half of IMIs andoccurs in isolation in approximately 3% ofall MIs. It is rarely associated with AMIs. Itis important to recognize post-infarctionRV dysfunction because the use of drugsthat are standard in LV infarction, such asdiuretics and nitrates, may lower RV pre-load, reduce cardiac output, and causehypotension in RV infarction.

In RV infarction echocardiographydemonstrates hypokinesis of the RV free wallassociated with an inferior LV wall motionabnormality. The RV apex is usually suppliedby the LAD coronary artery and its wallmotion is usually normal or hyperdynamicwhen RV infarction complicates an IMI. TheRV cavity is enlarged, the percentage changein RV cavity area reduced, and septum flat-tened in diastole. Paradoxical septal motionwith preserved septal thickening resultsfrom an elevated RV end-diastolic pressure.RV filling pressure is elevated as shown byIVC enlargement, which persists throughinspiration and by RA enlargement withbowing of the interatrial septum to the left.Right-to-left shunting through a patentforamen ovale may cause hypoxemia.Tricuspid regurgitation due to cavityenlargement or papillary muscle involve-ment in the infarction has a low velocitydue to poor RV systolic function andelevated RA pressure.


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The four cardiac valves normally open toallow unimpeded forward flow and closesecurely to prevent retrograde blood flow(Figure 7.1). Conditions that impair thesetwo functions alter chamber sizes, cardiacfunction, and hemodynamics, in propor-tion to their severity. Doppler echocardiog-raphy is ideally suited to assess obstructionto forward flow, regurgitant flow, and their

consequent effects on cardiac architecture,function, and hemodynamics.

THE MITRAL VALVE

Mitral valve anatomy

The annulus of the mitral valve (MV) is anintegral part of the fibromuscular cardiacskeleton, being attached to and supportedby the aortic annulus anteriorly and on theleft and right by the two fibrous trigones.The posterior annulus connects with thebasal ventricular myocardium at the atrio-ventricular (AV) groove. The annulus isshaped like the letter ‘D’ with the straightside of the D lying beneath the aortic valve.The anterior and posterior MV leaflets haveapproximately the same surface area but theposterior leaflet occupies approximately60% of the perimeter of the annulus.However, the anterior leaflet is the longerand more excursive of the two leaflets. Theanterior leaflet divides the LV into inflowand outflow tracts (LVIT and LVOT), and istriangular in shape with a rounded (convex)free edge, whereas the posterior leaflet isnearly rectangular. The normal mitral valveleaflets are �2 mm thick and are separatedby two commissures, anterolateral andposteromedial, which do not extend allthe way to the annulus. Two indentations

VALVULAR HEART DISEASE

CONTENTS ● The Mitral Valve ● The Aortic Valve ● The Tricuspid Valve ● The PulmonicValve ● Endocarditis ● TEE Versus TTE in Endocarditis ● Surgical Treatment of ValvularHeart Disease

7

A

A

A

R

R

N L

L

SP

P

Figure 7.1 Diagram of the spatial relations of the valves atthe base of the heart. The aortic (red) and mitral (blue)valves are in fibrous continuity while the pulmonic (green)and tricuspid (yellow) valves are separated by theinfundibulum. The pulmonic valve is twisted approximately60� from the plane of the aortic valve (R, right; L, left;A, anterior; P, posterior; N, noncoronary; S, septal).

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divide each leaflet into medial, central, andlateral scallops. The divisions are moreprominent for the posterior leaflet. Thescallop extending from the anterolateralcommissure is designated P1, P2 is central,and P3 extends from the posteromedialcommissure. Chords (chordae tendineae)(Figure 7.2) from the posteromedial papil-lary muscle attach to the medial half ofboth leaflets, and chordae from the antero-lateral papillary muscle attach to the lateralhalf of both mitral leaflets. The anteriorleaflet has no chordal attachments to itsbasal portion as does the posterior leaflet.Contraction of the papillary muscles inearly systole brings the leaflets together andinitiates valve closure.

Mitral stenosis

The normal diastolic mitral orifice is ellipti-cal in shape with an area of 4–6 cm2. Mitralstenosis (MS) typically causes symptoms ofexertional dyspnea when the orifice isreduced to 1.5–2.0 cm2 and MS is criticalwhen the orifice is �1.0 cm2.

EtiologyMS is almost invariably the result of rheu-matic fever but may rarely be congenitalresulting from anomalies of the leaflets orsubvalvular apparatus. Congenital MS isusually associated with chordal attachmentsfrom both leaflets to a single papillary mus-cle termed a parachute MV. Mitral annularcalcification (MAC) is a common finding inelderly people, particularly elderly women.It is also associated with systemic hyperten-sion, renal disease, and aortic stenosis. MAC(Figure 7.3) is usually confined to theventricular side of the posterior annulus

Figure 7.2 Apical long axis view. The continuity of thepapillary muscles, chordae tendineae (arrows) and mitralvalve leaflets is demonstrated in the image from a normalsubject (LV, left ventricle; LA, left atrium; AO, aorta).

Figure 7.3 Parasternal short axis view at the level of themitral valve. There is extensive mitral annular calcification(arrow) that causes shadowing and partially obscures distalstructures (RV, right ventricle; LV, left ventricle).

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at the base of the posterior leaflet but canspread to the entire posterior annulus caus-ing obstruction to left ventricular (LV) fillingthat is usually mild.

Rheumatic MS results from fusion of thetwo leaflets at the commissures, whichnarrows the orifice producing a funnel witha minimal cross-sectional area usually at theleaflet tips. The leaflets thicken, fibrose,cicatrize, and calcify over time. The rheu-matic process begins at the leaflet tips andextends to the body of the leaflets and thechordae. Thickening and fusion of the chor-dae close off interchordal communicationsand worsen the obstruction. Progressivenarrowing of the MV orifice elevates leftatrial (LA) pressure causing LA enlargement,and increased the likelihood of atrial fibril-lation and thrombus formation. Loss ofatrial contraction impairs diastolic filling.Elevated LA pressure is transmitted to thepulmonary vasculature causing pulmonaryhypertension. Pulmonary hypertensioncauses right ventricular hypertrophy (RVH),tricuspid regurgitation (TR), and ultimatelyright heart failure with hepatic congestionand peripheral edema. Symptoms of MS aresimilar to those of left heart failure; dyspneaon exertion, orthopnea, and paroxysmalnocturnal dyspnea but the LV is relativelyunaffected by MS.

M-mode echo findingsThe M-mode of the MV in MS shows dimin-ished early opening (D to E excursion), aflattened E–F slope and anterior motionof the posterior leaflet in diastole (Figure7.4). The latter finding is due to fusion ofthe leaflets at their tips so that the posteriorleaflet is pulled along with the anteriorleaflet. Bright reflections representing calci-fication may obscure posterior structures.LV size is normal and diastolic filling is slowand prolonged. Paradoxical septal motiondue to RV pressure and volume overloadmay be present or the interventricular sep-tum (IVS) may dip leftward in early diastolereflecting relatively enhanced RV filling.The LA is usually enlarged and the aorticvalve may also be affected by rheumatic dis-ease. The M-mode of the pulmonic valve(PV) shows loss of the A wave and may

show mid-systolic closure in pulmonaryhypertension.

Two-dimensional echo findingsCommissural fusion produces doming ofthe MV, which is best seen in the paraster-nal long axis view. A ‘hockey-stick’ or ‘bentknee’ appearance is seen in diastole whenthe body of the anterior leaflet is still pliable(Figure 7.5). The leaflets become moreimmobile, as thickening and calcificationprogress and diastolic leaflet doming is lost(Figure 7.6). Subvalvular involvement in therheumatic process can be assessed from theparasternal long axis and apical views byshifting the plane medially and laterally toinspect the chordae and papillary muscles.By carefully scanning through the funnel ofthe MV in the short axis plane the charac-teristic fish-mouth-shaped orifice can berecognized (Figure 7.7). The minimal mitralorifice area can be visualized and planime-tered in approximately 80% of all patientsbut this method is difficult to apply whenthere is extensive calcification or whenthere has been distortion of the valve fol-lowing balloon valvuloplasty. Gain settingsshould be high enough to visualize thewhole orifice without drop-out, but lowenough to prevent ‘blooming’ of echoesfrom the valve, which would cause the

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Figure 7.4 M-mode of the mitral valve in a patient withmitral stenosis.

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orifice area to be underestimated. Theeffects of MS on other cardiac structuresand the effects of the rheumatic process onthe other valves must also be assessed. LAenlargement will be present and LA throm-bus may be seen but cannot be excludedby transthoracic echocardiography (TTE)alone. Right heart enlargement, RVH andabnormal septal motion is expected andreflects the severity of pulmonary hyperten-sion. Relative chamber sizes are best seen inthe apical four-chamber view (Figure 7.8).

Doppler findingsPulmonary artery systolic and diastolicpressures should be assessed from the spec-tral Doppler velocity signals of tricuspidand pulmonic regurgitation, respectively, inall patients, but are especially important inpatients with MS. Most patients with MShave some degree of mitral regurgitation(MR), which should be carefully evaluated.

The Doppler flow velocity across the MVcan be assessed from the apical windowin almost all patients. Pulsed-wave (PW)


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Figure 7.5 Parasternal long axis view in a patient withmitral stenosis (MS) demonstrating the ‘hockey-stick’ or‘bent knee’ deformity that is present in MS while theanterior leaflet is still pliable (LV, left ventricle; LA, leftatrium; AO, aorta).

Figure 7.6 Parasternal long axis view in a patient withmitral stenosis. The mitral valve is thickened and immobile.The aortic valve is also thickened. The left atrium (LA) andright ventricle (RV) are enlarged (LV, left ventricle).

Figure 7.7 Parasternal short axis at the tips of the mitralvalve in early diastole in a patient with mitral stenosis (RV,right ventricle).

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Doppler (Figure 7.9) usually provides aclearer envelope but continuous wave (CW)Doppler will ensure that the peak velocitiesare included in the sample (Figure 7.10).Peak and mean pressure gradients across theMV can be calculated from peak and meanDoppler velocities using the modifiedBernoulli equation (Figure 7.11), where pres-sure � 4 � (peak velocity2). The gradientsalone, however, do not necessarily reflectthe severity of the stenosis. They are in part

determined by the amount of blood flow,which varies with cycle length and presenceof MR. The rate of equilibration of LA andLV pressure is a more fiducial measure of MSseverity and can be obtained from the spec-tral envelope of the transmitral Dopplerflow velocity. The time required for thepeak transvalvular gradient to decrease byone-half, the pressure half-time (P1/2), is areliable measure of the rate of pressureequilibration. Since velocity is quadratically

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Figure 7.8 Apical four-chamber view in a patient with severe mitral stenosis and moderate tricuspid stenosis andregurgitation. Note that the left atrium (LA) and right heart chambers are enlarged but the left ventricle is underfilled.A pericardial effusion is also seen (*) (RV, right ventricle; RA, right atrium).

Figure 7.9 Pulsed-wave Doppler with thesample volume at the tips of the mitral valveleaflets in a patient with moderate mitralstenosis. The peak velocity across the valve isapproximately 240 cm/s indicating a peakgradient of 23 mmHg. This patient is in atrialfibrillation and no A wave is seen.

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related to pressure, the P1/2 time will equalthe time from peak velocity to peak velocitydivided by the square root of 2 (1.414). Thepressure half-time is independent of heartrate or coexistent MR and is related to themitral orifice area by the formula: MVA �220/P1/2.

A pressure half-time of 220 ms equals avalve area of 1.0 cm2 (Figure 7.12).

When the E to F slope of the transmitralflow velocity spectrum is nonlinear, themid-diastolic slope is used. The mid-diastolic slope is extrapolated back to thetime of peak velocity and the pressure half-time is recalculated. The pressure half-timemethod underestimates the severity of MSin the presence of aortic regurgitation (AR).Competitive retrograde filling of the LVfrom the aorta increases LV diastolic pres-sure and quickens the rate of transmitralpressure equilibration. Similarly, the pres-ence of an atrial septal defect (ASD) willdecompress the LA and cause the P1/2method to underestimate the severity ofthe MS.

The cross-sectional area of the MV can alsobe estimated from the continuity equation.Blood flow across the MV in diastole mustequal blood flow through the LVOT in sys-tole if there is no aortic or mitral regurgita-tion. LVOT stroke volume can be calculatedas the product of the LVOT flow velocityintegral and the LVOT cross-sectional area.The MV area is equal to the LVOT stroke vol-ume divided by the transmitral flow velocityintegral. The pulmonary artery (PA) strokevolume can be substituted for the LVOTstroke volume if there is important AR butthe PA diameter can be difficult to measureaccurately.

Another application of the continuityequation, the proximal isovelocity surfacearea (PISA) method, can be used to measureMV orifice areas. Blood flow accelerates as itconverges toward a narrowing from a largerchamber. Blood flow within the funnel ofthe stenosed MV accelerates toward the lim-iting orifice in a series of concentric hemi-spheres whose velocity can be determinedby color Doppler (Figure 7.13). The colorDoppler scale and baseline are adjusted sothat the first PISA is clearly seen and theradius of the first isovelocity hemisphere ismeasured. The area of the hemisphere is cal-culated as 2p(r2). The velocity of the bloodat all points on the hemisphere is equal tothe first aliasing velocity taken from thecolor Doppler map. The product of the areaof the PISA and the velocity at the PISA is


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Figure 7.10 Continuous wave Doppler in a patient withmoderate mitral stenosis.

LV

LA

Figure 7.11 Left atrial (LA) and left ventricular (LV)pressure tracings in a patient with mitral stenosis. Apressure gradient (red) exists as LA pressure remainssignificantly higher than LV pressure throughout diastole.

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the volume flow rate and it is equal to theproduct of the peak transmitral velocityand area of the MV orifice (Figure 7.14).

MVA � 2p(r2) � V(Nyquist)/V(peak)

The PISA method assumes that the MVorifice is circular and that the PISA is ahemisphere and these assumptions are notalways warranted.

Percutaneous balloon valvuloplasty isused to increase the MV orifice area by split-ting the commissures. The interatrial sep-tum (IAS) is punctured and a balloon tippedcatheter is positioned in the MV orifice andrapidly inflated. Shunting across the IAS iscommon immediately after the procedurebut is not typically seen at late follow-up.Transesophageal echocardiography (TEE) isnecessary to rule out LA thrombus prior tothe procedure and TEE or TTE is often usedto assess results following each ballooninflation. Echocardiography is used to pre-dict the clinical outcome of percutaneousballoon valvuloplasty using a scoringsystem devised at Massachusetts GeneralHospital. A numeric value from 1 to 4 inorder of ascending severity is assigned forfour characteristics of the MV; subvalvularinvolvement, leaflet thickening, mobilityand calcification. A score of �8 indicates a

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Figure 7.12 Pressure half-time method for determining the mitral valve area. The red vertical arrows indicate 1 m/s and thered horizontal arrows indicate 200 m/s. The peak velocity of the continuous wave Doppler signal on the left is 207 cm/s and thepeak velocity of the signal on the right is 160 cm/s. The velocity at pressure half-time is 146 cm/s for the patient on the left(207/1.414) and 113 cm/s for the patient on the right (160/1.414). The patient on the left reaches the pressure half-time in241 ms (white arrow) and has a valve area of 0.9 cm2 (220/241). The patient on the right reaches the pressure half-time (whitearrow) in 147 ms and has a valve area of 1.5 cm2 (220/147).

MV

LV

LA

MV

Figure 7.13 Blood accelerates as it approaches anarrowing in the flow stream. The color Doppler signalaliases each time the velocity crosses a multiple of theNyquist limit and a series of concentric hemispheres ofalternating colors are formed. The cross-sectional area ofthe proximal hemisphere is determined from themeasured radius (2p(r2)). The area of the proximalisovelocity surface area (PISA) � the Nyquist limit velocity� the mitral valve (MV) orifice area � the peak transmitralvelocity therefore, MV area � PISA area � Nyquistlimit/peak mitral velocity (LV, left ventricle; LA, left atrium).

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good likelihood of success when there islittle MR.

Mitral regurgitation

Mechanisms Mild MR can be detected in 70–80% ofnormal people by color Doppler.Hemodynamically significant MR can resultfrom any disease process that affects thestructural components of the MV: thepapillary muscles, myocardium, chordae,leaflets, or the annulus. TransthoracicDoppler echocardiography can assess theetiology and severity of MR and the effectsof MR on LV, LA, and right heart chambersize and function, pulmonary artery systolicpressure (PASP), and identify any associatedlesions.

Chronic MRIn chronic severe MR, the LV initiallyincreases its stroke volume to accommodateforward and retrograde flow. The LV inchronic severe MR may remain compen-sated for many years, however, the effects ofthe volume overload are progressive. The LVdilates and assumes a more spherical shape.As the LV enlarges the mitral annulusdilates and the papillary muscles are pulledlaterally and apically disrupting leafletcoaptation and further exacerbating theMR. In chronic MR the LA progressivelydilates forming a reservoir that can accom-modate the regurgitant volume withouttransmitting systolic LV pressure back to thepulmonary vasculature. However, in acutesevere MR due to papillary muscle rupture,there is no time for the LA to dilate or adaptto the regurgitant volume, so that LA and leftpulmonary pressures are acutely elevatedresulting in pulmonary edema.

In chronic MR preload is initiallyincreased while LV afterload and wall stressare low because the LV can eject (unload)partly into the LA, which is a low-pressuresink. Ejection phase indices of LV systolicfunction are inversely related to wall stressexplaining the supernormal ejection frac-tion. Thus, a normal ejection fraction inchronic severe MR indicates LV dysfunc-tion. As LV systolic volume increases, wallstress increases, LV systolic function deteri-orates, and this deterioration can becomeirreversible.

The MV frequently appears normal in MRbut careful examination of the valve and itssubunits often reveals the etiology of theMR. In rheumatic heart disease, MR coexistswith MS resulting from scarred rigid leafletswith commissural fusion and shortenedchordae that prevents valve closure. MACcan inhibit LV posterior basal wall motionand impede posterior MV leaflet motionproducing MR.

Ischemic MRIschemic MR can result from infarction orischemia of a papillary muscle (usually theposteromedial) or of the LV wall that sup-ports the papillary muscle. MR may beacute and torrential (see Chapter 6) or


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Figure 7.14 Apical two-chamber view showing theproximal isovelocity surface area (PISA). The radius of thefirst isovelocity surface area is 0.9 cm (arrow). Theisovelocity surface area of the PISA is 5.1 cm2 (2p(r2)). TheNyquist limit taken from the Doppler color map is 40 cm/sand the peak transmitral velocity is 200 cm/s. The mitralvalve area is equal to 0.8 cm2 [(5.1 � 40)]/250) (LA, leftatrium).

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intermittent causing episodic flash pul-monary edema. Contraction abnormalitiesof the myocardium subjacent to the papil-lary muscle are generally evident and thesewalls may be thinned and noncontractile.The papillary muscle may be scarred andatrophied and motion of one of theleaflets is often restricted in ischemic MR.Dyssynchronous contraction of the papil-lary muscles and subjacent myocardiumdue to an intraventricular conductiondefect affects the timing and coordinationof valve closure and promotes MR. Cardiacresynchronization therapy coordinates pap-illary muscle contraction and significantlyand immediately reduces MR severity insome patients.

MR may also result from LV remodelingpost-infarction or in dilated cardiomyopa-thy and it can be difficult to determinewhether the MR caused the LV dysfunctionor resulted from it. MR resulting from cavityenlargement usually produces a centralregurgitant jet.

Mitral valve prolapse (MVP)MVP is the most common cause of isolatedMR occurring in 2–4% of the population.

The valve leaflets are thickened, redundant,and hypermobile. The annulus is usuallydilated, the chordae are stretched, elon-gated, and prone to rupture. Folds of leaflettissue billow or prolapse into the LA insystole. The posterior leaflet is more com-monly affected than the anterior leafletbut both leaflets and other cardiac valvesmay be affected. In a subset of patientsleaflet deformity is severe and the degreeof MR and LV dysfunction are progressive.Chordal rupture may produce flail leafletsegments and severe (acute on chronic)MR.

The prolapse and regurgitation may beholosystolic or late systolic. Doppler colorflow has shown that posterior MV leafletprolapse causes the MR jet to be directedanteriorly while the MR jet from anteriorleaflet prolapse is directed posteriorly. Thediagnosis of MVP should not be madeunless leaflet thickness is �5 mm and pro-lapse of either leaflet or their point ofcoaptation reaches 2.0 mm beyond theplane of the mitral annulus in the paraster-nal long axis view (Figure 7.15). The extentof the MVP should not be determined fromthe apical four-chamber view because the

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Figure 7.15 Parasternal long axis view in a patient with prolapse of the posterior mitral valve leaflet (arrow) (LV, leftventricle; RA, right atrium; LA, left atrium; AO, aorta; Dao, descending thoracic aorta).

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MV annulus is saddle-shaped and closer tothe apex in this view.

Other causes of MROther causes of MR include: infiltration ofany portion of the valve apparatus withamyloidosis or sarcoidosis; collagen vascu-lar disease, such as systemic lupus erythe-matosus or rheumatoid arthritis; andcongenitally cleft mitral valve as part of anendocardial cushion defect and trauma(although trauma to the tricuspid valve(TV) is more common than to the MV).Prolonged exposure to the anorexigensphenteramine and fenfluramine (�6months) can result in encasement of theposterior leaflet in a substance similar tothat seen in carcinoid heart disease.

Evaluation of severity of MR M-mode imagingThe LA is usually enlarged and expands insystole, causing an exaggerated anterior dis-placement of the aorta. In severe MR theaortic valve leaflets drift closed in systoledue to diminished forward stroke volume(Figure 7.16). LV size and function isassessed by measuring LV internal diametersand calculating fractional shortening.

Two-dimensional imaging This can assess LA size and LV size and func-tion. The apical views are best to visualizethe subvalvular apparatus and to determineif the chordae are thickened, redundant,and if leaflet motion is restricted. Cardiacchamber sizes, and coexistent valvularabnormalities must be ascertained. The PApressure should also be assessed, as thedevelopment of pulmonary hypertension isassociated with increased surgical mortality.

Color Doppler flow mappingThe color signal of MR will alias many timesas the MR jet is driven by the pressure differ-ence between the LV and the LA. This resultsin a bright, multicolored, mosaic jet, whichis very easy to detect visually (Figure 7.17).Color Doppler is exquisitely sensitive fordetecting MR but jets may be eccentric sothat multiple views should always be used.Angling the beam through the orthogonal

or azimuthal plane helps the operator con-struct a three-dimensional appreciation ofthe extent of the color disturbance. Theseverity of the MR is graded on a scale of 1to 4 depending on the spatial extent of thecolor disturbance. The spatial extent of thecolor can also be indexed to the LA area.When the color Doppler signal occupies20–40% of the LA, the MR is considered tobe moderate, less than 20% mild and greaterthan 40% severe.

The regurgitant volume is determined bythe pressure gradient between the LV andLA, the shape and orientation of the jet, thesize and shape of the regurgitant orifice andthe compliance of the LA. The regurgitantjet in acute MR will be small relative to itsregurgitant volume because of high LA pres-sure. Jets that collide with the LA wall tendto adhere to it (Coanda effect) losing energy


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Figure 7.16 M-mode echocardiogram of the aorta (AO)and left atrium (LA) in a patient with chronic, severe mitralregurgitation. The left atrium is 10 cm in diameter. Theaortic valve leaflets begin to drift closed in mid-systole(RVOT, right ventricular outflow tract).

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in the process. Color Doppler grading ofMR overestimates central jets and under-estimates eccentric jets, particularly thosethat hug the wall. In addition, jets may bemultiple and usually vary through systole.

Measurement of the vena contracta width,the narrowest central portion of a color jetwith the greatest velocity, correlate wellwith regurgitant orifice areas and angio-graphically determined regurgitant gradesand is independent of load. The parasternallong axis view and the apical views offeropportunities for multiple measurements.Zoom mode should be employed and theminimum diameter measured in the framethat shows the maximum MR for each view.MR is classified as moderate when the venacontracta width is between 0.3 cm and0.5 cm. It is mild when below this rangeand severe if �0.5 cm. These measurementscan be made in approximately 90% of allpatients and can differentiate mild fromsevere MR but there is overlap between mildand moderate and moderate and severe MR(Figure 7.18).

Spectral DopplerSpectral Doppler of the LV inflow tract(LVIT) demonstrates a high velocity E waveconsistent with rapid LV filling. The contin-uous wave Doppler signal of MR becomeseasier to obtain and its signal intensityincreases as the severity of the MR increases,because signal intensity is proportional tothe number of scatterers in the regurgitantjet. A CW Doppler signal of MR that matchesthe antegrade flow in intensity representssignificant MR.

Pulmonary vein DopplerThe S wave of the pulmonary venous wave-form is blunted or reversed when there issignificant MR but this finding may beabsent when the LA is large and compliantor difficult to interpret when the jet is eccen-tric and aimed directly at the pulmonaryvein under interrogation (Figure 7.19).

Regurgitant volume is the difference betweenthe stroke volume calculated fromplainimetry of two-dimensional images of

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Figure 7.17 Parasternal long axis view with colorDoppler showing severe mitral regurgitation in a patientwith mitral valve prolapse (LV, left ventricle; LA, leftatrium; AO, aorta).

Figure 7.18 Measurements (arrows) of the vena contractawidth in a patient with moderate mitral regurgitation (MR)(left panel) and in a patient with severe MR (right panel)(LV, left ventricle)

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the LV in diastole and systole and the strokevolume calculated as the product of theflow velocity integral (FVI) of the pulsedwave Doppler signal of flow in the LVOTand the LVOT cross-sectional area. The for-mer stroke volume includes the regurgitantvolume whereas the latter does not.Similarly, the transmitral stroke volume canbe calculated as the product of the mitralannular area, which is assumed to be circu-lar and the FVI of the transmitral diastolicflow taken at the same location. This strokevolume also includes the regurgitant vol-ume and can be substituted for the strokevolume derived from LV images. A strokevolume calculated from the PA diameterand FVI could be substituted for the LVOTDoppler stroke volume. Regurgitant frac-tion is calculated as regurgitant volumedivided by total (forward plus regurgitant)stroke volume. All methods used for deter-mination of stroke volume are limited.Quantitation of LV volumes from two-dimensional images is operator dependentand reliant upon good image quality. PWDoppler methods are dependent on accu-rate measurements of diameters and smallerrors are magnified as the diameters aresquared to obtain areas. The assumptionthat the MV annulus is circular may betrue in some patients but not others.

Nevertheless, calculation of regurgitantfraction can classify MR as mild, moderateor severe with reasonable accuracy. A regur-gitant fraction of 30–50% denotes moderate(2–3) MR, less than 30% is mild (1) andgreater than 50% is severe (4).

The PISA method calculates volumetric flowas the product of the cross-sectional area(CSA) of the flow stream and the FVIrecorded at the same location, and relies onthe fact that volume flow through a vessel isconstant and independent of the diameterof the vessel (Figure 7.20). As blood in theLV converges toward the regurgitant orificeof the MV the flow velocity increases. Thiszone of flow convergence consists ofconcentric hemispheres radiating from the


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Figure 7.19 Pulmonary vein pulsed wave Doppler. The Swave of this tracing is blunted by the mitral regurgitantflow.

Figure 7.20 Apical four-chamber view with color Dopplerin a patient with mitral regurgitation. The color Dopplerscale is reduced to 25 cm/s to increase the size of theproximal isovelocity surface area (PISA). The PISA radius is1.4 cm (arrow). The cross-sectional area of the PISA is 12cm2 (2p(r2)). The peak velocity of the mitral regurgitation(MR) continuous wave Doppler signal is 5 m/s. The mitralvalve regurgitant orifice area (ROA) is 0.6 cm2 ((12 � 25)/500)(PISA flow/MR peak velocity � ROA) indicating severe MR(LV, left ventricle; LA, left atrium).

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regurgitant orifice. The shell of the inner-most hemisphere has the smallest cross-sectional area but the fastest flow velocity.Shells further from the regurgitant orificewill have larger cross-sectional areas andlower velocities. The products of the cross-sectional area and velocity are equal foreach shell indicating that the flow at eachshell is constant. This flow is equal to theregurgitant flow and can be calculated asthe product of the velocity and area wherearea � 2p(r2), when r is the radius of thehemispherical shell. Using color Doppler ashell is identified as an arc of color change,red to blue or blue to red, which appearswherever the flow velocity exceeds a multi-ple of the Nyquist velocity. By adjusting thecolor Doppler baseline shift and scale func-tions, the first aliasing velocity (the proxi-mal shell) can be visualized and the radiusor distance to the valve orifice measured.The area of the shell, its PISA is calculated as2p(r2), the velocity at the PISA is given bythe Nyquist limit of the color Doppler mapthat is displayed on the screen. The regurgi-tant flow is the product of the two. Flow atthe PISA must be equal to flow through theorifice so that:

VelocityPISA � CSAPISA � VelocityMR � CSAMR

or the PISA flow divided by the peak veloc-ity of the CW signal of MR is equal to theregurgitant orifice area (ROA). The regurgi-tant volume is equal to the ROA multipliedby the FVI of the MR by CW Doppler.

PISA flow/MR peak velocity � ROA

ROA � FVIMR � Regurgitant volume

An ROA between 20 mm2 and 40 mm2 indi-cates moderate (2–3) MR. An ROA belowthis range can be considered mild (1) andabove this range, severe (4).

Difficulties with this technique remain.The assumption that the concentric flowfields are hemispheric may not be justifiedwhen the jet is constrained by adjacentstructures. When the jet is constrained, theangle of the unimpeded flow convergence ismeasured (angle a) and the ROA equation iscorrected for the degree of flow constraintby multiplying it by a/180�.

THE AORTIC VALVE

Aortic valve anatomy

The aortic valve is in close proximity to allfour cardiac chambers. The aortic annulusseparates the LVOT from the aorta and givesoff three spurs, which form the three com-missures and sinuses that terminate at thesinotubular junction. The valve cuspsseparate in systole to form a nearly circularorifice. In diastole the three cusps appose inthe center of the aortic lumen and preventregurgitant flow. The nodules of Arantiusare small mounds of fibrous tissue at thecenter of the closing edges of each cuspthat facilitate complete closure. The valveleaflets extend for a few millimetersbetween the closing edge and the free edgeof each cusp. The aortic sinuses of Valsalvaare outpouchings of the aortic wall behindeach cusp. The diameter of the aorta at thelevel of the sinuses is larger than at theannulus or sinotubular junction. The coro-nary arteries arise from the right and leftaortic sinuses of Valsalva close to the sino-tubular junction. The plane of the aorticvalve faces superiorly, rightward andslightly posteriorly so that the direction ofblood flow in systole is toward the rightshoulder. The aortic valve can be easily visu-alized echocardiographically from the leftparasternal window and flow assessed byDoppler from the apical, suprasternal, andright parasternal windows.

Bicuspid aortic valve

Bicuspid aortic valve (BAV) is the most com-mon congenital cardiac abnormality occur-ring in approximately 1% of the populationwith a 2:1 male to female predominance. ABAV usually has two leaflets of nearly equalsize with the commissure running obliquelyfrom lower left to upper right in theparasternal short axis image but leaflet ori-entation is variable. When the two cusps areof unequal size, the larger may contain araphe, which is a fibrous ridge at the site offusion between two congenitally conjoinedcusps. A raphe may cause the valve to appeartricuspid in diastole, but the systolic orifice

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is elliptical (Figure 7.21). Approximately50% of cases of coarctation of the aorta areassociated with BAV.

Most bicuspid valves are at least mildlyregurgitant and in younger patients withBAV significant AR is much more commonthan significant aortic stenosis (AS).Significant regurgitation is usually due toprolapse of the larger of the two aorticcusps. BAVs are prone to accelerated calcifi-cation and are the most frequent causeof AS in the fifth to sixth decades. Valvecalcification usually involves the base of thecusps and the raphe.

Aortic root dilatation and ascending aor-tic aneurysm are commonly associated withBAV and occur out of proportion to thehemodynamics of concomitant aorticstenosis or regurgitation suggesting anintrinsic defect of the aortic root tissue. BAVis present in approximately 15% of proxi-mal (type A) aortic dissections; the risk ofaortic dissection is increased ninefold bythe presence of a BAV. The morphology ofthe BAV can be defined echocardiographi-cally in short axis images in greater than90% of cases. It is helpful to move thetransducer approximately 1 cm laterallyand angle the beam medially. Subcostalshort axis views of the base may alsodemonstrate aortic valvular anatomy and

are especially useful when parasternalviews are suboptimal.

In the parasternal long axis view the clo-sure line in diastole is often eccentric inBAV. Stenosed BAVs often exhibit systolicdoming (Figure 7.22), the minimal orifice


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Figure 7.21 Short axis of the aortic valve in zoom mode. The aortic valve appears to be trileaflet in the diastolic frame but isshown to be bicuspid with a raphe in systole.

Figure 7.22 Parasternal long axis view of the aortic valvein systole. This bicuspid aortic valve exhibits systolicdoming and mild stenosis (LV, left ventricle; LA, left atrium).

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area is at the tips of the leaflets. M-mode orshort axis imaging at the base of the cuspsmay underestimate the degree of stenosis.The Doppler color flow jet of AR is ofteneccentric in BAVs when the two cusps areunequal in size. Imaging of the ascendingaorta distal to the sinotubular junction isrequired in patients with BAV and is bestaccomplished from the right parasternalwindow with the patient in the right lateraldecubitus position.

Aortic stenosis

Congenital AS Congenital AS is either acommissural orunicommissural. In the acommissural typethe valve functions as a diaphragm with asmall central orifice and there is markedsystolic doming. A unicommissural valvehas two raphes, usually between the rightand left cusps and between the right andnoncoronary cusps leaving only a small slit-like orifice between the left and noncoro-nary cusps (Figure 7.23). The stenosiscaused by either type is usually severe andpatients present in infancy. Coarctation ofthe aorta should be excluded in all patients

with congenitally abnormal valves by care-ful imaging and Doppler interrogation ofthe descending aorta from the suprasternalnotch.

Senile calcific ASIn senile AS, calcification affects the bodiesof the cusps beginning at the base with ini-tial sparing of the commissures. It is themost common cause of AS in patients �70years. The rate of progression of calcifica-tion varies greatly, but is associated with thesame risk factors as atherosclerosis: hyper-tension, hypercholesterolemia, smoking,male sex, diabetes, and advanced age. Aorticvalve sclerosis without hemodynamicallyimportant stenosis marks the early stage ofthe disease process.

Rheumatic ASRheumatic valvulitis causes thickening ofthe cusps, commissural fusion, and progres-sive stenosis, which may become significantprior to the development of calcification. Itis invariably associated with rheumatic MVdisease.

Subvalvular ASObstruction to LV outflow can occur proxi-mal to the aortic valve and may be fixed ordynamic. Dynamic LVOT obstruction asso-ciated with systolic anterior motion of theMV is a feature of hypertrophic obstructivecardiomyopathy (see Chapter 8). Fixed out-flow tract obstruction at the subvalvularlevel is caused by a discrete outcropping oftissue in the form of a membrane or shelfthat narrows the outflow tract (Figure 7.24).Typically a ridge of tissue arises from theIVS a few millimeters proximal to the rightcoronary cusp. Alternatively, it may encirclethe LVOT or more rarely arise from theanterior MV just proximal to the aorticvalve. The extension of the membrane intothe outflow tract is usually triangular inshape being broader at the base than at thetips. Severe subaortic obstruction usuallypresents in infancy. Subvalvular obstruc-tions are best visualized echocardiographi-cally in the parasternal or apical long axisplanes or in the apical five-chamber view.The pressure gradient across the obstruction

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Figure 7.23 Parasternal short axis view in a patient witha unicommissural aortic valve. There are two raphes(arrows) seen in this systolic frame (RA, right atrium; LA,left atrium; PA, pulmonary artery).

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can be reliably assessed by CW Doppler.LVOT membranes are usually echo-brightbut if thin may be difficult to recognize. Ajet of AR that is redirected upon striking theobstruction may first suggest subaorticstenosis. The aortic valve may be damagedby the high velocity jet from the obstruc-tion causing the commonly associatedaortic regurgitation. Subaortic stenosis mayrecur after successful surgery.

Supravalvular ASCongenital supravalvular AS results from anarrowing of the ascending aorta. Theobstruction usually occurs just above thesinotubular junction and the narrowingmay be focal or tubular. This type of obstruc-tion is associated with stenoses of the pul-monary arteries, usually at the bifurcation orin branch vessels. Supravalvular aorticstenosis is a feature of William syndrome,which is characterized by mental retarda-tion, pulmonic stenosis, hypercalcemia, and

elfin facies. Severe supravalvular obstructionexposes the coronary arteries to elevatedpressures and accelerated atherosclerosis.Coronary ostial lesions are common. Rarely,supravalvular obstruction may also occurfrom deposition of large atheroscleroticplaques in the ascending aorta as occurs infamilial homozygous hypercholesterolemia.

Symptoms of ASThe prognosis in AS relates to developmentof symptoms, 75% of patients die within3–5 years of the onset of symptoms of chestpain, syncope or dyspnea attributable to thestenosis without surgical relief of obstruc-tion. Progression to heart failure caused bydeteriorating systolic function occurs late inthe course of the disease and is associatedwith myocyte degeneration and fibrosis.The prognosis of a patient with symptomsat rest is poor.

Doppler-echocardiography in ASM-modeDiminished leaflet excursion and leafletcalcification seen on M-mode does notpredict the severity of aortic stenosis. Thepresence of the normal box-shaped aorticvalve pattern on M-mode echocardiogra-phy excludes the diagnosis of significantAS except when the valve is congenitallyabnormal and exhibits systolic doming.

Two-dimensional echo Two-dimensional echo imaging from theparasternal LV long axis (Figure 7.25) andshort axis (Figure 7.26) show thickenedand calcified leaflets with restricted leafletmotion. Concentric LV hypertrophy (LVH)is invariably present in hemodynamicallysignificant AS and is best assessed from theparasternal long and short axis views(Figure 7.27) or if these are inadequate,from the subcostal short axis. LVH can bedefined as a relative wall thickness (end-diastolic wall thickness�2/end-diastolic LVcavity radius) �0.42. In ‘compensated’ AS,systolic function is preserved and LV cavitysize remains normal because the LVH nor-malizes systolic wall stress. When wallstress can no longer be normalized byfurther LVH, LV dilatation occurs, systolic


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Figure 7.24 Parasternal long axis view in a patient withfixed left ventricular (LV) outflow tract obstruction from asubaortic ridge of tissue (arrow) (RV, right ventricle; LA, leftatrium; AO, aorta).

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function deteriorates and ‘decompensated’AS ensues.

Doppler echoThe pressure gradient (Figure 7.28) acrossthe aortic valve in AS is measured with CWDoppler from the imaging windows thatallow the beam to be aligned parallel totransaortic flow. CW Doppler velocity sig-nals should be obtained from the apicalfive-chamber (Figure 7.29) or apical longaxis, right parasternal (Figure 7.30) andsuprasternal notch views in every patientwith AS. The non-imaging or CW transduceris important in obtaining the maximumvelocity because its small footprint allows itto be manipulated in the intercostal spacesfor optimum alignment with flow. Two-dimensional imaging identifies the optimallocation for placement of the non-imagingprobe and color flow Doppler identifies thedirection of transaortic flow. The angle ofthe CW beam is adjusted incrementallyusing the audio signal and the spectral dis-play until a complete spectral envelope isobtained from each window. The highestvelocity obtained is used to estimate the

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Figure 7.25 Parasternal long axis in a patient with aorticstenosis. Aortic valve excursion is markedly reduced in thisearly systolic frame (LV, left ventricle; LA, left atrium; AO,aorta).

Figure 7.26 Parasternal short axis views in a patient with aortic stenosis and regurgitation. The systolic frame showsmoderate reduction in the aortic valve cross-sectional area. The diastolic frame shows a small, central regurgitant orifice (RA,right atrium; LA, left atrium; PA, pulmonary artery).

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Figure 7.27 Parasternal short axis images of the left ventricle (LV) from a patient with severe aortic stenosis demonstratesevere concentric LV hypertrophy and normal systolic function.

LV

AO

Figure 7.28 Aortic (red, AO) and left ventricular (LV)pressure tracings (black) in a patient with aortic stenosis.The pressure gradient measured by continuous waveDoppler is the peak instantaneous gradient (long verticalarrow) and not the peak to peak gradient (short verticalarrow) measured at cardiac catheterization.

Figure 7.29 Continuous wave Doppler tracing of aorticstenosis. The transducer is at the apex and flow is awayfrom the transducer. The peak velocity of the signal isapproximately 4 m/s indicating a peak instantaneoustransaortic gradient of 64 mmHg.

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pressure gradient across the aortic valve andassess the severity of AS as Doppler veloci-ties can be underestimated when the beamis not aligned with the flow but they cannotbe overestimated. The Doppler peak instan-taneous pressure gradient is determinedfrom the transaortic flow velocity by theformula:

Pressure gradient �4(VelocityAOV

2 VelocityLVOT2)

where VelocityAOV is the maximumrecorded CW velocity through the aorticvalve and VelocityLVOT is the maximum PWDoppler velocity recorded in the LVOT. Thelatter is best obtained by placing the PWsample volume in the region of flow accel-eration immediately proximal to the aorticvalve and gradually withdrawing it until asmooth thin envelope representing laminarflow with a well-defined peak velocity isachieved. The sample volume will beapproximately 0.5–1.0 cm proximal to thevalve. Peak flow velocity in the LVOT nor-mally ranges from 0.7 m/s to 1.5 m/s andvaries with stroke volume. When peakvelocity of LVOT flow is 1 m/s or less, theVelocityLVOT term in the pressure gradientequation can be ignored and the formulasimplifies to

Pressure gradient � 4(VelocityAOV2)

Omission of VelocityLVOT when it is highwill overestimate the transaortic gradient.

The pressure gradient may be elevated outof proportion to the severity of AS whenstroke volume is increased as in AR orbradycardia. Conversely, the transaortic gra-dient will be low when there is severe steno-sis and poor LV pump function. Calculationof the aortic valve area is mandatory inthese conditions.

The aortic valve area calculated using theconservation of energy principle/continuityequation is independent of stroke volumeand is therefore an integral part of the eval-uation of AS severity (Figure 7.31). The con-tinuity equation assumes that all of thestroke volume passing through the LVOTpasses through the aortic valve. LV strokevolume is calculated as the product of theLVOT FVI and the cross-sectional area of theLVOT. The LVOT is circular and its cross-sectional area is calculated from the LVOTdiameter measured from the parasternallong axis view in early systole as the dis-tance between the insertion points of theright and noncoronary cusps of the aorticvalve.

LVOT stroke volume (LVOTFVI � LVOTCSA)is equal to aortic valve stroke volume(AOVFVI � AOVCSA). The equation isrearranged to estimate aortic valve area:

AOVCSA � LVOTFVI � LVOTCSA/ AOVFVI

The PW Doppler envelope of the LVOTflow and the CW envelope of transaorticflow must be clear and complete for accurate

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Figure 7.30 Continuous wave Dopplertracing of aortic stenosis. The transducer isat the second right intercostal space andflow is toward from the transducer. Thepeak velocity of the signal is approximately5.2 m/s indicating a peak instantaneoustransaortic gradient of 108 mmHg. There isalso aortic regurgitation.

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valve area determination. The LVOT diame-ter measurement is critically important aserroneous measurements are squared in theLVOTCSA calculation. The aortic valve areafor adults is approximately 3.0 cm2 (2.6–3.6cm2). Critical AS is defined as an aortic valvearea �0.7 cm2, severe AS as 0.7–1.0 cm2 andmoderate AS as 1.0–1.5 cm2.

In some patients with AS and poor LVfunction it may be difficult to determinethe predominant condition and aortic valvearea may increase with increased stroke vol-ume. Dobutamine stress echo may be usedto establish whether aortic valve areaincreases significantly with dobutamine, ifso, severe AS is not present. If the trans-aortic gradient increases with increasedstroke volume the AS is severe. Patients whodo not demonstrate an increase in strokevolume or transaortic gradient with dobuta-mine have mild AS, which is not the causeof their LV dysfunction.

Impaired relaxation with a decreased Ewave and augmented A wave on transmitralDoppler and a prolonged isovolumic relax-ation time are common in AS. Coexistantmitral regurgitation by Doppler color flowis frequent and the severity of MR decreasesfollowing aortic valve replacement inapproximately 50% of patients. The pres-ence of coexistent AR and MR is easily

demonstrated using color Doppler in theparasternal long axis and apical views.

Aortic regurgitation

AR results from congenital or acquiredabnormalities of the valve cusps or fromenlargement of the aortic root. The mostcommon cause of AR is aortic root dilata-tion secondary to hypertension. Aortic rootenlargement prevents normal leaflet coap-tion causing central AR. Congenital andacquired AS are usually associated withsome degree of AR. Rheumatic AR resultsfrom commissural fusion, which interfereswith effective valve closure. Prolapse of atrileaflet aortic valve may be caused bymyxomatous degeneration of the leaflet tis-sue or annulus in association with mitraland tricuspid valve prolapse. Marfan syn-drome is usually associated with progressiveaortic enlargement limited to the aortic rootand ascending aorta, myxomatous degener-ation, and prolapse of the MV and increasedrisk for aortic dissection.

AR causes LV volume overload so that LVcavity volume increases to accommodateforward and regurgitant stroke volumes(Figure 7.32). In contrast to MR where theLV discharges its regurgitant volume intothe low pressure LA, in AR the LV stroke


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Figure 7.31 The measurements required for calculation of the aortic valve area by the continuity equation are displayed. Theyellow vertical arrows in the middle and right panels indicate the velocity calibration of 1 m/s. A left ventricular outflow tract(LVOT) diameter of 2.2 cm is measured (left panel), the LVOT cross-sectional area is therefore 3.8 cm2. The pulsed-wave Dopplersample volume is placed in the LVOT and the flow velocity integral is measured at 20 cm (middle panel). The flow velocityintegral of the continuous wave signal of flow through the valve is measured at 104 cm. The aortic valve area �(3.8 cm2 � 20 cm)/104 cm � 0.7 cm2 indicating critical aortic stenosis.

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volume is ejected into the high-pressuresystemic circuit. AR presents the LV withboth a pressure and volume overload. TheLV responds to increased diastolic load (wallstress) by cavity enlargement and eccentrichypertrophy that initially preserves strokevolume, and the increased systolic load(wall stress) induces concentric hypertro-phy that normalizes the increased systolicwall stress. An equilibrium may be sus-tained for many years wherein the patientremains asymptomatic with little change inLV size, however, the disease is generallyprogressive such that LV volumes continueto increase and the LV becomes morespherical. In severe AR concentric hyper-trophy becomes inadequate to normalizesystolic wall stress and systolic functiondeteriorates.

Patients usually first present with symp-toms of dyspnea on exertion or effort intol-erance and valve surgery is indicated at theonset of symptoms. Symptom onset isrelated to LV size and LV cavity enlargementis a marker of incipient LV systolic dysfunc-tion and increased mortality. To preventirreversible damage to the LV, surgery forasymptomatic patients is generally recom-mended when the LV end-systolic diameterexceeds 55 mm, when the LV end-diastolicdimension is greater than 75 mm or whenthe resting LV ejection fraction falls below50%.

Assessment of the severity of ARM-mode echoThe M-mode echo of the left ventricle in apatient with chronic AR is characterized byLV cavity enlargement and LVH with pre-served systolic function (Figure 7.33). Wall

thickness is normal or increased and theseptum exhibits a biphasic systolic excur-sion pattern. The AR jet often impingesupon the anterior MV leaflet limiting itsdiastolic excursion and causing high fre-quency fluttering of the anterior mitralleaflet or chordae, neither of these findingscorrelate with the severity of AR. The M-mode of the aortic valve in AR usuallyappears normal even when the AR is severe.

Two-dimensional echo Aortic valve morphology in chronic AR canbe precisely characterized in the largemajority of patients and the etiology deter-mined by a thorough examination of thevalve in the parasternal short and long axisviews. Diastolic aortic leaflet prolapse,leaflet perforation, vegetative endocarditisand systolic doming are best visualized inparasternal long axis and when this view is

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NL AS AR

Figure 7.32 Illustrates the relative muscle(blue) to cavity (red) ratios from a normalsubject (NL), a patient with severe aorticstenosis (AS), and a patient with severe aorticregurgitation (AR). Left ventricular musclemass is increased in AS and AR. AS causespressure overload hypertrophy and AR causesvolume overload hypertrophy.

Figure 7.33 M-mode echocardiogram of a patient withchronic aortic regurgitation. The left ventricle is enlarged,systolic function preserved and the interventricular septumexhibits biphasic systolic excursion.

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unavailable, apical long axis or apical five-chamber images in zoom mode should beattempted.

The severity of chronic AR is directlyrelated to LV chamber size and the LV canbecome enormously dilated (cor bovinum).As the LV enlarges it becomes more spheri-cal. LV size, shape, and function can beassessed from the apical four-chamber andother apical views but care must be takento image the full length of the ventriclewithout foreshortening.

DopplerAR from trivial to severe can be detected bycolor flow Doppler as a brightly colored

mosaic jet in the LVOT in diastole that iseasily seen in the parasternal long and shortaxis views, and the apical five-chamber andlong axis views (Figure 7.34). The AR jet isdriven by the pressure difference betweenthe aorta and the LV in diastole. The colorjet of AR must therefore alias several timesas this gradient equates to a CW Dopplervelocity of 3.5–4.5 m/s. The severity of theAR can be semiquantified by the spatialextent of the color disturbance, 1 ARwhen the color signal is within 1 cm of theaortic valve, 2 AR when the color jetextends to the MV leaflet tips, 3 AR whenit extends to the papillary muscles and 4AR when the color disturbance fills the LV.Regurgitant volume in AR is not the onlydeterminant of the size of the Doppler colorflow. It is also determined by the pressuregradient between the aorta and the LV, thedirection of the jet, shape of the regurgi-tatant orifice and the compliance of the LV.Regurgitant AR jets that run along the ante-rior MV or septum may not propagate dueto loss of momentum and result in underes-timation of the severity of AR (Figure 7.35).


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Figure 7.34 Apical long axis with color Doppler showingmoderate aortic regurgitation (LV, left ventricle; LA, leftatrium).

Figure 7.35 Parasternal long axis view showingmoderately severe aortic regurgitation with an eccentricjet.

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Measurement of jet width indexed to theLVOT diameter is used to assess the severityof AR (Figure 7.36). A color jet width �65%of the LVOT diameter corresponds toangiographic grade 4 (severe) AR, while acolor jet �25% of the LVOT diameterindicates angiographic grade 1 (mild) AR.Measurement of the area of the color signalin the LVOT in short axis immediately sub-jacent to the aortic valve plane indexed tothe LVOT cross-sectional area at this levelalso correlates with angiographic severity ofAR. When the color jet cross-sectional areaoccupies �50% of the cross-sectional area ofthe LVOT in this plane, the regurgitation issevere, whereas if it is �25% the AR is mildor mild to moderate.

Aortic regurgitant volume and regurgi-tant fraction can be determined by compar-ing two measured stroke volumes, one that

includes regurgitant volume, and one thatdoes not. Stroke volumes derived from dias-tolic and systolic volumes quantified fromapical images or from the LVOT diameterand PW Doppler FVI include regurgitantvolume (Figure 7.37). Stroke volumes quan-tified from PW Doppler FVI and cross-sectional area measurements of the PA ormitral annulus do not include regurgitantvolume.

Color Doppler signals of AR are rarelyadequate by TTE for the PISA method forregurgitant orifice area determination butthis area can be estimated by the continuityprinciple. Retrograde flow in the aorta canbe detected by PW Doppler in moderateand severe AR (Figure 7.38). The PW samplevolume is placed in the aorta approximately2 cm distal to the aortic valve andaligned with transaortic flow from the

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Figure 7.36 Measurements of thewidth of the color jet of aorticregurgitation (arrow) and the ratio of jetwidth to left ventricular outflow tractdiameter are facilitated by the use ofcolor M-mode.

Figure 7.37 Pulsed-wave (PW) Doppler with the sample volume in the left ventricular outflow tract (LVOT) in a patient withaortic regurgitation. Stroke volume calculated from LVOT diameter and the flow velocity integral of the PW Doppler signalincludes the regurgitant volume. Stroke volume calculated from RVOT diameter and FVI does not. Comparison of the twostroke volumes yields the regurgitant volume.

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suprasternal or high right intercostal posi-tion. The product of the FVI of aortic retro-grade flow and the cross-sectional area(CSA) of the aorta at the same level is equalto the regurgitant volume, which is equal tothe FVI of the CW signal of AR multipliedby the unknown regurgitant orifice area.

FVIAO � CSAAO � FVIAOV � CSAAOV orFVIAO � CSAAO/FVIAOV � CSAAOV

The assumption that coronary blood flowcontributes little to the diastolic FVI maycause the regurgitant orifice area to beslightly overestimated. Regurgitant fractioncan also be estimated as the ratio of forwardstroke volume to regurgitant volume. Thesevolumes are obtained by placing the PWsample volume in the ascending ordescending aorta (Figure 7.39) from thesuprasternal notch. The forward stroke vol-ume is the product of the systolic FVI andthe cross-sectional area of the aorta and theregurgitant volume is the product of thediastolic FVI and aortic cross-sectional area.Systolic and diastolic aortic diameters can-not be assumed to be equal and should bemeasured individually as the large forwardstroke volume causes a significant increasein the size of the aorta.

The magnitude of retrograde aortic bloodflow is proportional to the severity of theaortic incompetence. Holodiastolic retro-grade flow sampled in the abdominal aorta(Figure 7.40) from the subcostal window

represents severe AR provided that there isno patent ductus arteriosus. Holodiastolicretrograde flow in the descending aortasampled from the suprasternal notch repre-sents severe or moderate to severe regurgita-tion depending on the FVI of the diastolicsignal.

The velocity of the CW Doppler signal ofAR decelerates through diastole and the rateof deceleration reflects the rate of equilibra-tion of aortic and LV pressures. The slope of


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Figure 7.38 Pulsed-wave Dopplerwith the transducer at the apex andthe sample volume in the aortaapproximately 2 cm distal to theaortic valve. Retrograde flow in theaorta caused by aortic regurgitationis shown as flow toward thetransducer.

Figure 7.39 Pulsed-wave Doppler with the transducer inthe suprasternal notch and the sample volume in theproximal descending thoracic aorta. Retrograde flow in theaorta caused by aortic regurgitation is shown as flowtoward the transducer.

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the CW signal of AR is a marker of the sever-ity of the regurgitation. More severe ARcauses a faster rate of equilibration and asteeper deceleration slope (Figure 7.41). Adeceleration slope of less than 200 cm/sindicates mild regurgitation and a slopeof greater than 400 cm/s indicates severeregurgitation.

Acute severe ARSevere AR may develop acutely when thereis destruction of the leaflets from infectionor from loss of commissural support and

prolapse of the aortic valve into the LVOTwith aortic dissection. The LV cannot adaptacutely to the regurgitant volume by cavityenlargement. Aortic and LV pressures equil-ibrate rapidly in diastole so that LV diastolicpressure rapidly exceeds LA pressure caus-ing premature MV closure and diastolic MR.LV diastolic pressure and pulmonary venouspressure rise dramatically causing pul-monary edema. LV systolic function isacutely reduced rather than being hyper-dynamic as in chronic compensated AR dueto the sudden hemodynamic burden. AcuteAR can be difficult to assess echocardio-graphically. High LV diastolic pressure tendsto minimize the findings of retrograde flowin the aorta and tachycardia can make thecolor jet small and difficult to visualize.However, acute severe AR can be diagnosedfrom the slope of the CW signal of AR(Figure 7.42), which is very steep andreaches the baseline before the QRS com-plex of the ECG indicating equilibration ofaortic and ventricular pressure in diastoleand by premature MV closure detectable onM-mode in the absence of first degree A-Vblock (Figure 7.43). The cause of the regur-gitation may also be recognized on two-dimensional imaging. An intimal flapmay be seen in the lumen of the proxi-mal ascending aorta from type A aorticdissection, or there may be avulsion ofthe aortic valve leaflets due to vegetativeendocarditis.

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Figure 7.40 Pulsed-wave Doppler with the transducer inthe subcostal region and the sample volume in theabdominal aorta. Holodiastolic retrograde blood flowindicates severe aortic regurgitation.

Figure 7.41 The slope of the continuous wave Doppler signal of aortic regurgitation (AR) describes the rate of equilibrationof aortic and left ventricular diastolic pressures. The steeper the slope the more severe the AR. Moderate AR is indicated by theslope of the AR signal in (A) and severe AR indicated in (B).

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THE TRICUSPID VALVE

Anatomy

The TV annulus is larger than the mitralannulus, its leaflets are thinner, and thereare three leaflets of unequal size: theanterior, the posterior, and the septal. Theanterior and septal leaflets are seen inthe apical four-chamber view where the TVis distinguished from the MV by the moreapical insertion of the septal leaflet of theTV. There are three principal papillarymuscles, named for the leaflets to which

they attach, but accessory papillary musclesare common for the TV. The septal leaflet,which is attached at its base to the mem-branous and muscular interventricularseptum, also has direct chordal connectionsto the septum. The posterior is the smallestof the three leaflets and opens along thediaphragmatic surface of the RV. The poste-rior and anterior leaflets are seen in the RVinflow tract (RVIT) view. The PW signal oftrans-tricuspid flow is biphasic but variesmore with the respiratory cycle than doestransmitral flow.

TV annular calcification (TAC) occursmore commonly in elderly people and inpatients with altered RV hemodynamics.Calcification of the TV annulus is much lesscommon than MAC. It is usually seen as anecho-dense reflection from the annulusadjacent to the anterior tricuspid leaflet inthe apical four-chamber view.

Tricuspid stenosis

The etiology of tricuspid stenosis (TS) isalmost always rheumatic heart disease(RHD) that is associated with rheumatic dis-ease of the mitral and aortic valves, whichdictates the clinical course. The chronicinflammation occurring in RHD causes TVleaflet thickening, commissural fusion,chordal thickening, and retraction thatresults in restricted leaflet motion anddecreased TV orifice area (Figure 7.44). PureTS is rare and is more commonly combinedwith TR. The RA and inferior vena cava (IVC)


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Figure 7.42 The continuous wave Doppler signal in apatient with acute severe aortic regurgitation. There israpid equilibration of aortic and left ventricular diastolicpressure and they are nearly equal at end-diastole.

Figure 7.43 Premature mitral valve(MV) closure (downward pointing arrows)caused by acute severe aorticregurgitation. MV closure occurs beforethe next QRS complex (upward pointingarrows).

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are enlarged. RV size will be determined bythe degree of pulmonary hypertensionsecondary to mitral valve disease and thedegree of TR.

M-mode echoThe E–F slope of the TV by M-mode echo isreduced, the leaflets are thickened and theirmobility is restricted.

Two-dimensional echoThe M-mode echo features described aboveare corroborated by two-dimensional imag-ing of the TV which is optimally visualizedeither in the parasternal RVIT view, theapical or subcostal four-chamber views.Diastolic doming will be evident on two-dimensional imaging in TS (Figure 7.45).

DopplerThe Doppler velocity waveform of trans-tricuspid flow in TS is similar to that ofMS, but the peak and mean velocities andgradients are lower (Figure 7.46). A meangradient of 4 mmHg is consistent with severeTS. The TV orifice can rarely be seen from thesubcostal short axis view but usually cannotbe planimetered. The slope of trans-tricuspidflow reflects the rate of equilibration of RAand RV diastolic pressures and the orificearea can be calculated from the pressurehalf-time as TVA � 220/P1/2. This empiricequation is less well validated for TS thanMS. A careful examination of the TV ismandatory for all patients with RHD.

Tricuspid regurgitation

Mild TR occurs commonly in normal indi-viduals. It is present in 90% of patients witha PA systolic pressure �40 mmHg, and isnearly universal in patients with severepulmonary hypertension (Figure 7.47).Pathological TR can result from dilatationof the tricuspid annulus, damage to thevalve leaflets, papillary muscles or RVmyocardium. Annular dilatation results

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Figure 7.44 Apical four-chamber view in a patient withrheumatic heart disease. There is severe mitral stenosisand moderately severe tricuspid stenosis (arrow) (RV, rightventricle; LV, left ventricle; RA, right atrium; LA, leftatrium).

Figure 7.45 RA/RV view indiastole showing diastolic domingof the tricuspid valve andmoderate tricuspid stenosis.

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from RV cavity enlargement, that can besecondary to cor pulmonale, left heartfailure, or left-to-right shunting. Annulardilatation interferes with normal coaptationof the leaflets resulting in incomplete clo-sure and central regurgitation. The tricuspidleaflets can be damaged by blunt chesttrauma, radiation therapy, infection, RHD,or RV biopsy. Myxomatous degeneration ofthe TV causing prolapse, ruptured chordsand flail leaflet segments is usually seen inassociation with MV prolapse.

Severe TR allows RV systolic pressure tobe transmitted back into the systemic veinsresulting in systemic venous hypertension,jugular venous distension, and flow rever-sal causing a pulsatile liver. Venous hyper-tension can cause liver and renaldysfunction. Sodium and fluid retentioncontribute to lower extremity edema, ascites,and anasarca in severe TR. Cardiac outputis reduced in severe TR and often associ-ated with symptoms of fatigue and effortintolerance.

Assessment of severity of TRTwo-dimensional echoIn severe TR the RA and RV are enlarged.Paradoxical septal motion is frequently seen

with RV volume overload, the RV becomesmore globular and forms the cardiac apex.Severe TR causes the IVC to becomeengorged and expand in systole.

DopplerThe severity of TR is graded by the spatialextent of the color disturbance. It is 1 ifthe TR color signal is seen only within 1 cmof the valve and 4 if the color signal isseen throughout the RA. Systolic flow rever-sal in the middle hepatic vein (MHV) andsuperior vena cava (SVC) are markers ofsevere TR. The MHV and SVC are ideal forPW Doppler interrogation because they areparallel to the ultrasound beam.

The peak velocity of the CW Doppler sig-nal of TR in conjunction with an estimateof RA pressure is used to assess PA pressures.The CW Doppler waveform of TR loses itscharacteristic bell-shaped appearance andbecomes dagger shaped when the tricuspid


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Figure 7.46 Continuous wave Doppler signal of flowvelocities through the tricuspid valve in a patient withtricuspid stenosis and regurgitation. The peak diastolicgradient is 16 mmHg.

Figure 7.47 Apical four-chamber view with color Dopplershowing severe tricuspid regurgitation (TR) (RV, rightventricle; LV, left ventricle; LA, left atrium).

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regurgitation is severe. The peak velocityoccurs earlier and the velocity returns tobaseline more quickly in severe TR indicat-ing a more rapid equilibration of RV and RApressures.

Carcinoid heart disease

Carcinoid heart disease is caused by a rare,malignant tumor that secretes a serotonin-like amine and other vasoactive substancesthat damage the tricuspid and pulmonicvalves. Most (90%) carcinoid tumors arelocated in the gastrointestinal tract but onlymetastatic carcinoid tumors to the livercause carcinoid heart disease. The reasonthat right heart valves are predominantlyaffected is because the secreted vasoactivesubstances are inactivated in the liver andlungs. The TV and PV leaflets become thickand ridged and ultimately fixed in a partiallyopened position (Figure 7.48) such that TRusually predominates but TS is also present(Figure 7.49). This characteristic appearance

of the TV and PV and the absence of leftheart valve involvement allows carcinoidheart disease to be distinguished from RHD(Figure 7.50).

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Figure 7.48 Apical four-chamber view showing diastolicdoming of the tricuspid valve in a patient with carcinoidheart disease. The mitral valve opens normally (RV, rightventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

Figure 7.49 Continuous wave Doppler signal of tricuspidstenosis and regurgitation in a patient with carcinoid heartdisease.

Figure 7.50 Long axis of the pulmonary artery (PA) insystole showing moderate pulmonic stenosis in a patientwith carcinoid heart disease (LV, left ventricle; RVOT, rightventricular outflow tract).

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THE PULMONIC VALVE

Anatomy

The PV annulus occupies a plane that is off-set by 60–90� from the plane of the aorticannulus so that the PV annulus points tothe left mid-scapular line facing almostdirectly posteriorly with a slight leftwardand superior tilt, while the aortic valve ispointed to the right shoulder. The normalPV has three cusps of approximately equalsize: the anterior, left posterior, and rightposterior. The infundibular septum is subja-cent to the commissure between the leftand right PV cusps, which is aligned withthe commissure between the left and rightaortic valve cusps. The free wall of theinfundibulum subtends the remainder ofthe PV annulus. The infundibulum hasprominent trabeculations, which extend tothe valve sinuses. A limb of the septal bandextends to the left posterior sinus and tra-beculations running parallel to the parietalband extend to the right posterior sinus.

The PV is the least well visualizedechocardiographically of all the valves in

normal patients and the PV cannot usuallybe visualized in short axis. Two leaflets ofthe PV can be seen bridging the PA in dias-tole but in systole the leaflets are difficultto distinguish from the walls of the PA. ThePV and PA are ideally situated for Dopplerinterrogation of blood flow velocity becausethe PA is parallel to the ultrasound beam inthe parasternal short axis of the aorticvalve. In this view, normal systolic flowacross the PV is laminar and less than 0.9m/s. Color flow Doppler is very sensitive fordetecting pulmonary insufficiency (PI) anda minor amount of PI is present in mostnormal individuals.

Pulmonic stenosis

The PV may rarely become stenosed in RHDbut almost all cases of pulmonary stenosis(PS) are congenital in origin (Figure 7.51).Congenital PS results from fusion of theleaflet tips leaving a central orifice or whenthe valve is dysplastic. In dysplastic PS thevalve is thick and immobile and often asso-ciated with annular hypoplasia. This severe


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Figure 7.51 The pulmonary artery (PA) bifurcation is seen in this short axis view. The patient has mild to moderatepulmonary stenosis (arrow right panel). The right coronary artery is also seen (arrow left panel) (RA, right ventricle; AO, aorta).

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type of stenosis usually requires relief of theobstruction in infancy. In the nondysplastictype of valvular PS the leaflets are initiallymobile with systolic doming. Over time thistype of valve becomes fibrosed and thick-ened and is associated with post-stenoticdilatation of the PA. In carcinoid heart dis-ease, the PV thickens, the PV leaflets scarand shrivel and the annulus constrictsresulting in PS of mild-to-moderate severity.

Assessment of severity of PSM-mode echoM-mode echo of PS shows a deep, exagger-ated A wave if the leaflet is pliable becausewith atrial contraction, right ventriculardiastolic pressure approaches PA diastolicpressure. RVH with abnormal septal thick-ness and motion are present in proportionto the severity of PS.

Two-dimensional echoTwo-dimensional echo enables completeassessment of RV size, wall thickness, cavityarchitecture, semi-quantification of systolicfunction and direct visualization of the PVleaflets and their excursion.

DopplerThe peak systolic gradient is easily deter-mined by CW Doppler (Figure 7.52). A peaksystolic gradient greater than 75 mmHg isconsidered severe, moderate PS is 50–75mmHg, and mild PS is a gradient of less than

50 mmHg and is generally well tolerated.The continuity equation is not applied forthe determination of PV cross-sectional areabecause the PW Doppler sample of bloodflow obtained in the RVOT is not represen-tative of flow across the lumen and the truediameter of the RVOT is difficult to obtain.

RVOT obstruction can also occur at thesubvalvular level from hypertrophy of theinfundibulum muscle bands. This hypertro-phy is often associated with valvular PS butmay occur in isolation. The subcostal shortaxis view of the base of the heart is best forthe Doppler evaluation of infundibularstenosis as the ultrasound beam can bealigned parallel to flow.

Supravalvular PS may be caused by tubularor shelf-like narrowings, which can bemultiple. They sometimes occur at thebifurcation causing left or right pulmonaryartery stenosis. The right pulmonary arterycan be seen in long axis from the suprasternalnotch projection but the distal left pul-monary artery is rarely seen. Branch stenosesdistal to the bifurcation cannot be reliablyevaluated with TTE. Mild supravalvular PSsometimes occurs at the site of anastomosisin orthotopic heart transplant recipients(Figure 7.53).

Pulmonic insufficiency

Hemodynamically significant PI is usuallysecondary to dilatation of the pulmonary

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Figure 7.52 Continuous waveDoppler signal of pulmonic stenosis.The peak velocity is approximately 3.8m/s, which yields a peak gradient of58 mmHg. Mild pulmonaryinsufficiency is also seen.

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artery. This commonly occurs in pulmonaryhypertension and following surgery fortetralogy of Fallot or after a balloon valvu-loplasty for PS. PI is usually clinically silent,but severe PI may cause RV volume over-load. The severity of PI is assessed from thespatial extent of the Doppler color flow dis-turbance but this may be misleading as it isoften difficult to completely visualize thejet in one plane (Figure 7.54). Measurementsof the jet width at the annulus and the ratioof jet to annular diameter are the preferredmethods. The deceleration slope of PI canbe helpful and severe PI will have a rapidslope indicating a rapid equilibration of PAand RV pressures but a rapid PI slope alsooccurs with decreased RV compliance, suchas in RV infarction. If diastolic retrogradeflow in the main branches of the PA ispresent the PI is at least moderately severe.

ENDOCARDITIS

Infective endocarditis is defined as a focalinfection of the endocardial lining of theheart usually involving a valve that is dam-aged or congenitally abnormal. Aortic andmitral valve endocarditis is associated morewith incompetent than stenotic valves(Figure 7.55). Endocarditis of the TV is oftenassociated with intravenous drug use or pro-longed use of indwelling catheters. The TVis usually intrinsically normal when theinfection is the result of IV drug use. The PVis the least affected, but congenital abnor-malities such as PS and tetralogy of Fallotare associated with infective endocarditisof the PV. Ventricular septal defects andpatent ductus arteriosus and complex con-genital heart disease predispose to endo-vascular infection. The endocardium may


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Figure 7.53 Parasternal short axis view showing thebifurcation of the pulmonary artery (PA). Color Dopplershows moderate pulmonary insufficiency. A suture line(arrow) is present in the PA approximately 2 cm distal tothe pulmonic valve in this patient with a heart transplant(AO, aorta).

Figure 7.54 Parasternal short axis view showing thebifurcation of the pulmonary artery (PA). Color Dopplershows moderately severe pulmonary insufficiency. The PAis mildly dilated (AO, aorta).

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be damaged by high velocity jets across aVSD or by jets of AR and become the site ofinfection. Patients with hypertrophic car-diomyopathy are prone to endocarditis dueto abrasion of the mitral valve from sys-tolic contact with the septum and damageto the aortic valve from the high velocitysystolic jet.

The clinical course of infectious endo-carditis may be insidious with fever, chills,malaise and weight loss. A murmur maydevelop or change in character and initiatean echocardiographic examination for evi-dence of vegetative endocarditis. Vegetativeendocarditis can cause acute, severe valvularregurgitation from destruction of the valveleaflets, septicemia, and shock culminat-ing in irreversible heart failure. The overallmortality for endocarditis is approximately10%.

Two-dimensional echo

A vegetation is a mass of microorganisms,platelets, inflammatory cells, and fibrin.Echocardiographically they appear as low-density, globular, hypermobile masses and

exhibit chaotic high-frequency oscillations.They are usually attached to the undersurfaceof a valve (i.e. the atrial aspect of the mitralvalve or the ventricular side of the aorticvalve) but can also be attached to the endo-cardial surface of a cardiac chamber or tothe chordal apparatus. Endocarditis causesvalve dysfunction through leaflet destruc-tion, perforation, chordal rupture and flailleaflets and when vegetations mechanicallyinterfere with valve coaptation.

Aortic valve vegetations are usually focal,attached to one leaflet or two adjacentleaflets. They are associated with AR of vary-ing severity and appear as shaggy massesattached to the cusps that often prolapseinto the LVOT in diastole (Figure 7.56).Aortic valve vegetations and flail aorticvalve leaflets are best seen in the parasternallong-axis view. Aortic valve vegetations mayinvolve the anterior MV leaflet or chordalstructures from the AR jet or spreaddirectly through the intervalvular fibrosa.Direct extension of infection to the annu-lus and surrounding structures is more

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Figure 7.55 M-mode echocardiogram of the mitral valvein a patient with mitral valve (MV) endocarditis. Shaggyechoes on the posterior MV leaflet are consistent with avalvular vegetation.

Figure 7.56 Parasternal long axis view. There is a largevegetation attached to the aortic valve that prolapses intothe LV outflow tract in diastole (RV, right ventricle; LV, leftventricle; LA, left atrium; AO, aorta).

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common in the aortic than other valvesand may result in the formation of abscess(Figure 7.57) or fistulous communication tothe myocardium, pericardium or other car-diac chamber. Thickening of the aortic root,vegetations attached to the annulus orecholucent pockets adjacent to the annulussuggest perivalvular spread of the infectionand abscess formation that requires emer-gent TEE. TEE is superior to TTE for assessingperivalvular abscess, fistula, compression ofthe coronary ostia or pseudoaneurysm,which are indications for emergency sur-gery. Periannular extension of aortic valveinfection often occurs at the weakestportion of the annulus, near the membra-nous septum and AV node. New AV blockor bundle branch block suggests abscessformation.

Vegetations most commonly affect themitral valve (Figure 7.58). They are focaland attach to the atrial side of the valveleaflets. Vegetations may occasionally belarge enough to cause LVIT obstruction.


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Figure 7.57 Parasternal short axis view. A large, septatedabscess (AB) is seen adjacent to the aortic valve annulus.There is a large mobile aortic valve vegetation (arrow). Thispatient had acute severe aortic regurgitation and requiredemergent surgery (LA, left atrium; AO, aorta).

Figure 7.58 Parasternal long axis view. There is a large, mobile vegetation attached to the anterior mitral valve leaflet(arrow) (LV, left ventricle; LA, left atrium; AO, aorta).

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Endocarditis most commonly occurs ondamaged valves and it may be difficult todistinguish small vegetations from focalleaflet thickening, calcification and myxo-matous degeneration of the MV, althoughmyxomatous degeneration is usually non-focal. Mechanical destruction of the MV,such as chordal rupture, leaflet perforation,or avulsion, acutely increases MR severityand can cause LV dysfunction and heartfailure. Periannular extension of MV infec-tion occurs more commonly with prostheticvalves but may affect native valves.Pericardial effusion in the setting of mitral oraortic endocarditis suggests a communica-tion between an abscess and the pericardiumor concomitant purulent pericarditis.

Right heart endocarditis accounts for 10%of all cases of endocarditis and has a 10%in-hospital mortality. Most cases involve theTV alone (Figure 7.59). TV vegetations tendto be large and are seen on the atrial side ofthe valve where they may be confused withRA thrombus. TV endocarditis is rarely asso-ciated with intracardiac abscess formation.Isolated endocarditis of the PV (Figure 7.60)is extremely rare even in intravenous drugusers but PV vegetations may rarely coexistwith vegetations on the other valves.

The risk of embolization of vegetations isdetermined by their size, mobility, and loca-tion. MV vegetations embolize more fre-quently than aortic vegetations particularlyif the vegetation involves the anterior MVleaflet. Vegetations �10 mm in diameter

and those that are mobile or pedunculatedare at increased risk of embolization. Earlyuse of antibiotics reduces the risk ofembolization. Serial echocardiograms areclinically useful for monitoring response totherapy.

Vegetations in fungal endocarditis tend tobe large, mobile and echo-dense with aheterogeneous echo texture (Figure 7.61).

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Figure 7.59 Apical four-chamberview. There is a vegetation (arrow)attached to the tricuspid valvecausing severe tricuspidregurgitation. The mitral valve isdensely calcified (RV, rightventricle; LV, left ventricle; RA,right atrium; LA, left atrium).

Figure 7.60 Parasternal short axis view. A vegetation(arrow) is identified on the pulmonic valve (RV, rightventricle; LA, left atrium; PA, pulmonary artery; AO, aorta).

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They are prone to perivalvular spread andembolization. Fungal endocarditis is associ-ated with negative blood cultures, immuno-suppression, prolonged use of antibiotics,prolonged use of indwelling catheters, andthe implantation of cardiac devices. Themortality for fungal endocarditis is greaterthan for bacterial endocarditis and valvesurgery is almost always necessary.

NONBACTERIAL THROMBOTICENDOCARDITIS

Nonbacterial thrombotic endocarditis(NBTE) or marantic endocarditis is notcaused by an infecting organism but is asso-ciated with malignancies, disseminatedintravascular coagulation and other hyper-coagulable states. Friable vegetations com-posed largely of platelets and fibrin formon but do not destroy the valve leaflets.The left heart valves are more commonlyaffected, but multiple valve involvement,

multiple vegetations, and embolization arecommon features of NBTE.

Libman–Sacks verrucous endocarditis is aNBTE occurring in systemic lupus erythe-matosus. Wart-like vegetations composed offibrin, 3–4 mm in size, appear on the valvu-lar or mural endocardial surface of the heartassociated with mild MR or AR. The poste-rior MV leaflet is most commonly affected,embolization is rare and this form of endo-carditis is usually clinically silent. Loffler’sendocarditis is a manifestation of the hyper-eosinophilic syndrome, which is discussedin Chapter 8. Lambl’s excrescences are fila-mentous structures that project linearlyfrom the tips of the valve cusps that areseen usually in elderly people by TEE orrarely by TTE and should not be mistakenfor vegetations.

Fibroelastomas are rare benign tumorscomposed of connective tissue that canattach to any of the heart valves and can bedifficult to distinguish from vegetations.They occur most frequently on the aorticvalve. They may be multiple, typically havemultiple frond-like excrescences that exhibitchaotic motion, are prone to embolizationand are associated with minor valvularregurgitation.

TEE VERSUS TTE IN ENDOCARDITIS

The specificity of TTE for detecting vegeta-tions in patients with proven endocarditisis approximately 98% but its sensitivity isonly 60–70%. Infective endocarditis cannotbe definitively excluded by TTE alone onnative or prosthetic valves particularlywhen image quality is technically limited.TTE cannot usually detect vegetations lessthan 3 mm in diameter. TEE is as specific asTTE and its sensitivity is 90–95%. In mostcases TEE is not indicated as the initialexam for endocarditis but becomes neces-sary when TTE is nondiagnostic, when theTTE is negative but clinical suspicion is highand when prosthetic valve endocarditis orperivalvular infection/abscess are suspected.When TTE clearly visualizes valvularanatomy there is no indication for TEE


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Figure 7.61 Large vegetations are present on the aorticand mitral valves of this patient with fungal endocarditis(RV, right ventricle; LV, left ventricle; LA, left atrium; AO,aorta).

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unless periannular abscess or fistulae aresuspected. TTE can guide and focus the TEEand should be done prior to TEE except inMV prostheses where TTE is unable to visu-alize the atrial surface of the valve due toshadowing and reverberation artifact.Similarly, regurgitation through a prostheticMV can be difficult to detect with TTE butcan be reliably assessed by TEE, which candistinguish the normal central regurgitationof some prostheses from pathological regur-gitation. A negative TEE does not alwaysexclude the diagnosis of early or nonvegeta-tive endocarditis and should be repeatedwithin 7–10 days if clinical suspicion per-sists. Neither TTE nor TEE can distinguishbetween healed or active vegetations.

SURGICAL TREATMENT OF VALVULARHEART DISEASE

Valve repair is preferred to replacement formitral and tricuspid valve disease and avariety of surgical techniques are usedincluding chordal lengthening or shorten-ing procedures, chordal translocation andinsertion of artificial chords, quadrangularor triangular leaflet resection and oftenreduction in the annular circumference,which usually involves the implantation ofan annular ring. If replacement is necessary,surgery that retains chordal integrity is pre-ferred as cutting the chordae prevents themuscle fibers that attach to the cardiacskeleton by way of the papillary musclesfrom contributing effectively to contractionand maintaining LV shape. Similarly, sur-gery that spares and realigns the aortic valveleaflets while repairing or replacing theaortic root is often applicable in aortic rootdissection or dilatation.

Valve replacement surgery has proved tobe vastly superior to medical managementfor patients with advanced valve diseaseand about 80 different models of valve pros-theses have been developed and approvedfor use for valve replacement.

There are three types of valve prosthesisin general use (Figure 7.62): biologic hetero-grafts, homografts, and mechanical valves.

Biologic prostheses contain some biologictissue, porcine valve cusps or bovinepericardium shaped for use as valve leaflets,and they are usually mounted onto a cloth-covered sewing ring or stent. Mechanicalprostheses are composed primarily of metalor pyrolytic carbon and like biologic valvesare generally sutured to the valve annulususing a fabric-covered sewing ring after thediseased valve has been removed. A homo-graft is a valve from a human donor, anautograft is a valve that is translocated fromone position in the heart to another, such asin the Ross procedure where the PV is usedto replace the aortic valve and the PV isreplaced with a homograft.

The biologic tissue in valves like theCarpentier–Edwards porcine valve (Figure7.63) and the Ionescu–Shiley bovine peri-cardial valve are resistant to thrombosiscompared to mechanical valves andanticoagulation is not required after theimmediate postoperative period. However,the biologic leaflets are prone to progressivecalcification and rigidity that can result in

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Figure 7.62 Prosthetic heart valves. (A) Starr–Edwardsball and cage valve. (B) Bjork–Shiley tilting disk valve. (C)Carpentier–Edwards bovine pericardial valve. (D) St Judebileaflet mechanical valve.

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tearing of the leaflets and valvular regurgi-tation or more rarely, prosthetic stenosis.Pannus formation is the gradual ingrowthof fibrous tissue over the sewing ring seen inboth biologic and mechanical valves thatcan cause obstruction to flow and serve as anidus for thrombus.

Mechanical prostheses are more durablethan biologic valves, with a life expectancyof 20–30 years. All mechanical prosthesesconsist of a sewing ring, a housing, and anoccluder within the housing. There are threetypes of occluder: central occluders, inwhich a ball or a disk moves forward withinthe housing to permit forward flow and ispressed back toward the sewing ring to pre-vent regurgitant flow, monoleaflet tiltingdisk valves, and bileaflet valves. TheStarr–Edwards valve with a ball and cagecentral occluder was first implanted in 1968and is still being used today. It has no recordof structural failure but it offers significantobstruction to central flow. The motion ofthe central occluders in the left heart valvesis toward and away from the apex. An M-

mode directed from the apex is ideal for thetiming of valve opening and closure in thistype of valve. Tilting disk valves such as theBjork–Shiley and the Omniscience valvehave a single wafer-thin disk that pivots on ahinge or strut with an opening angle of60–70� and provide good central flow.Bileaflet mechanical prosthetic valves havetwo occluding leaflets made of pyrolytic car-bon, which tilt open in parallel and offertrivial resistance to forward flow. They arethe most commonly used valves for the aor-tic position. As with most mechanicalvalves, trivial regurgitation in bileafletvalves is built-in to minimize thrombosis.

Mechanical valves are thrombogenic andrequire anticoagulation (Figure 7.64). Whenanticoagulated, the risk of an embolic eventin a patient with a mechanical valve issimilar to that of a patient with a bio-logic valve, approximately 1% per year.Mechanical heart valves are rarely used inthe right heart because low velocity flow isprothrombotic.

Thrombosis of a prosthetic valve maycause acute hemodynamic deterioration orit may present with gradually worseningsymptoms of heart failure. Evidence ofvalvular obstruction can be determined byDoppler interrogation, but thrombus mustbe differentiated from pannus on anobstructed mechanical valve. The visualiza-tion of multiple, mobile, masses attached tothe prosthesis establishes the diagnosis ofthrombus. TEE is required for adequatevisualization of a mechanical mitral pros-thesis and usually required for prostheses inother positions.

Homografts are aortic valves within theirproximal aortas that are harvested fromhuman cadavers. They have low risk ofthrombosis and infection and because theyhave no sewing ring they have larger effec-tive orifice areas than stented bioprostheses.Structural failure is usually due to progres-sive aortic root dilatation with aortic regur-gitation. Their supply is limited but they areused in aneurysms or dissections of theproximal aorta when aortic repair andvalve resuspension cannot be performedand in patients with small aortic roots.Their resistance to infection makes them


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Figure 7.63 M-mode echocardiogram through a normallyfunctioning porcine valve in the mitral position.

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especially useful in active endocarditiscomplicated by abscess or dehiscence of aprosthetic valve.

The Ross procedure, first performed in1967, is a PV autograft to the aortic positionwith a homograft to the pulmonic position.It does not require anticoagulation, has alow risk of infection and provides excellenthemodynamic results with no LVOT gradi-ent. It is particularly beneficial for childrenrequiring aortic valve surgery because thePV graft retains the ability to grow. Theprocedure is technically demanding andlate complications include progressiveaortic dilatation with AR and PS.

All aortic valve replacements with theexception of homografts and stentless het-erografts are inherently stenotic. Bileafletmechanical valves have larger effectiveorifice areas (EOA) than stented biologicprostheses and ball and cage valves. Valvegradients vary with EOA and can be highdespite normal prosthetic function depend-ing on the valve type and size. When theannular size is reduced it may be neces-sary to insert a smaller than optimalreplacement. This usually occurs in valvereplacement for AS, which is often associ-

ated with annular calcification and LVHand results in a prosthesis–patient mis-match, which exists when the valve is toosmall for the patient. In prosthesis–patientmismatch the gradients are higher, there isless clinical improvement and incompleteregression of LVH.

Prosthetic valvular endocarditis

Endocarditis affects approximately 1–1.5%of prosthetic valves per year. The risk ofendocarditis is lowest in homografts. Theinfection usually begins at the sewing ringwhere the valve is anchored to the annulus.Vegetations may intrude on the valve cuspsor occluders and interfere with valve closureor more rarely valve opening. Apart fromthe cloth-covered sewing ring the materialin mechanical prostheses does not allowadherance of microorganisms when it is freeof thrombus. In biologic valves the infec-tion is generally confined to the leafletsand the risk of spread to the sewingring (Figure 7.65) and annulus is muchlower than for mechanical valves. Abscess(Figure 7.66), fistula formation (Figure7.67), and perivalvular regurgitation result

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Figure 7.64 Parasternal long axis view. (A) Bjork–Shiley tilting disk valve is in the mitral position. The prosthesis is encased inthrombus and cannot open fully (RV, right ventricle; LV, left ventricle; LA, left atrium).

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from annular necrosis and can cause pros-thetic valve dehiscence. Partial dehiscenceof the prosthesis secondary to annularnecrosis can cause rocking of the sewingring when �40% of annulus is dehisced.Mitral prostheses are occasionally sewn to asmall rim of leaflet tissue rather than theannulus when the annulus is calcified andthis increases the mobility of the sewingring but it should not be confused with therocking of a dehisced valve.

Subclinical hemolysis can be detected inthe majority of patients with a normallyfunctioning mechanical valve but severehemolytic anemia is rare and is usuallyassociated with perivalvular regurgitationand the need for reoperation.

Doppler/echocardiography is used toevaluate prosthetic valves in the same waythat it is used to evaluate native valves buttechnical factors can make the evaluation ofprosthetic valves more difficult. Mechanicalvalves make imaging difficult because ofshadowing and reverberation artifacts,


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Figure 7.65 Parasternal short axis view. A periannularabscess (*) has developed from infection of the sewingring of the bioprosthesis (RA, right atrium; LA, left atrium;PA, pulmonary artery).

Figure 7.66 Parasternal long axis view of a periannularabscess (arrow) adjacent to the sewing ring of a biologicaortic valve prosthesis (RV, right ventricle; LV, left ventricle;LA, left atrium; AO, aorta).

Figure 7.67 Parasternal short axis view. Color flowDoppler reveals a fistulous communication (arrow)between the left ventricular (LV) outflow tract just proximalto the biologic aortic prosthesis and the right atrium (RA)(RV, right ventricle; LA, left atrium; PA, pulmonary artery;AO, aorta).

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whereas biologic leaflet tissue may beobscured by echoes from the sewing ring.Scarring from the surgery often hampersTTE and post-operative images from theright parasternal window are usually lim-ited. Doppler examination of eccentric jetsfrom valves with central occluders mayunderestimate true pressure gradients,whereas elevated gradients due to pressurerecovery distal to the minimal valve orificeare seen in some valves. In patients with

aortic valve replacements the posterioraortic root is not well seen by TTE and theanterior aortic root is not well seen by TEE.Despite these limitations a combination ofTTE and TEE is almost invariably successfulin evaluating prosthetic valve function,hemodynamics and the complications ofreplacement. Echocardiographic assessmentin the early postoperative period beforedischarge is invaluable as a baseline forfuture comparison.

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The term cardiomyopathy (CM) shouldbe reserved for primary diseases of themyocardium of unknown etiology but it isoften applied to conditions whose cause isknown, such as ischemic CM or left ventric-ular dysfunction attributable to cardiotoxicagents (Figure 8.1), parasitic infections or

infiltrative processes. The three types of CMare dilated (DCM), hypertrophic (HCM),and restrictive (RCM) and these are definedby characteristic abnormalities of ventric-ular architecture, and diastolic and systolicdysfunction but there is some overlapbetween the groups.

CARDIOMYOPATHIES

CONTENTS ● Dilated Cardiomyopathy ● Hypertrophic Cardiomyopathy ● RestrictiveCardiomyopathy

8

Figure 8.1 Parasternal long axis view in a patient with left ventricular (LV) systolic dysfunction secondary to X-radiationtherapy. A pleural effusion (PL) is seen posterior to the LV (LA, left atrium).

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DILATED CARDIOMYOPATHY

DCM affects 40–50 people per 100 000 pop-ulation. Its exact etiology is unknown inmost cases, but there is an importantgenetic component. Approximately 20%of patients with DCM have a first-degreerelative with evidence of DCM. Myocarditisfrom a viral infection is an important causeof DCM. There is myocardial involvementin 5% of all viral illnesses. Patients withmyocarditis may present with severe biven-tricular congestive heart failure (CHF),ventricular arrhythmias and sudden deathor there may be a long latent period. About15% of patients with myocarditis progressto DCM.

Regardless of the etiology, the heartresponds to damage with cavity enlarge-ment. Stroke volume is preserved at theexpense of ejection fraction. Left ventricular(LV) cavity enlargement causes increasedwall stress, which is a stimulus for LV hyper-trophy but the increased wall thickness isoften inadequate to normalize wall stress.Ejection fraction falls and LV volumes riseas wall stress increases. Typically, progres-sive LV enlargement is followed by left atrial(LA) enlargement, which is secondary to

elevated filling pressures and mitral regurgi-tation (MR). As the LV enlarges it becomesmore spherical and orientation of the papil-lary muscles to the annulus is changed,

Figure 8.2 M-mode echocardiogram in a patient withdilated cardiomyopathy. The left ventricular cavity isenlarged (left ventricular internal dimension at end-diastole � 7.8 cm) and the percent fractional shorteningis decreased.

Figure 8.3 Parasternal long axis view in a patient with dilated cardiomyopathy. The LV is markedly enlarged and LV globalsystolic function is severely impaired (RV, right ventricle; LV, left ventricle; LA, left atrium; AO, aorta).

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CARDIOMYOPATHIES

resulting in mal-coaptation of the leafletswith central MR. Enlargement of the rightheart chambers may be due to the myo-pathic process but it is usually secondaryto elevated pulmonary pressures. Patientsusually present with symptoms of CHF,which are progressive, but arrhythmias andsudden death may be the first symptoms.

The dilated, hypocontractile LV is pre-disposed to thrombus formation andthromboembolism may occur at any stageof the disease.

Echocardiographically, LV enlargementand decreased systolic function are themajor findings in DCM. An M-modeechocardiogram at the ventricular leveldemonstrates cavity enlargement anddecreased fractional shortening (Figures 8.2,8.3). The relative wall thickness is greatlydecreased. Interventricular septal motion isoften abnormal because of left bundlebranch block (LBBB) or nonspecific intra-ventricular conduction delay. An M-modeof the mitral valve displays an increasedE-point–septal separation (Figure 8.4) andthere may be an A–C shoulder indicatingan increased LV end-diastolic pressure(LVEDP). In short axis at the level of theaorta and LA, the M-mode demonstrates LAenlargement, reduced anterior motion ofthe aorta during systole and there may betruncation of the aortic valve motion pat-tern in systole indicating reduced forwardflow.

Two-dimensional echocardiographydemonstrates variable degrees of four-chamber enlargement. Systolic dysfunctionis almost always global (Figure 8.5).

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Figure 8.4 M-mode echocardiogram of the mitral valvein a patient with dilated cardiomyopathy. The E pointseptal separation is increased and the fractionalshortening is greatly diminished.

Figure 8.5 Apical four-chamber view in a patient with dilated cardiomyopathy. There is four-chamber enlargement but leftheart chamber enlargement predominates. LV diastolic volume is �1 L (RV, right ventricle; LV, left ventricle; RA, right atrium;LA, left atrium).

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Spontaneous echo-contrast is often seenwhen LV enlargement and systolic dysfunc-tion are severe and are associated withincreased risk of thrombus formation.Thrombus typically forms at the apex andapical mural thrombus must be distin-guished from apical trabeculations, whichbecome prominent when the LV dilates. Theapical short axis is especially useful for this.The diagnosis of apical mural thrombusshould only be made when the thrombus isseen in two different and preferably orthog-onal echocardiographic planes. The rightventricle (RV) is dilated to a variable degreeand the angle of the moderator band to the

interventricular septum may approach 90�in marked RV enlargement but LV enlarge-ment predominates and the RV does notbecome apex forming. A central jet of MRis almost invariably present in DCM andmay be severe (Figure 8.6). It can be diffi-cult to distinguish primary DCM with MRfrom chronic severe MR with secondaryLV dysfunction. The restrictive pattern oftransmitral flow with an augmented E waveand rapid deceleration is often present andreflects increased LVEDP and the effects ofthe mitral regurgitant volume (Figure 8.7).Tricuspid regurgitation (TR) is also very com-mon and pulmonary artery pressure shouldbe estimated from the peak TR jet velocity(Figure 8.8).

Despite the nearly identical cardiacmorphology and common clinical path indifferent forms of DCM, some distinctetiologies deserve emphasis.

Alcoholic cardiomyopathy

Alcoholic cardiomyopathy accounts forapproximately a third of all cases of DCM.Alcohol depresses myocardial contractilityacutely even in non-alcoholic normal volun-teers. Cardiac enlargement and subclinicalmyocardial depression can be appreciatedin alcoholics without cardiac symptoms.Biventricular enlargement, decreased LVsystolic function and symptoms of heartfailure, orthopnea, dyspnea on exertion,edema, and fatigue can progress graduallyor rapidly. Unlike other forms of DCM, theprogression of alcoholic DCM can beslowed and sometimes reversed with totalabstinence in the early stages.


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Figure 8.6 Same patient as in Figure 8.5. There ismoderately severe mitral regurgitation (MR) (RV, rightventricle; LV, left ventricle).

Figure 8.7 The restrictivepattern of transmitral flow isoften seen in dilatedcardiomyopathy and reflectsincreased left ventricular end-diastolic pressure and the effectsof the mitral regurgitant volume.

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Peripartum cardiomyopathy

DCM that presents in the last trimester ofpregnancy or within the first few monthspost-partum is termed peripartum cardio-myopathy and is indistinguishable fromidiopathic forms of DCM. Most womenhave a full clinical recovery with return tonormal of LV size and function usuallywithin 6 months of delivery. However,some patients continue to deteriorate, andprogress to death or cardiac transplantation(Figure 8.9).

HIV/AIDS cardiomyopathy

Human immunodeficiency virus (HIV) DCMaccounts for 3–4% of all cases of DCM and isthe cause of a third of HIV-related deaths.HIV DCM occurs late in the course of the dis-ease, is associated with a greatly decreasedCD4 count and has a higher mortality thanother forms of DCM (Figure 8.10).

Anthracycline cardiomyopathy

Doxorubicin and daunarubicin are anthra-cyline chemotherapeutic drugs that have a

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Figure 8.8 Moderately severe tricuspid regurgitation isseen with color Doppler in this apical four-chamber view ina patient with dilated cardiomyopathy (RV, right ventricle;LV, left ventricle; RA, right atrium; LA, left atrium).

Figure 8.9 Apical four-chamber view in a patient with peripartum cardiomyopathy (RV, right ventricle; LV, left ventricle; RA,right atrium; LA, left atrium).

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dose-related cardiotoxicity. They can causeglobal, irreversible LV systolic dysfunction.Initially, systolic volume is increased withlittle increase in diastolic volume and thereis further cavity enlargement over time.The LV myocardium in anthracyclinecardiomyopathy is highly echo-reflective(Figure 8.11).

Chagas’ disease

Chagas’ disease is a major health problemin Central and South America affecting as

many as 20 million people. It is caused bythe hemoflagellate protozoan, Trypanosomacruzi, that enters the body with the bite of ablood-sucking insect, the reduviid bug.Chagasic myocarditis can present withincessant ventricular tachycardia or otherarrhythmia, sudden death, or with biven-tricular failure. There may be four-chamberdilatation indistinguishable from othertypes of DCM, but apical aneurysms, similarto those caused by apical myocardial infarc-tion, may also be present. The RV apex mayalso be aneurysmal and apical thrombus and


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Figure 8.10 A long axis view from a low transducer position demonstrates very poor global systolic function in this patientwith HIV/AIDS. A left pleural effusion (PL) is seen posterior to the LV (DAO, descending aorta; LV, left ventricle; LA, left atrium).

Figure 8.11 Parasternal long axis view in a patient with dilated cardiomyopathy from adriamycin cardiotoxicity (LV, leftventricle; LA, left atrium).

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systemic and pulmonary thromboemboliare common.

Prolonged tachyarrhythmias

Prolonged rapid atrial pacing (�180 bpm)can produce models of DCM in experi-mental animals and DCM can be causedby prolonged tachyarrhythmias in humans,particularly in children. Incessant or repet-itive episodic ventricular tachycardia,supraventricular tachycardia, or even atrialfibrillation can cause DCM, which is oftenreversible with the restoration of normalheart rate and rhythm (Figure 8.12).

Muscular dystrophies

Duchenne muscular dystrophy and theless severe Becker muscular dystrophycause pseudohypertrophy and atrophy ofthe skeletal muscle as muscle fibers aresurrounded by fat and fibrous tissue. It islinked to the X chromosome, affectingyoung males and typically affects the heartat the onset of puberty. The LV lateraland posterobasal walls and posterobasalpapillary muscle are progressively replacedwith fibrous tissue resulting in segmentaldysfunction, which may become globalas the LV enlarges and systolic functiondeteriorates.

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Figure 8.12 Parasternal longaxis view in a patient withglobal left ventricular (LV)systolic dysfunction (A)associated with prolonged boutsof SVT. Systolic function returnedto normal (B) with resolution ofthe arrhythmia (LA, left atrium;AO, aorta).

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LV noncompaction

LV noncompaction is a rare congenitalabnormality, whereby the myocardium isnot uniformly compacted and large inter-trabecular sinusoids persist (Figure 8.13).The LV myocardium is divided into two lay-ers, a thin compacted epicardial layer andan endocardial layer that is not compactedbut composed of a loose network of hyper-trophied trabeculations and endomyocar-dial recesses that communicate with the LVcavity. The endocardial layer is generally atleast twice the thickness of the epicardiallayer. The sinusoids are distinct from thoseof the ‘spongy myocardium’ seen in severecongenital aortic stenosis, which com-municate with the coronary circulation.The noncompaction predominates at theapex and at the mid-lateral and mid-inferiorwalls but systolic dysfunction is global andnot limited to those regions. Intratrabecularrecesses are prone to thrombus formation,and thromboembolism, arrhythmias, andCHF are common in this condition.

Half of all referrals for cardiac trans-plantation are for DCM and while hearttransplantation offers an 85% 1-year and68.5% 5-year survival rate, only about 2000heart transplants are performed annually inthe United States due to the shortage ofdonors. Left ventricular remodeling and notcontractile dysfunction is now recognizedas the principal lesion in DCM and in otheretiologies of systolic failure and this viewhas led to the development of surgical anddevice-based therapies that can return thefailing heart to a more normal size andgeometry.

HYPERTROPHIC CARDIOMYOPATHY

In HCM, LV hypertrophy (LVH) is geneti-cally determined and occurs in the absenceof any hemodynamic stimulus. Systolicfunction is normal or supernormal butdiastolic dysfunction is common. Typically,the anterior interventricular septum ispredominantly affected and asymmetricseptal hypertrophy (ASH) is present (Figure8.14). In some cases hypertrophy is limitedto the upper anterior septum resulting indisproportionate upper septal thickness(DUST) or the hypertrophy may extend tothe LV free wall, posterior septum, inferiorwall, or RV free wall while the posterior wallis usually spared. In hypertensive hyper-trophic disease of the elderly the upperseptum is disproportionately thickened andangled into the LV outflow tract (LVOT).This condition is more common in womenand associated with concentric LVH andaortic root dilatation secondary to hyper-tension. Hypertrophy confined to the apexaccounts for approximately 2% of HCMcases in the United States but up to 25%of HCM cases in Japan (Figure 8.15). Thisvariant, known as ‘spade heart’ because ofthe characteristic shape of the LV cavity isassociated with giant inverted T waves inthelateral precordium on the electrocardiogram(EKG).

The hypertrophied interventricular sep-tum budges into and narrows the LVOT. Thepapillary muscles are often hypertrophied


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Figure 8.13 Apical four-chamber view in a patient withleft ventricular (LV) noncompaction cardiomyopathy. Thenoncompacted layer is composed of a dense network oftrabeculations and endocardial recesses in communicationwith the LV cavity (RV, right ventricle; LA, left atrium).

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Figure 8.14 Parasternal long axis view in a patient with hypertrophic cardiomyopathy. The interventricular septum (blackarrow) is massively thickened at �3.5 cm in diastole (LV, left ventricle; LA, left atrium).

Figure 8.15 Apical four-chamber view in a patient with apical hypertrophic cardiomyopathy or spade heart. The apex ishypertrophied and there is a systolic disturbance in the color Doppler signal near the apex caused by systolic entrapment ofblood between the hypertrophied apical walls (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

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and displaced anteriorly and superiorly. Themitral leaflets and chords are elongated inhalf of all patients with HCM and the pointof coaptation is abnormal, occurring at thebody of the leaflets rather than at their tips.

These factors cause dynamic subaorticLVOT obstruction that varies through sys-tole in some patients with HCM. Theincreased systolic flow velocity through thenarrow LVOT pulls the portion of the mitralvalve apical to the coaptation point intocontact with septum by the Venturi effect.This displacement of the mitral valve isreferred to as systolic anterior motion (SAM)(Figure 8.16) which causes obstruction tooutflow and a posteriorly directed MR jet.Patients with HCM are often characterizedas having obstructive (HOCM) or non-obstructive (HNOCM) types (Figure 8.17)but the presence and severity of a LVOTobstruction is dynamic and can be alteredby changes in LV loading conditions.Factors that decrease preload or afterload orincrease contractility or heart rate reduceend-systolic volume and increase the gradi-ent in patients with obstruction or mayprovoke an obstruction in a patient whohas HNOCM.

Neither ASH nor dynamic LVOT obstruc-tion with SAM is completely sensitive andspecific for HCM. ASH is also seen in amy-loid, glycogen and lipid storage diseases,Freidreich ataxia, and pheochromocytoma.A proportion (10–15%) of patients with


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Figure 8.16 Parasternal long axis view in a patient withobstructive hypertrophic cardiomyopathy. Systolic anteriormotion of the mitral valve blocks the left ventricularoutflow tract (LV, left ventricle; LA, left atrium).

Figure 8.17 Parasternal long axis view in a patient with nonobstructive hypertrophic cardiomyopathy. There is massiveseptal hypertrophy but no systolic anterior motion of the mitral valve and no left ventricular outflow tract obstruction (LV, leftventricle; LA, left atrium).

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systemic or renovascular hypertension haveASH rather than concentric hypertrophy.ASH also occurs in RV pressure overloadand in normal subjects, particularly inendurance athletes with physiologic hyper-trophy. SAM is absent in the majority ofpatients with HCM but can be provoked inmany patients without HCM by dobuta-mine. HCM in children will sometimespresent with RVOT obstruction mimickingcongenital infundibular stenosis.

The symptoms of HCM are similar tothose of aortic stenosis: syncope, dyspnea,and angina. Syncope is usually associatedwith arrhythmias or may be caused bytransient increases in LVOT obstruction.Arrhythmias are common in HCM. Regionsof myofibrillar disarray and fibrosis are sub-strates for arrhythmias, particularly VF andVT. Sudden cardiac death is common inHCM especially with exertion, and HCM isthe most common cause of sudden cardiacdeath in the young. Atrial fibrillation cancause severe clinical deterioration andheart failure and increases the risk ofthromboembolism. Dyspnea is common inpatients with HCM and is usually attrib-utable to increased LA pressures secondaryto poor diastolic function and/or MR.Ischemia can cause angina in HCM in theabsence of epicardial coronary disease. LVHcan compress intramuscular coronaries andthere is a mismatch between coronaryblood flow and increased LV mass. Severesymptomatic CHF is rare except in atrial fib-rillation and in a subset of patients withend-stage disease. In approximately 5% ofpatients with HCM, progressive LV systolicdysfunction develops with wall thinningand cavity enlargement resembling DCM.

M-mode echocardiographic examinationdemonstrates LA enlargement secondary toMR or decreased LV compliance and theaortic valve often closes in mid-systolereflecting the time course of the dynamicLVOT obstruction (Figure 8.18). The MV M-mode shows SAM (Figure 8.19) and theduration of mitral–septal contact in HOCM.SAM is absent in hypertrophic HNOCM.The interventricular septum is usually thick(greater than 1.5 cm) but systolic thickeningis decreased. Septal hypomobility permits

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Figure 8.18 Mid-systolic notching on the aortic valve M-mode in a patient with hypertrophic cardiomyopathy anddynamic left ventricular outflow tract obstruction.

Figure 8.19 M-mode echocardiogram at the mitral valve(MV) level demonstrating systolic anterior motion of theMV and systolic anterior motion septal contact (arrows).

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hyperdynamic posterior wall motion, itssystolic excursion is relatively unopposed,and therefore it is relatively unloaded. ASHis defined as a ratio of septal to posteriorwall thickness of �1.3:1. Septal thicknessgreater than 3.0 cm at end-diastole is associ-ated with increased risk of sudden death. LVinternal diameter in diastole is almostalways less than 4.5 cm.

The parasternal long axis view reveals thebase to apex extent of the hypertrophy,allowing ASH to be distinguished fromDUST and serial short axis images demon-strate its circumferential involvement(Figure 8.20). The myocardium has anabnormal acoustic signature that is echo-bright and has a speckled or granularappearance. This type of brightly reflectingmyocardium is also seen in patients withcardiac amyloid and in some patients withchronic renal failure. Anterior displacementof the mitral valve and subvalvular appara-tus will be seen. The point of SAM–septalcontact can be precisely identified in theparasternal or apical long axis view (Figure8.21) and a small echo-bright friction lesionor callous on the septum or rarely on theMV can sometimes be seen at this point ofcontact.

Diastolic dysfunction is the hallmark ofHCM and should be carefully assessed withpulsed-wave (PW) Doppler of transmitraland pulmonary vein flow, propagation


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Figure 8.20 Parasternal short axis view in a patient with hypertrophic cardiomyopathy and marked asymmetric septalhypertrophy. Left ventricular (LV) systolic function is supernormal (RV, right ventricle).

Figure 8.21 Apical long axis view in zoom mode showingSAM–septal contact (LV, left ventricle; LA, left atrium).

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velocity, and tissue Doppler imaging (TDI)in patients suspected of having this disease.TDI may be especially useful in evaluatingpatients with HCM. Both longitudinal TDIdiastolic velocities from the apical windowand transmural TDI velocity gradientsacross the posterior wall from the paraster-nal window can differentiate the pathologichypertrophy of HCM from the physiologicLVH of athletes. In addition, abnormalitiesin TDI strain and strain rate imaging arepresent in carriers of the HCM genotypeprior to the development of hypertrophywhen other echo/Doppler findings arenormal.

Color Doppler interrogation of the LVOTis performed in long axis views from theapical and parasternal windows and turbu-lent blood flow is seen in systole beginningat the point of SAM–septal contact. In theapical variant of HCM a small turbulent jetmay be appreciated in the LV cavity nearthe apex. Mitral regurgitation is invariablypresent when there is obstruction and theseverity of MR is related to the degree of

obstruction. The MR jet in HOCM is poste-riorly directed (Figure 8.22). If the jet ismore complex, there may be another etiol-ogy for the MR. The subaortic gradient canbe assessed with continuous wave Dopplerfrom the apical window, the right paraster-nal and especially suprasternal approachesare generally not helpful. The gradientpeaks in late systole and the LVOT spectralenvelope has a dagger shape (Figure 8.23).Combined subaortic and valvular aorticstenosis can coexist and the late peakingflow from the subaortic stenosis can besuperimposed on the more symmetricalenvelope of the valvular stenosis. Mild aor-tic regurgitation (AR) is present in a quarterto a third of patients with HOCM and prob-ably reflects damage to the aortic valvecaused by the high velocity systolic jet.

Patients with no gradient at rest maydemonstrate a gradient with a change inloading conditions. A gradient may beprovoked with maneuvers that decrease LVsystolic volume, such as, inhalation of amylnitrate, which decreases both pre- and

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Figure 8.22 Parasternal long axis view in systole withcolor Dopper in a patient with obstructive hypertrophiccardiomyopathy showing turbulent flow in the leftventricular outflow tract (white arrow) and a posteriorlydirected jet of mitral regurgitation (black arrow) (LV, leftventricle; LA, left atrium; AO, aorta).

Figure 8.23 Continuous wave Doppler of the leftventricular outflow tract in a patient with hypertrophiccardiomyopathy. The velocity reaches a maximum in latesystole. The peak pressure gradient is 88 mmHg.

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afterload, or the Valsalva maneuver, whichdecreases preload during the ‘strain’ phase.Between 40% and 50% of patients withHCM have no LVOT obstruction at rest orwith provocation.

Surgical relief of LVOT obstructionresulting in exercise-limiting symptoms ofsyncope, angina or DOE can be accom-plished with MV replacement using alow-profile prosthesis and chordal preser-vation or more commonly by septalmyotomy-myectomy. A trough of septalmuscle is surgically removed through theaortic valve often under epicardial echo-cardiographic guidance. LVOT gradientscan also be abolished by the selectivedestruction of the obstructive part of theleft upper septum by the injection ofalcohol into the first or first and second septalperforating arteries (Figure 8.24). Gradientreduction and symptomatic improvementwith this technique is similar to that withsurgical myotomy-myectomy but neithertechnique alters the natural history of thedisease. Diastolic dysfunction and thepropensity for ventricular arrhythmias,often requiring an automatic implantablecardiovertor defibrillator, persist.

RESTRICTIVE CARDIOMYOPATHY

The RCMs are rare and consist of a relativelyheterogeneous group of diseases. LV size isusually normal but LV wall thickness isnormal or increased. The LV systolic func-tion may be normal or decreased and ifdecreased it may be globally or regionallyaffected. Right heart failure with peripheraledema and ascites may predominate. Theunifying factor in RCM is increased resist-ance to diastolic filling. Symptoms of CHFare caused by elevated filling and the inabil-ity to increase cardiac output on exertion.RCMs can be divided into two principalcategories, primary (as in endomyocardialfibrosis) and secondary (as in the infiltrativemyocardial diseases).

Primary RCMs

Endomyocardial fibrosis Endomyocardial fibrosis (EMF) causes 25%of all cardiovascular deaths in east Africaand South America and is thought to bethe result of hypereosinophilia. Eosinophilsinfiltrate the endocardium causing necrosis


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Figure 8.24 Off-axis apical four-chamber views in a patient with obstructive hypertrophic cardiomyopathy in the cardiaccatheterization lab for a percutaneous transluminal septal myocardial ablation (PTSMA). The left panel is the baseline prior tothe procedure. In the middle panel contrast has been injected into the first septal perforator to assess the location and extentof myocardium supplied by that vessel. In the right panel, 2 mL of 99% alcohol (ETOH) has been injected into the septalperforator to selectively destroy a portion of the upper septum (LV, left ventricle; RA, right atrium, LA, left atrium).

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of the endocardium and subendocardialmuscle fibers. Dense sheets of pearly whitefibrous tissue replace the endocardium ofboth ventricles beginning at the apices withgradual spread to the atrioventricular (AV)valves. The outflow tracts are spared. Muralthrombus forms over the fibrous tissue andmay obliterate the apices. The posteriormitral leaflet may become entrapped inthrombus resulting in severe MR.

Loffler’s endocarditisLoffler’s endocarditis, also known as fibro-plastic endocarditis or eosinophilic endo-myocardial disease, is similar to tropicalEMF and is associated with idiopathichypereosinophilia. There is extensive endo-cardial scarring and thrombus formationwith cavity obliteration in advanced cases,but thromboembolic events are uncommon(Figure 8.25). Echocardiographic findingsincluded biatrial enlargement and smallto normal ventricular cavity sizes. Right

and left ventricular walls are thick andhypokinetic and the endocardium is highlyecho-reflective. MR and TR are present andmay be severe. Transmitral Doppler veloci-ties show a restrictive pattern of diastolicfilling pattern, and all indices of diastolicfunction are severely depressed.

In idiopathic RCM there is restriction toventricular filling without endocardialthickening, fibrosis or infiltrative process.Familial forms exist and are sometimes asso-ciated with distal skeletal muscle disease(Figure 8.26).

Secondary RCMs (infiltrative diseases)

Infiltration of the heart with toxic, insolu-ble amyloid protein fibrils is the mostcommon cause of RCM. There are severaltypes of amyloidosis, the amyloid proteinsare morphologically distinct for each type.

Amyloid heart diseaseIn amyloid heart disease intracellularamyloid is deposited in the left and rightventricular myocardium where it disruptsdiastolic function and later in the course ofthe disease, systolic function (Figure 8.27).Amyloid also accumulates in the atrial walls,interatrial septum, coronary arteries, valves,and conduction system. Sinu-atrial disease,heart block, and atrial fibrillation arecommon. Progressive biventricular failuremarked by restrictive filling ensues. Themyocardium in cardiac amyloid is highlyecho-reflective and has a sparkling, groundglass appearance. Two-dimensional echo-cardiography reveals a normal-sized, thick-walled LV that contracts poorly and fillsslowly (Figure 8.28). ASH occurs in approxi-mately a third of patients with amyloidheart disease (Figure 8.29). Small pericardialeffusions without hemodynamic signifi-cance are common. LV and RV walls areusually thick, bright, and hypocontrac-tile. Patients with amyloid and an LV wallthickness �1.5 cm have a mean survival of1.5 years, if LV wall thickness is �1.5 cmmean survival is 0.4 years. Mild AR and mod-erate AV valve regurgitation is common.Diastolic dysfunction progresses inexorably

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Figure 8.25 Apical four-chamber view in a patient withLoffler’s endocarditis. There is extensive thrombus, whichhas obliterated the RV and LV apices (RV, right ventricle; LV,left ventricle; RA, right atrium; LA, left atrium).

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Figure 8.26 Apical four-chamber view in a patient with idiopathic restrictive cardiomyopathy. The ventricles are small andthere is marked biatrial enlargement (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

Figure 8.27 Apical four-chamber view in a patient with amyloid heart disease. The ventricular walls are thick and highlyecho-reflective. There is biatrial enlargement and a small pericardial effusion (*) is noted adjacent to the RA free wall(RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

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from abnormal relaxation to pseudonormalto restrictive patterns of filling. A decel-eration time of the transmitral DopplerE wave of �150 ms predicts a 90% 1-yearsurvival rate. One-year survival is reduced

to 50% in patients with a deceleration timeof �150ms.

HemochromatosisHemochromatosis results in excessive irondeposits in the liver, pancreas, skin, andheart. Excess iron accumulates due to ahereditary defect leading to the absorptionof excessive iron from the intestines.Similar iron deposition occurs in hemo-siderosis from multiple (�100 units) bloodtransfusions over many years. Iron isdeposited in the muscle cells of the epicar-dial third of the myocardium and this isassociated with destruction of myocytesand replacement fibrosis. The walls do notbecome thickened with iron infiltrationas with amyloid infiltration. Initially wallthickness is normal and systolic function ispreserved but with time the heart enlarges(Figure 8.30) and patients usually presentwith left and/or right heart failure andechocardiographic features of DCM. Thereis a spectrum of diastolic dysfunction withrestrictive disease being the most severe.

SarcoidosisSarcoidosis is a multisystem disease ofunknown etiology wherein noncaseatingepitheloid granulomas (epitheloid cell

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Figure 8.28 Parasternal short axis in a patient with amyloid heart disease. The left ventricular (LV) walls are thick and highlyecho-reflective. A small pericardial effusion is seen posterior to the LV (*).

Figure 8.29 M-mode echocardiogram in a patient withamyloid heart disease. There is asymmetric septalhypertrophy and systolic contraction and diastolic fillingare impaired.

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tubercles) are formed in the skin, lungs,or eyes. Diffuse infiltration of the lungparenchyma with pulmonary hypertensionand cor pulmonale is common. Cardiacinvolvement is rare but granulomas canform in the heart and have a predilection forthe basal septum and LV free wall causingregional contractile dysfunction and lessoften diastolic dysfunction. Granulomascause interstitial inflammation and fibrosisand may affect the conduction system andpapillary muscles.

Uhl’s anomalyUhl’s anomaly or arrhythmogenic RV dys-plasia (ARVD) is characterized by geneticallydetermined progressive atrophy and fibro-fatty replacement of the RV myocardiumextending from epicardium to endocardium.ARVDis associated with arrhythmias includ-ingVTand sudden death. There is a spectrumof RV involvement ranging from segmentalRV thinning and akinesis to severe global RVand occasionally LV dysfunction. RV apicalaneurysms are most common and thesemay involve the RV inferior, lateral, or freewall (Figure 8.31). The RV dilates andsystolic function progressively deteriorates.


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Figure 8.30 Apical four-chamber view in a patient with hemochromatosis. There is moderate four-chamber enlargement andreduced global systolic function (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

Figure 8.31 Apical four-chamber view in a patient withUhl’s anomaly or arrhythmogenic right ventricular (RV)dysplasia. The RV is enlarged and there is an RV apicalaneurysm (A) (LV, left ventricle; RA, right atrium; LA,left atrium).

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ANATOMY

The pericardium envelops the heart and iscomposed of serous and fibrous layers. It isabout 2 mm thick and receives oxygenatedblood from the internal mammary arteries.The thin inner serous visceral pericardiumis the epicardium. It covers the outer surfaceof the heart including the proximal greatarteries, where it melds with their adventi-tia, and the terminal portions of the super-ior vena cava (SVC) and pulmonary veinsand reflects back on itself as the parietalpericardium which lines the fibrous peri-cardium. The outer surface of the fibrouspericardium is firmly attached to the centraltendinous and left muscular portions ofthe diaphragm, and more loosely to thesternum, costal cartilages, parietal pleurae,vertebral bodies, esophagus, and descendingthoracic aorta (DAO). These attachmentslimit displacement of the heart. The inferiorvena cava (IVC) enters the pericardiumdirectly through the central diaphragm andis therefore not covered by the fibrous peri-cardium. The reflections of the serous peri-cardium, i.e. the junctions of visceral andparietal layers, form two prominent sinuses.The transverse sinus is a tunnel-like projec-tion of the pericardium anterior to the SVCand atria and posterior to the great arteries.The oblique sinus is an inverted U-shapedcul-de-sac located behind the left atriumbetween the right and left pulmonary veins.

The space between the visceral andparietal layers of the pericardium normallycontains 15–30 mL of fluid secreted bymicrovilli on the pericardial surface. Thisfluid contains phospholipids, which act as alubricant allowing the two layers to slideover each other with minimum friction.Pericardial fluid is normally drained bythe lymphatic system of the parietal peri-cardium into the thoracic duct or by wayof the right pleural space into the rightlymphatic duct.

The pericardium acts as a barrier to thespread of infection, inflammation, andmalignancy from contiguous organs, but itsmost important function is to limit acutediastolic distension of the cardiac cham-bers. The fibrous pericardium allows onlyminor increases in intrapericardial volume,beyond this point it is inelastic with anearly vertical relation between pressureand volume. However, when the increasein intrapericardial volume is gradual, thepericardium will stretch to accommodate it.

PERICARDITIS

Pericarditis may be idiopathic or due to viralinfection with or without accompanyingmyocarditis. Patients with pericarditis aretypically febrile and have positional chestpain, aggravated by cough and respiration

DISEASES OF THE PERICARDIUM

CONTENTS ● Anatomy ● Pericarditis ● Pericardial Effusion ● Tamponade● Constrictive Pericarditis ● Specific Etiologies

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and relieved by sitting with the trunk bentforward. The pericardium may react toinflammation with exudation of fluid andfibrin but in most cases of pericarditis thereis no significant accumulation of fluid. The

pericardial surfaces become thickened andrough. A normal echocardiogram does notexclude the diagnosis of pericarditis.

PERICARDIAL EFFUSION

Pericardial effusions can accompany peri-carditis from any etiology. They can be dueto trauma, malignancy, heart failure, failureof lymphatic drainage or may be of iatro-genic origin. Pericardial fluid may be serous,serosanguineous, or purulent depending onthe etiology. The pericardium can accom-modate a large amount of fluid (�2 L) with-out sudden hemodynamic collapse if itdevelops slowly. A small effusion (�150 mL)that accumulates rapidly, however, can raiseintrapericardial pressure dramatically andcause fatal tamponade.

Echocardiography is the diagnosticmodality of choice for detecting, quantify-ing, and assessing the hemodynamic impactof pericardial effusions and can oftenprovide additional information about thepericardial contents. A small amount ofpericardial fluid (�20 mL) is often visible as

Figure 9.1 M-mode echocardiogram shows a smallposterior pericardial effusion as a separation between thevisceral and parietal layers of the pericardium (arrow) thatpersists throughout the cardiac cycle.

Figure 9.2 Parasternal short axis view in a patient with a moderate sized, circumferential pericardial effusion (PE). A smallleft pleural effusion (PL) is also seen (RV, right ventricle; LV, left ventricle).

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a slight separation between the visceraland parietal layers of the pericardium by M-mode echo in normal patients. It is generallynecessary to reduce the gain so that only thepericardial reflectors remain. A separationthat persists through diastole as well assystole represents a small effusion (Figure9.1). Small effusions tend to pool at the base

of the heart. Moderate-sized effusions arevisible circumferentially as echo-free regionsanterior to the right ventricular (RV) freewall and posterior to the left ventricle fromthe parasternal imaging window (Figure 9.2)and superior to the right atrum (RA) fromthe apical four-chamber view but small oreven moderate-sized effusions may beobscured if excessive gain is employed. Anisolated anterior hypoechoic zone probablyrepresents a fat pad rather than fluid.

As an effusion enlarges, it extends apically,laterally and then anteriorly becomingcircumferential. Effusions may be loculatedand seen adjacent to only one or two cardiacchambers. In this case fluid is walled off byadhesions between the visceral and parietallayers (Figure 9.3). It is essential to distin-guish pericardial effusions from pleuraleffusions (Figure 9.4). The vast majority ofpericardial effusions terminate at the level ofthe posterior atrioventricular (AV) grooveregardless of their size and unlike pleuraleffusions they are not visible posterior tothe left atrium (LA). Occasionally, large peri-cardial effusions extend into the obliquepericardial sinus. Pericardial effusions can bedistinguished from pleural effusions bylocalizing the effusion relative to the DAO inthe parasternal long axis view (Figure 9.5).

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Figure 9.3 Subcostal four-chamber view in a patient witha loculated pericardial effusion (PE) (RV, right ventricle; LV,left ventricle; RA, right atrium; AO, aorta).

Figure 9.4 Apical four-chamber view in a patient with a small pericardial effusion (PE) and a larger pleural effusion (PL).Most but not all pericardial effusions terminate at the level of the atrioventricular groove (RV, right ventricle; LV, left ventricle;LA, left atrium; Dao, descending thoracic aorta).

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Pericardial effusions are anterior to theDAO and pleural effusions are posterior andlateral to the DAO. The heart may swingfreely within a large pericardial effusion andthis motion corresponds to the phasic varia-tion in QRS amplitude termed electricalalternans. The pericardial contents can be

qualitatively evaluated by assessing itsdensity and heterogeneity. An effusion withan echo density greater than that of fluidmay represent hematoma or infection(Figure 9.6). Nodular thickening of thepericardial surface may represent tumor.Regions of increased echo density within


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Figure 9.5 Parasternal long axis view of a patient with a pericardial effusion (PE) and a pleural effusion (PL). PEs areanterior to the descending thoracic aorta (Dao) and PLs are posterior and lateral to the Dao in this view (RV, right ventricle; LV, left ventricle).

Figure 9.6 Subcostal short axis view in a patient with a large, dense, hemorrhagic pericardial effusion (PE) (LV, left ventricle).

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an effusion may represent fibrin (Figure 9.7)or hematoma. Fibrin strands attached toboth pericardial surfaces are often seen aspericardial effusions begin to organize andform fibrous adhesions (Figure 9.8).

TAMPONADE

Tamponade occurs when the heart is com-pressed by the pericardial contents to theextent that cardiac filling is impaired. Intamponade, diastolic pressures are elevatedbut true filling pressure is equal to the trans-mural pressure, which is diastolic pressureminus intrapericardial pressure. Whenintrapericardial pressure is equal to ventric-ular diastolic pressure, filling pressure iszero and continued cardiac output becomesdependent on respirophasic variations inventricular filling and ventricular interde-pendence. In tamponade, the inspiratoryfall in intrathoracic pressure is not trans-mitted to the pericardial space, pulmonarycapillary wedge pressure falls and with itleft ventricular (LV) filling. RV filling andoutput are augmented in inspiration. Theinterventricular septum shifts to the leftand further impedes LV filling. In expira-tion the situation is reversed, LV filling andoutput are accentuated at the expense of RVfilling and output.

Systolic blood pressure (BP) rises and fallswith the respiratory cycle in tamponade.The difference between the inspiratory andexpiratory systolic BP is the pulsus paradoxusand in tamponade it is usually greater than

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Figure 9.7 The echodense region adjacent to the right ventricular free wall (arrow) within the pericardial effusion (PE) in thisparasternal short axis view may represent fibrin deposits or hematoma (LV, left ventricle).

Figure 9.8 Parasternal short axis view in a patient with amoderate-sized pericardial effusion (PE). Fibrin strands areseen, one of which (arrow) is attached to both the visceraland parietal pericardial surfaces (RV, right ventricle; LV, leftventricle).

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10 mmHg. Pulsus paradoxus is not patho-gnomonic of tamponade, and it is absentwhen elevated pericardial pressure impactson the RV and LV unequally, as occurs whenpreexisting heart failure has caused chronicelevation in LV filling pressure or when pul-monary hypertension has caused chronicelevation in RV filling pressure. Pulsus para-doxus is also absent when the inspiratoryincrease in RV filling is matched by aninspiratory increase in shunt flow throughan atrial septal defect (ASD) or when there issignificant retrograde filling of the LV fromaortic regurgitation that is independent ofrespiration. In addition, pulsus paradoxusoccurs in patients with chronic obstructivepulmonary disease (COPD), asthma, RVinfarction, and pulmonary embolism in theabsence of a pericardial effusion.

Tamponade is a clinical diagnosis and nota diagnosis that can be made echocardio-graphically. However, Doppler/echocardio-graphy is sensitive to the exaggeratedrespiratory variation and ventricular inter-dependence that is driven by increased


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Figure 9.9 Parasternal short axis view in a patient with a large pericardial effusion (PE) and cardiac tamponade showing rightventricular (RV) diastolic indentation in early diastole that reverses by end-diastole. The RV free wall indents when RV fillingpressure is exceeded by intrapericardial pressure (LV, left ventricle).

Figure 9.10 Diastolic indentation of the right ventricularoutflow tract (arrow) is evident in this diastolic frame (PE,pericardial effusion; RV, right ventricle; LV, left ventricle;LA, left atrium; AO, aorta).

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intrapericardial pressure, and it can assessthe hemodynamic impact of a pericardialeffusion. When pericardial pressure exceedsthe pressure in a cardiac chamber, the wallsof the chamber are forced inward orindented. Collapse of the RA wall is an earlyand sensitive sign of increased intrapericar-dial pressure. Abnormal posterior motion ofthe RV free wall in early to mid-diastoleindicates that pericardial pressure exceedsRV filling pressure (Figure 9.9). RV diastolicindentation can be clearly demonstrated inthe subcostal views and in the parasternallong axis view (Figure 9.10) as the RV out-flow tract is the most distensible part of theRV free wall. Timing of the indentation isfacilitated by M-mode interrogation fromeither projection using a fast sweep speed(Figure 9.11). When RV filling pressure is lowas in the hypovolemic patient, RA and RVindentation will occur early at a relativelylow pericardial pressure. Conversely, thissign may be absent in a patient with RVHand pulmonary artery hypertension whenRV filling pressure is high and LV free wallindentation may precede RV indentation(Figure 9.12). Respirophasic variation inventricular filling can be identified by recip-rocal changes in ventricular dimensions asthe interventricular septum shifts leftwardwith inspiration and back during expira-

tion. The IVC is enlarged and does notcollapse with inspiration when RA pressureis greater than 15 mmHg (Figure 9.13).

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Figure 9.11 M-mode echocardiogramat the level of the aorta (AO) and leftatrium (LA). There is diastolicindentation of the right ventricular (RV)outflow tract (RVOT) (arrows). M-modeechocardiography facilitates recognitionof the timing of RV indentation (LA,left atrium).

Figure 9.12 M-mode echocardiogram of a patient with aloculated posterior pericardial effusion (PE) and cardiactamponade. There is diastolic indentation of the leftventricular posterior wall (PW, posterior wall; IVS;interventricular septum).

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Respirophasic variations in Doppler flowvelocities mirror the hemodynamics intamponade. On the first beat of inspiration,transmitral E wave velocity falls, reflectingthe decreased gradient between the extra-cardiac pulmonary veins and the LA. Aninspiratory fall in the transmitral E wave isnormally less than 10%. When greater than25% it is suggestive of tamponade and this

finding is associated with RV diastolicindentation (Figure 9.14). LV isovolumicrelaxation time (IVRT) is prolonged withinspiration and the MV may open onlywith atrial contraction. LVOT flows aresimilarly affected (Figure 9.15). A normalexpiratory decrease in the transtricuspid Ewave can be as high as 25%. A variation of�50% is consistent with tamponade (Figure9.16). Systemic venous flow velocity pro-files can be obtained from the SVC whenthe transducer is positioned in the leftsupraclavicular fossa and the beam is angledcaudad and parallel to the spine and fromthe middle hepatic vein from the subcostalposition where the beam can be alignedwith blood flow. There are normally twonegative peaks representing forward flowin systole and diastole. The systolic waveis normally higher than the diastolic andboth increase with inspiration. There mayalso be a small retrograde deflection causedby atrial contraction. In tamponade, totalintrapericardial volume is constant and fill-ing occurs predominantly in systole whenblood is ejected during which pericardialpressure falls. Systemic venous flow is pre-dominantly systolic and diastolic flow isreduced, absent or reversed. Inspiratoryaugmentation may be normal or reducedin tamponade but on the first beat afterexpiration and coincident with minimumtranstricuspid velocity, diastolic and oftensystolic velocities fall or reverse.

Pericardiocentesis is performed emergentlyin patients with tamponade and may be life


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Figure 9.13 The inferior vena cava (IVC) and hepaticveins are markedly enlarged and the IVC diameter doesnot vary with respiration in this patient with a pericardialeffusion and cardiac tamponade.

Figure 9.14 Pulsed-wave Doppler withthe sample volume at the tips of themitral valve leaflets in a patient withcardiac tamponade. There is markedrespirophasic variation in transmitralflow velocities. The E wave velocityincreases phasically with expiration anddecreases with inspiration.

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saving. Needle aspiration of pericardial fluidis also performed to obtain a sample foranalysis especially when there is a suspicionof a malignant or infectious etiology. Thepatient’s head is elevated to facilitateinferior and anterior pooling of fluid. Thesubcostal route is preferred as it avoids thepleural space and internal mammary andmajor coronary arteries. Blind pericardio-centesis carries a risk of damage to the liver,

lung, or heart. Pericardiocentesis is generallyperformed in the cardiac catheterizationlaboratory with hemodynamic monitoringand fluoroscopic guidance or increasinglywith echocardiographic guidance.

CONSTRICTIVE PERICARDITIS

In constrictive pericarditis the pericardiumis stiff and fibrotic and restricts diastolicfilling. The pericardial layers are usuallyfused by dense adhesions and the peri-cardial space obliterated. In late stages ofthe disease the pericardium may calcify.Constriction begins with a pericarditis thatis usually accompanied by an effusion. Theeffusion is reabsorbed but the pericardiumremains inflamed. In patients with end-stage pericardial constriction, symptomsof ascites, peripheral edema, and hepaticinsufficiency predominate and can mimicRV failure.

Diastolic compliance is normal in patientswith constriction and early diastolic fillingis unimpaired but terminated abruptlywhen the limits of the pericardium arereached. This is seen as a rapid early poster-ior deflection of the posterior LV wall onM-mode that abruptly plateaus. An inter-ventricular septal notch or bounce is seenon the M-mode echo (Figure 9.17). The sep-tum moves sharply to the left in early dias-tole and then quickly back to the right. Thisfinding is independent of cycle length and

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Figure 9.15 Pulsed-wave Doppler withthe sample volume in the left ventricularoutflow tract (LVOT) in a patient withcardiac tamponade. There is markedrespirophasic variation in the peak LVOTflow velocity. The peak velocity increasesphasically with expiration and decreaseswith inspiration.

Figure 9.16 Pulsed-wave Doppler with the samplevolume at the tips of the tricuspid valve leaflets in apatient with cardiac tamponade. There is markedrespirophasic variation in transtricuspid flow velocities.The E wave velocity increases phasically with inspirationand decreases with expiration.

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seen even in patients with atrial fibrillation.It is more prominent with inspiration andreflects a transient inequality in the nearlyequal left and right filling pressures. TheIVC is dilated and does not decrease in sizewith inspiration reflecting elevated RApressure. The pericardium may be thick andif it is very thick or calcified, echo imagesmay be very difficult to obtain.

The Doppler transmitral E wave velocityis high, the E–F slope rapid, and the IVRTis characteristically short. The respirophasicvariations in ventricular output and LV fill-ing are similar to those seen in pericardialtamponade because the constricting shelldoes not permit the inspiratory fall inintrathoracic pressures to be transmitted tothe cardiac chambers. Pulsus paradoxusand reciprocal changes in ventricular sizeare common. Early transmitral flow veloc-ity falls with the first beat of inspirationand early transtricuspid flow velocity fallswith expiration. The S2 and D peakvelocities in the pulmonary venous wave-form are enhanced with expiration and fallwith inspiration. These changes are more

conspicuous than the variation in transmi-tral velocities and occur independently ofcardiac cycle length.

Early diastolic RA filling is rapid and sys-tolic filling is preserved, so that the middlehepatic venous waveform is biphasic with a‘W’ pattern. Forward flow is accentuatedwith inspiration and diastolic flow isreversed in expiration. This respirophasicpattern is also seen in patients with COPDor asthma when strong respiratory effortexaggerates changes in intrathoracic pres-sure. Respirophasic SVC flow reflectschanges caused by pulmonary disease morethan changes in cardiac disease. A varia-tion in SVC flow of �20 cm/s favors thediagnosis of pulmonary disease and�20 cm/s indicates constriction. The mini-mum transmitral E wave is coincident withthe second or third beat of inspiration whenthe variation is due to COPD but coincideswith the first beat of inspiration whencaused by constriction.

Constrictive pericardial disease can bedifficult to distinguish from noninfiltrativerestrictive cardiomyopathy and this


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Figure 9.17 M-mode echocardiogram in a patient with constrictive pericarditis. The interventricular septum moves sharply tothe left and then quickly back to the right in early diastole (downward pointing arrows). This septal bounce or notch is acommon finding in constrictive pericardial disease. There is rapid posterior motion of the posterior wall in early diastole butthis motion is terminated abruptly when the limit of the constricting pericardium is reached and there is little further motionthrough the rest of diastole. It is sometimes possible to distinguish the visceral and parietal pericardial layers (upward pointingarrow) and in constrictive pericardial disease they are usually fused together – the separation between them is constantthroughout the cardiac cycle (LV, left ventricle).

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distinction is important because pericardialstripping can be curative. The distinctionbetween the two conditions is based uponthe finding that blood flow velocities arerespirophasic in constrictive disease but notin restrictive disease and because myocar-dial relaxation is normal in constriction butnot in restriction. Respirophasic variationin transmitral E wave ((E expiration � Einsiration)/E inspiration) is �10% in RCMbut �25% in constrictive pericarditis. Asmall minority of patients with constrictionmay not demonstrate respirophasic varia-tions in flow velocities initially, but thesefindings can be provoked by pharmacologicinterventions that reduce preload. Color M-mode propagation velocities (Vp) and tissueDoppler indices of early filling (E�) are nor-mal (�50 cm/s and �8 cm/s, respectively) inconstrictive pericarditis and significantlyreduced in RCM. Equivocal findings will bepresent in cases of mixed pericardial/muscledisease (Table 9.1).

SPECIFIC ETIOLOGIES

Bacterial or purulent pericarditis

This was usually secondary to pneumonia orempyema before the introduction of antibi-otics. Today it is usually due to extension ofendocarditis, early postoperative infectionor hematogenous spread during bacteremia.

Purulent effusions result in extensive adhe-sions with loculations and localized fusionof the pericardial space. Pus cannot be aspi-rated and suspected purulent effusionsrequire surgical exploration, drainage withpericardial lavage, intrapericardial installa-tion of antibiotics, and usually extensivepericardiectomy. The mortality for purulentpericarditis is greater than 50%.

Post-infarction pericarditis

This occurs within four days of infarctionand is exudative. Pericarditis occurs inapproximately 6% of patients with an infarc-tion and 20% of patients with large anteriorwall infarcts. It is often patchy, adjacentto the infarcted myocardium. Dressler syn-drome or post-infarction syndrome occursin approximately 5% of patients from weeksto months after an infarction and consistsof recurrent fevers, pleuritis, and pericardi-tis. It affects the pericardium diffusely andis probably immunologically mediated.Post-pericardiotomy syndrome is seen lateafter cardiac surgery, catheter perforationor cardiac trauma. It is similar to Dresslersyndrome and is thought to be an immuneresponse to bleeding into the pericardial sacand mediastinum.

Post-cardiac surgery

Pericardial effusions and tamponade candevelop following cardiac surgery frombleeding at suture sites and from epicardialpacemaker leads (Figure 9.18). The peri-cardium is generally left open after surgeryand the usual signs of increased intrapericar-dial pressure will be absent. Alternatively,the cut edges of the pericardium may adhereto the sternum. Effusions that develop inthis setting will be loculated posteriorly.Postoperative hematomas often exert a localhemodynamic effect on one or two cardiacchambers and may need to be surgicallyevacuated.

Congenital pericardial cysts

These are circumscribed pouches or diver-ticula that form in utero. Ninety percent

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RCM CP

Septal shift No YesTissue Doppler Indices � 8 No YesAtria enlarged ��

Respiratory variation No YesShortened deceleration time Yes YesMHV expiratory diastolic

flow reversal No YesE/E� �15 �8 Normal

Table 9.1 Restrictive cardiomyopathy (RCM) versusconstrictive pericarditis (CP)

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form at the right costophrenic angle andare seen along the superomedial margin ofthe right atrium in the apical four-chamberview. They are usually anechoic having theacoustic signature of clear fluid, but may befilled with a proteinaceous slurry that canbe seen to move in real-time imaging. Theyare benign and asymptomatic and usuallypresent as an incidental finding on a chestX-ray or computed tomography.

Congenital complete absence of theparietal pericardium

This is rare and usually asymptomatic. It isusually the left parietal pericardium that isdeficient and this causes the heart to shiftto the left. There is paradoxical septalmotion and the right heart appears to beenlarged when viewed from the parasternaltransducer position but not from the apicalwindow. The LA or left atrial appendage canherniate through a defect in the pericardiumand sudden death from strangulated herniashas been reported.


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Figure 9.18 Apical four-chamber view in a patient withpericardial effusion (PE)/hematoma in cardiac tamponaderesulting from postoperative bleeding following coronarybypass surgery (RV, right ventricle; LV, left ventricle; RA,right atrium; LA, left atrium).

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ANATOMY

The ascending aorta curves anteriorly,superiorly, and to the right from the aorticannulus. It is approximately 5 cm long and3 cm in diameter and terminates at theorigin of the innominate artery. The aortacontinues as the aortic arch or transverseaorta, which travels leftward and posteri-orly, arching over the right pulmonaryartery. This segment is about 4 cm long andextends from the innominate artery to theligamentum arteriosum directly oppositethe left subclavian artery (Figure 10.1). Thedescending aorta (DAO) extends from theligamentum arteriosum and is divided intothoracic and abdominal segments at thediaphragm. The abdominal DAO is adja-cent to the left margin of the vertebralcolumn, parallel, posterior, and leftward to

the inferior vena cava (IVC) and bifurcatesinto right and left iliac arteries at the levelof the umbilicus.

The thin inner layer of the aorta, theintima, is comprised of the endothelium andsurrounding elastic fibers and connective

DISEASES OF THE AORTA

CONTENTS ● Anatomy ● Atherosclerotic Disease ● Aortic Dissection

10

RSC

RCC LCC

TAO

AAOPA

DAO

Diaphragm

LSC

In

Figure 10.1 Drawing of the aorta. The ascending aorta(AAO) crosses over the right pulmonary artery (PA) andcontinues as the transverse aorta (TAO) or aortic arch.Three arteries arise from the superior aspect of the aorticarch. They are from proximal to distal the inomminate,which branches into the right subclavian (RSC) and rightcommon carotid (RCC) arteries, the left common carotid(LCC) and the left subclavian (LSC). The descending aorta(DAO) begins at the ligamentum arteriosum (arrow) and isdivided into thoracic and abdominal sections at thediaphragm.

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tissue. The medial layer is approximately1 mm thick and contains smooth musclecells, collagen, and elastin. The outer adven-titial layer is composed of tough connectivetissue.

The aorta can be damaged by trauma,inflammation, infection, atherosclerosis,degenerative changes and hereditary con-nective tissue disease. Elastic elements in theintima and media stretch with systole andstore energy, which is released in diastolehelping to propel blood to the periphery.These elements are attenuated with agingand the aorta becomes less distensible,enlarges, and elongates. Atherosclerosiscan cause focal fibrosis and calcificationof the aortic wall, which can lead toaneurysm formation, embolic events, and

dissection. Hypertension accelerates bothatherosclerotic and degenerative changes.

ATHEROSCLEROTIC DISEASE

The spectrum of atherosclerotic disease ofthe aorta extends from mild focal thickeningof the aortic wall to large, raised, calcifiedplaques that protrude into the lumen andmay be associated with thrombus (Table10.1). Alternatively, ulcerated plaques canpenetrate into the aortic wall and producean intramural hematoma or a pseudo-aneurysm (contained rupture) of theaorta (Figure 10.2). Atherosclerotic aorticaneurysms result from weakening of the

Normal Mild Moderate Severe

Intimal thickening �2.0 mm �3.0 mm �5.0 mm �5.0 mmLuminal irregularities None None Raised plaques Protruding plaques and/or debris

Table 10.1 Aortic atherosclerosis classification

Figure 10.2 Parasternal long axis in a patient with a pseudoaneurysm or contained rupture of the descending thoracic aorta(Dao), which has been walled off by thrombus. A pleural effusion (PL) is also seen (RV, right ventricle; LV, left ventricle; LA, leftatrium; AO, aorta).

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aortic wall from extension of atheroma intothe medial layer with destruction of themuscular and elastic tissues. Aneurysms area localized dilatation of the aorta of greaterthan 50% of the normal diameter (Figure10.3). Fusiform aneurysms involve theentire circumference of the aorta. Saccularaneurysms affect only a part of the circum-ference. Surgery is generally indicated foraneurysm �5 cm as the risk of rupture isproportional to size. The abdominal aorta ismore commonly affected than the thoracicaorta with both occlusive and aneurysmalatherosclerotic disease (Figure 10.4).

In addition to atherosclerosis, aneurysmscan result from inflammation, as in Takayasuor giant cell arteritis; infection, as in syphliticaortitis; or mycotic aneurysm from emboliza-tion of infected material or from medialnecrosis associated with hereditary condi-tions including Marfan and Ehlers–Danlossyndrome. Congenital aneurysms of thesinus of Valsalva can rupture into theright atrium (RA), right ventricle (RV), orpulmonary artery (PA) or may compress oneof the coronary arteries (Figure 10.5).

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Figure 10.3 Subcostal four-chamber view in a patientwith a giant (9.7 cm) aneurysm of the descending thoracicaorta (Dao) (RV, right ventricle; LV, left ventricle; RA, rightatrium; LA, left atrium).

Figure 10.4 Subcostal views of the abdominal aorta in long axis (left panel) and short axis (right panel) in a patient with agiant aneurysm of the abdominal aorta, which is partially filled with thrombus (Dao, descending aorta; LA, left atrium; AO,aorta).

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AORTIC DISSECTION

In aortic dissection a tear in the intimallayer allows pulsatile blood flow to tearthrough the medial layer and divide theaortic wall into intimal-medial and medial-adventitial components. The inner layerforms a flap within the aortic lumen thatseparates it into true and false channels.

The tear commonly originates at the rightanterior aortic wall just superior to the rightcoronary artery, or at the ligamentumarteriosum near the innominate artery, andcan propagate longitudinally in antegrade,retrograde, or both directions (Table 10.2).Absent pulses or neurological deficits canresult when the dissection extends into thewalls of branch arteries and compromisesblood flow. Acute type A aortic dissectionhas a mortality rate of approximately 1–2%per hour without surgical repair whereastype B aortic dissections may be managedmedically with blood pressure reduction.The primary cause of death is aortic ruptureinto the pericardium causing tamponade.Acute severe aortic regurgitation (AR)results from retrograde extension of the dis-section with disruption of the commissuresor interference with aortic valve closure bythe dissection flap (Figure 10.6). Aortic rup-ture into the left pleural space is a commonterminal event in distal dissection.

Echocardiography

The diagnosis of an aortic dissection rests onthe visualization of an intimal flap dividingtrue and false lumens (Figure 10.7). The true


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Figure 10.5 Parasternal long axis view in a patient with a sinus of Valsalva aneurysm (arrow) of the noncoronary sinus (LV,left ventricle; LA, left atrium; AO, aorta).

DeBakey classificationDeBakey type 1 Originates in the ascending aorta,

propagates at least to the aortic archand usually for a variable distancebeyond the arch

DeBakey type 2 Originates in and is confined to theascending aorta

DeBakey type 3 Originates in the descending aorta Type 3A stops above the diaphragmType 3B extends below thediaphragm

Stanford classificationType A Involves the ascending aortaType B Doesn’t involve the ascending aorta

Table 10.2 Aortic dissection classification

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lumen expands in systole and may collapsein diastole. The false lumen may containthrombus or spontaneous echo contrast(smoke). Color Doppler demonstrates for-ward systolic flow in the true lumen andreduced, absent or retrograde flow in thefalse lumen, and is often able to identify thesite of origin of a dissection and fenestra-tions between true and false lumens. ColorDoppler is also used to assess the presenceand severity of AR. Transthoracic echocar-diography (TTE) has sensitivity for detectingaortic dissection of only 40%. The diagnosisof an aortic dissection cannot thereforebe excluded by TTE alone. Transesophagealechocardiography (TEE) alone or in combi-nation with TTE is the preferred diagnosticmodality for aortic dissections.

The aorta can be assessed almost com-pletely from the aortic valve to its bifurca-tion using a combination of imagingwindows. The left parasternal long axis(Figure 10.8) and short axis views demon-strate the aortic valve, sinuses of Valsalva

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Figure 10.6 Parasternal long axis view in a patient with aproximal aortic dissection. The dissection flap is indicatedby arrows. A pericardial effusion (*) is also seen and is anominous sign in this setting as the primary cause of deathin aortic dissection is tamponade from rupture of the aortainto the pericardial space (LV, left ventricle; LA, leftatrium). Figure 10.7 Suprasternal notch view of the descending

aorta (Dao) in a patient with a type B aortic dissection. Thedissection flap is indicated by an arrow (TAO, transverseaorta).

Figure 10.8 A parasternal long axis view from a highintercostal space shows aneurysmal dilatation of theascending aorta (Aao) in a patient with Marfan syndrome(LV, left ventricle).

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Figure 10.9 The apical five-chamber view demonstratesmarked aortic (AO) root enlargement in this patient withsevere aortic regurgitation (LV, left ventricle; LA, leftatrium; RV, right ventricle).

Figure 10.10 A dissection flap is seen in the long axis ofthe ascending aorta (Aao; arrow) from the second rightintercostal space in a patient with a type A aorticdissection.

Figure 10.11 Parasternal long axis view. A dissection flapis seen in the descending thoracic aorta (Dao) in thispatient with a type B aortic (AO) dissection. A large pleuraleffusion (PL) is also present (RV, right ventricle; LV, leftventricle; LA, left atrium).

Figure 10.12 The descending thoracic aorta (Dao) canoften be visualized in its long axis from the parasternalwindow. If the Dao is seen in the parasternal long axisview then the scan plane can be rotated 90� while holdingthe Dao in view (PE, pericardial effusion; LVOT, leftventricular outflow tract; LA, left atrium).

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and proximal ascending aorta and thesestructures are also seen from the apical five-chamber (Figure 10.9) and apical long axis

views. The ascending aorta is best seen fromthe upper right sternal border (Figure 10.10)when the patient is positioned in the rightlateral decubitus position. The suprasternalnotch transducer position is used to assessthe transverse and proximal descendingaorta although the proximal transverseaorta is usually less well seen. The DAO canusually be seen in a variation of the apicaltwo-chamber view in which the scan planeis angled medially and inferiorly. The DAOis seen in cross-section in the parasternallong axis view just superior to the atrio-ventricular groove (Figure 10.11) and it canbe seen in its long axis when the plane isrotated 90� clockwise while keeping it inview (Figure 10.12). The distal thoracic andabdominal aorta are seen from the subcostalwindow when from a short axis of theventricles, the plane is angled medially andinferiorly (Figure 10.13). Short axis imagingof the abdominal aorta is optimal withthe patient supine and the transducerplaced on the abdomen and angled directlyposteriorly.

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Figure 10.13 The abdominal aorta is visualized in itslong axis in this patient with an aortic atheroma (arrow)(DAO, descending thoracic aorta; RA, right atrium).

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Cardiac masses include thrombus (seeChapters 4 and 6), vegetations (see Chapter7), and tumors. Masses can be reliablydetected echocardiographically (Figure11.1), and distinguished from ultrasound

artifacts and implanted devices (Figure 11.2)by careful assessment of mass, location,size, shape, mobility, points of attach-ment, acoustic signature, and hemodynamicsignificance.

CARDIAC MASSES

CONTENTS ● Secondary Cardiac Tumors ● Primary Benign Cardiac Tumors ● PrimaryMalignant Cardiac Tumors

11

Figure 11.1 Apical four-chamber view in a patient with an apparent mass on the interatrial septum. The systolic framedemonstrated that the fossa ovalis is not thickened and that ‘mass’ is lipomatous hypertrophy of the interatrial septum, whichis a benign condition (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

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SECONDARY CARDIAC TUMORS

At least 95% of all cardiac tumors are metas-tases (Table 11.1). Cardiac metastases arepresent at autopsy in 10–12% of patientswith malignancies. Depending on their size

and location, tumors can cause obstructionto left or right ventricular inflow or out-flow tracts; arrhythmias and conductiondefects; coronary compression; pericardialeffusions; pericardial tamponade; andcardiac encasement with symptoms ofconstriction. However, most metastases aresmall and do not interfere with cardiacfunction. Cardiac involvement is clinicallysilent in 90% of cases but a pericardialeffusion or tamponade may be the initialsign of metastatic disease.

Tumors invade the heart by:● direct extension from contiguous struc-

tures (i.e. mediastinal lymphomas,esophageal carcinoma)

● hematogenous spread (i.e. melanomas)● retrograde lymphatic spread (i.e. broncho-

genic and breast cancer)● transvenous extension via the cavae

or pulmonary veins (i.e. renal cell andhepatocellular carcinoma) (Figure 11.3).

Lung cancer is the most common sourceof cardiac metastases, being the primarytumor in approximately 36% of cases. Itmay invade the pulmonary veins and causeobstruction and pulmonary venous hyper-tension (Figure 11.4) but it more commonlyinvolves the pericardium and epicardiumindicating retrograde lymphatic spread, asmost of the lymphatics that drain the peri-cardial cavity are located on the visceralpericardium. Secondary cardiac tumors canaffect any region of the heart but the greatmajority of them are pericardial.

Malignant pericardial effusions are usuallydue to metastatic spread to the pericardium(Figure 11.5). The epicardium can also beinvolved with tumor extension into themyocardium but this is rare. Breast cancer,lung cancer, lymphomas, and leukemiasaccount for 80% of all malignant effusionsand malignancy accounts for 50% of alleffusions that require intervention. Pleuraleffusions coexist in a third of cases.Malignant effusions are usually bloodyand tamponade can develop rapidly fromerosion of a pericardial blood vessel orcardiac chamber. The pericardium is oftendiffusely or focally thickened and effusive–constrictive disease is common. Malignant

Figure 11.2 Apical four-chamber view with an apparentmass in the left ventricular (LV) apex and another attachedto the tricuspid valve. Both masses are thrombus. Theformer was associated with apical akinesis and the latterwas covering a right ventricular (RV) pacing wire (RA, rightatrium; LA, left atrium).

Primary 5% of all cardiac tumorsBenign 75% of primary tumors

Myxomas 50% of benign tumorsLeft atrial 75% of myxomasRight atrial 23% of myxomas

Malignant 25% of primary tumorsSarcomas 95% of malignant tumors

Secondary 95% of all cardiac tumorsLung 36% of secondary tumorsNonsolid 20% of secondary tumorsBreast 7% of secondary tumorsEsophagus 6% of secondary tumors

Table 11.1 Cardiac tumors

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Figure 11.3 Subcostal view of the inferior vena cava (IVC) (left panel) and apical four-chamber view (right panel) in a patientwith renal cell carcinoma. The tumor has extended along the IVC and into the right atrium (RA) and now obstructs thetricuspid valve (RV, right ventricle; LV, left ventricle; LA, left atrium).

Figure 11.4 Subcostal four-chamber view in a patientwith a massive tumor (*) that has invaded the atria fromthe pulmonary veins. A large right pleural effusion (PL) isalso present (RV, right ventricle; LV, left ventricle; LA, leftatrium).

Figure 11.5 Parasternal short axis view in a patient witha metastatic tumor on the right ventricular (RV)epicardium (*) that has extended into the RV cavity (arrow)(LV, left ventricle).

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effusions usually indicate advanced diseaseand poor long-term prognosis.

PRIMARY BENIGN CARDIAC TUMORS

Only 5% of cardiac tumors are primary and75% of these are benign.

Myxomas

Half of all benign cardiac tumors are myxo-mas, 75% of these are located in the leftatrium (LA) (Figure 11.6), 23% in the rightatrium (RA) (Figure 11.7) and the remainderarise from the ventricles or mitral valve(MV) apparatus. Myxomas are more com-mon in females and 90% of myxomas arefound in patients between the ages of 30and 60 years. Atrial myxomas are usuallyattached to the fossa ovalis either by abroad base or by a narrow stalk or pedicle.

When large and mobile they can prolapsethrough the MV in diastole producingsymptoms that mimic mitral stenosis. Atrialmyxomas may also present with a non-specific systemic illness with fever, weightloss, joint pain, and fatigue. Portions of thetumor or thrombus on the tumor surfacemay embolize suggesting endocarditis orvasculitis.

Echocardiographically, myxomas have abright, speckled, gelatinous, heterogeneousappearance often with cystic echolucenciesdue to hemorrhage or liquefaction necrosisand may be �5 cm in diameter. Most myxo-mas are solitary and sporadic, but thereis a familial form, Carney complex, inwhich multiple myxomas occur in atypicallocations.

Rhabdomyomas

The most common tumors in children arerhabdomyomas, which are almost invari-ably multiple, pedunculated, mural massesin the ventricles. They are slow growingand spontaneous regression is common.They are associated with tuberous sclerosis,a congenital familial disorder marked bytumors and sclerotic patches of the brain,tumors of the eye and kidneys, epilepsy,and progressive mental deterioration.

Fibromas

Fibromas are usually solitary, well-circumscribed, benign connective tissuetumors that are often located within theinterventricular septum (Figure 11.8). Theytypically affect children and range from1 cm to 10 cm in diameter. They are echo-dense with a homogeneous consistency andoften have a central calcified core.

Papillary fibroelastomas

Papillary fibroelastomas generally arisefrom the ventricular aspect of semilunarvalves, the atrial sides of atrioventricularvalves and rarely from the chordae or rightor left ventricular endocardium. The leftheart valves account for 80% in adults butthe tricuspid valve is most commonly


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Figure 11.6 A low parasternal long axis view in a patientwith a left atrial myxoma (*) (RV, right ventricle; LV, leftventricle; AO, aorta).

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CARDIAC MASSES

affected in children. Fibroelastomas aresmall, usually �1.5 cm in diameter, andcan embolize or obstruct a coronary arterybut do not obstruct forward flow.Echocardiographically, they are very bright,shimmering, mobile masses attached to thevalve by a short stalk. Morphologically theyresemble a sea anemone, having multiplevillous fronds attached to a central core ofdense connective tissue.

Hemangiomas

Hemangiomas are vascular tumors thatarise from the epicardium or endocardiumbut are usually intramural and usually seenin the walls of the right heart. They are 2–4cm in diameter, subendocardial, and have aspongy, echodense acoustic signature.

Lipomas

Lipomas are bright, homogeneous tumorsthat are usually small, sessile, and asympto-matic. Twenty-five percent of lipomas areintramyocardial and most are subepicardial.

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Figure 11.7 Off-axis subcostal short axis at the base in a patient with a small right atrial myxoma (*) (RV, right ventricle; AO,aorta; PA, pulmonary artery; S, superior vena cava).

Figure 11.8 Parasternal long axis view in a patient with afibroma (*) within the interventricular septum. The tumoris echodense and casts an acoustic shadow, which partiallyobscures distal structures (RV, right ventricle; LV, leftventricle; LA, left atrium; AO, aorta).

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PRIMARY MALIGNANT CARDIAC TUMORS

Ninety-five percent of malignant primarycardiac tumors are sarcomas.

Angiosarcomas

Angiosarcomas occur almost exclusively inthe RA in the third to sixth decades of lifeand affect males twice as often as females.They present as broad-based masses at thecavo-atrial junction that invade the RAendocardium and extend into the peri-cardium. These tumors are aggressive anddirectly invade the mediastium (Figure 11.9),pleura, inferior vena cava, and tricuspidvalve and may metastasize to the lungs.Mean survival from diagnosis is rarely greaterthan six months. Echocardiographically,angiosarcomas are echo bright, heteroge-neous, large tumor masses with irregularmargins.

Rhabdomyosarcomas

Rhabdomyosarcomas can affect any cardiacchamber. They are invasive but they do not


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Figure 11.9 Parasternal short axis view in a patient withan angiosarcoma. The tumor has invaded the mediastinumand distorted the anatomy of the great vessels so that theaortic (AOV) and pulmonic (PV) valves almost occupy thesame plane (RA, right atrium; LA, left atrium).

Figure 11.10 Apical four-chamber view in a patient with a rhabdomyosarcoma that has a broad base of attachment to thelateral wall of the left atrium (LA) and has spread into the left ventricular (LV) lateral wall myocardium (RV, right ventricle; RA,right atrium).

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usually extend beyond the parietal peri-cardium. They generally have a broad baseof attachment and a heterogeneous tissuetexture (Figure 11.10).

Primary cardiac lymphomas

Primary cardiac lymphomas are rare andmost often encountered in patients with acompromised immune system, such aspatients with acquired immune deficiency

syndrome (AIDS) or organ transplant.There is occasionally diffuse infiltration ofthe right atrial and right ventricular wallsin which focal nodules may be appreci-ated. Infiltration of the myocardium cancause regional wall motion abnormalitiesand a heterogeneous echocardiographictexture of the walls involved. However,pericardial effusions are often the onlyechocardiographic finding in cardiaclymphoma.

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One percent of all children are born with acongenital heart defect and the number ofadults with congenital heart disease (CHD) isincreasing as a result of effective therapy ininfancy and childhood. The retrosternalcardiac position that often accompanies con-genital cardiac malformations and scar tissuefrom prior corrective or palliative surgeriesoften makes imaging difficult in the adultpatient with congenital heart disease.Careful attention to patient positioningand the use of off-axis imaging windows isfrequently necessary. Furthermore, whenevaluating complex congenital malforma-tions it is essential to follow a disciplined,sequential, segmental approach to identifyatrial situs and document veno–atrial,atrio–ventricular, and ventriculo–arterialconnections, and chamber and great vesselmorphology. Knowledge of the normalfetal circulation is necessary because somecongenital abnormalities are the result ofthe persistence of elements of the fetalcirculation after birth.

FETAL CARDIAC ANATOMY

In utero, oxygen is provided to the fetus bythe maternal placental circulation via theumbilical veins and inferior vena cava (IVC).The fetal lungs require only enough blood

flow to support development and the pul-monary circulation is largely bypassed.Oxygenated blood in the IVC is preferen-tially directed across the interatrial septum(IAS), through the foramen ovale, which isguarded by a flap valve, to the left side of theheart to facilitate the rapid growth of thehead. Relatively deoxygenated blood fromthe superior vena cava (SVC) is preferentiallydirected through the tricuspid valve (TV),pulmonic valve (PV) and the ductus arterio-sus (PDA) to the descending aorta (Figure12.1). The eustachian valve and Chiarinetwork help direct and separate the twostreams of blood.

At birth, the lungs expand and resistanceto blood flow into the lungs greatlydecreases. Flow through the PDA decreasesand the duct ultimately closes and becomesthe ligamentum arteriosum. Pressure in theleft atrium (LA) becomes greater than pres-sure in the right atrium (RA) and the flapvalve of the foramen ovale closes andusually seals shut becoming the fossa ovalisin the first months of infancy. However, apatent foramen ovale (PFO) is present inapproximately 20% of the normal adultpopulation. PFOs permit paradoxical emboliand have been increasingly recognized asa source of stroke. Additionally, PFOs canstretch in the presence of atrial enlargementand permit significant shunt flow, thedirection of which is dependent on therelative atrial pressures.

CONGENITAL CARDIACMALFORMATIONS

CONTENTS ● Fetal Cardiac Anatomy ● Echocardiography ● Shunt Lesions ● ObstructiveLesions ● Complex Congenital Cardiac Malformations

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In early embryonic life there are paired leftand right SVCs. With subsequent develop-ment venous return from the left arm andleft side of the head is diverted to the rightSVC via the brachiocephalic vein and thedistal left SVC becomes incorporated intothe coronary sinus and the rest withers tobecome the ligament of Marshall. When theleft SVC persists, blood from the left upperbody returns to the RA via the coronarysinus. A greatly enlarged coronary sinus seenin the parasternal long axis usually indicatesa persistent left SVC (Figure 12.2), which canbe imaged directly from the left supraclavic-ular fossa. This can be confirmed with aninjection of contrast medium into a vein inthe left arm. Contrast enters the RA from the

coronary sinus in the apical four-chamberedview with the scan plane angled posteriorly(dorsally) (Figure 12.3).

ECHOCARDIOGRAPHY

The segmental approach to echocardio-graphic diagnosis of complex congenitalabnormalities begins with the establishmentof the atrial situs, which can be ascertainedby examining the spatial relationship of theIVC and abdominal aorta. When the abdom-inal aorta is anterior to and slightly to theleft of the spine and the IVC is to the right ofthe spine then the atrial situs is normal (situssolitus) with the right atrium on the rightand left atrium on the left. Mirror imagereversal of the abdominal aorta and IVC(situs inversus) indicates mirror imagereversal of atrial situs (Figure 12.4). Atrial

RAPA

AO RPA LPA

LA

DAO

RV

LV

SVC

IVC

Figure 12.1 Diagram of the fetal circulation. Oxygenatedblood from the inferior vena cava (IVC) passes through theflap of the foramen ovale (arrow in right atrium (RA)) andrelatively deoxygenated blood from the superior vena cava(SVC) passes through the tricuspid and pulmonic valves andthen through the ductus arteriosus (arrow in PA) (RV, rightventricle; LV, left ventricle; RA, right atrium; LA, leftatrium; DAO, descending thoracic aorta; LPA, leftpulmonary artery).

Figure 12.2 This parasternal long axis view shows agrossly enlarged coronary sinus (CS) (RV, right ventricle; LV,left ventricle; LA, left atrium; AO, aorta).

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isomerism with bilateral right-sidedness(asplenia) is detected when the IVC is ante-rior to the abdominal aorta and both vesselsare on the same side of the spine. Bilateralleft-sidedness (polysplenia) is associatedwith interruption of the IVC in 70% ofcases. Atrial morphology is confirmeddirectly by identifying the flap of the fossaovalis opening into the LA and by visualiz-ing the limbus, which is situated on thesuperior right atrium wall and the elevatedrim of tissue surrounding the fossa ovalis,which is also right sided. The body of theLA has a smoother contour than that of theRA and lacks pectinate muscles except in itsappendage and the LA appendage has a nar-row base while the base of the right atrialappendage is broad. The systemic veins usu-ally enter the RA and the pulmonary veinsusually enter the LA but this is insufficientlyreliable for identifying the atrial type.

The atrioventricular (AV) connections arethen established. The TV inserts into theinterventricular septum (IVS) at a more api-cal position than the mitral valve (MV) butthis relationship is lost in complete endo-cardial cushion defect (ECD). The AV valvesare always concordant with the ventricles.

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Figure 12.3 The cause of the enlarged coronary sinus (CS) in Figure 12.2 is revealed by an injection of agitated saline into aleft arm vein. The contrast material enters the right atrium and ventricle (RV) via the coronary sinus demonstrating a persistentleft superior vena cava (LV, left ventricle).

Figure 12.4 The transducer is positioned in the subcostalregion and angled caudad to visualize the spatialrelationship of the abdominal aorta and the inferior venacava (IVC). There is a mirror image reversal of the normalrelationship or situs inversus. The IVC is on the patient’sright and the aorta is on the patient’s left. Situs solitus isshown in Figure 2.37 (B) (Dao, descending thoracic aorta).

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Identification of the AV valve aids in recog-nition of the ventricular type. The MV hastwo predominant papillary muscles; the TVhas multiple, smaller papillary muscles. TheTV has chordal insertions directly to the IVSbut the MV does not. Importantly, the rightventricle (RV) is more heavily trabeculatedat the apex than the left ventricle (LV)and contains the moderator band. This fea-ture of ventricular morphology is usuallydecisive. Atrioventricular connections areassessed to be either concordant (RA to RV),discordant (RA to LV), ambiguous or uni-laterally absent regardless of the position ofeach chamber within the chest.

To establish the ventriculo–arterial con-nections it is necessary to recognize that theaorta arches and the pulmonary artery (PA)bifurcates. From the left and right para-sternal and suprasternal notch transducerpositions, the aorta is seen to ascend anteri-orly and from it will arise the coronary andbrachiocephalic arteries. The bifurcation ofthe PA must be visualized to unequivocallyidentify the great vessels. This can beaccomplished from off-axis high parasternalviews, subcostal short axis views, or fromthe apical imaging window and permits

identification of ventriculo–arterial con-nections as concordant or discordant. Thecongenital abnormalities described belowmay be complex but can be resolved bythe application of the segmental chamberanalysis.

SHUNT LESIONS

Patent ductus arteriosus

When the ductus arteriosus remains patent(PDA) after birth, blood flows continuouslyfrom the aorta to the PA, the magnitude ofthe flow is determined by the size of theductus and by the aortic–pulmonary pres-sure gradient. The incidence of PDA ishigher in premature infants and up to 30times higher in people living at high alti-tudes (�5000 m). When a PDA is small itcan be well tolerated for many decades butwhen large it can cause pulmonary hyper-tension or heart failure from LV volumeoverload. Near equalization of systemic andpulmonary pressures causes the shunt tobecome bidirectional (right to left during


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Figure 12.5 The pulmonary artery (PA) is enlarged in the parasternal short axis image on the left. Color Dopplerdemonstrates a continuous jet entering the right PA just distal to the bifurcation from a persistent ductus arteriosus (AO,aorta).

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systole and left to right during diastole).PDAs are best visualized from the paraster-nal view of the bifurcation of the PA on theinferior aspect of the proximal right PA.Color Doppler of the PA reveals a brightcontinuous flow that extends several cen-timeters into the PA (Figure 12.5). Onceidentified, the site of the PDA can be inter-rogated by continuous wave (CW) Doppler

and systolic and diastolic aortic/PA pressuregradients assessed (Figure 12.6). PDAs maybe the site of endovascular infection.

Atrial septal defects

These occur in the midportion of the IAS inthe region of the fossa ovalis in 65–80% ofcases and are termed ostium secundumatrial septal defects (ASDs) (Figure 12.7).Ostium primum ASDs are anterior andinferior to the fossa ovalis and in continu-ity with mitral and tricuspid valve tissueinferiorly (Figure 12.8) and are frequentlyassociated with trisomy 21 (Down syn-drome). These are a type of an ECDcommonly associated with a cleft MV andmitral regurgitation of varying severity(Figure 12.9). Symptoms are generally moresevere in primum than secundum ASDs,and occur at an earlier age. Sinus venosusASDs are usually located at the roof of theatria close to the insertion of the SVC,which usually overrides the defect but aminority are adjacent to the IVC. Sinusvenosus ASDs are associated with partialanomalous pulmonary venous drainage,most often with a direct connection of the

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Figure 12.6 Continuous wave Doppler directed throughthe color jet in Figure 12.5 demonstrates a diastolicvelocity of 3 m/s and a systolic velocity of 4.5 m/s.

Figure 12.7 Apical four-chamber view in a patient with a large secundum atrial septal defect (*). Color flow Doppler (rightpanel) shows left to right flow across the defect (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

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right upper and middle pulmonary veins tothe SVC (Figure 12.10). A coronary sinusASD or unroofed coronary sinus is a raretype of ASD that results from a defect in thevessel wall separating the coronary sinusfrom the LA.

The goal of echocardiography in theevaluation of a patient with an ASD is toidentify the location and size of the defect,the relationship of the defect to the AVvalves, the pulmonary and systemic bloodflows (Qp/Qs), and PA systolic pressure.The IAS is normally thin and difficult tovisualize adequately when parallel to theultrasound plane, as from the apical four-chambered view. From the subcostal four-chamber, subcostal short axis and theupper right sternal transducer position theIAS is perpendicular to the beam whileshunt flow is parallel to it facilitatingpulsed-wave and color Doppler interroga-tion. Flow across the ASD is continuous and


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Figure 12.8 Apical four-chamber view in a patient with a primum atrial septal defect (ASD). The mitral and tricuspid valvesare coplanar (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

Figure 12.9 A short axis view in the same patient asFigure 12.8. There is a cleft in the anterior mitral valveleaflet.

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low velocity. Reducing the velocity scalefacilitates the recognition of shunt flow bycolor Doppler. Depending on the magni-tude of the shunt, the PA and right heartchambers may be dilated, the IVS may showparadoxical motion and the LV may besmall and under-filled.

An injection of agitated saline into aperipheral vein causes opacification of theright heart chambers and the appearance ofcontrast (bubbles) in the left atrium in thepresence of an ASD either at rest or with aValsalva maneuver. Bubbles must appear inthe left atrium within five cardiac cycles oftheir appearance in the RA to confirm thepresence of an ASD as the late arrival ofcontrast may occur through pulmonary AVmalformations. The magnitude of the shuntflow is expressed as the ratio of pulmonaryto systemic flows (Qp:Qs) and can be esti-mated as the ratio of the Doppler derivedRV outflow tract (RVOT) and LVOT strokevolumes. PA pressure may be estimatedfrom the peak velocity CW signal of the tri-

cuspid regurgitation (TR) jet. ASDs are oftenclinically silent but significant shunting(Qp:Qs �2.0) ultimately causes symptomsof dyspnea, pulmonary hypertension and/orright heart failure. ASDs are also associatedwith atrial arrhythmias and paradoxicalemboli. Surgical patch closure is one of thesafest and most effective cardiac surgicalprocedures and is generally recommended.Defects less than 2 cm in diameter whichare surrounded by atrial septal tissue areusually amenable to transcatheter deviceclosure. Transthoracic echocardiography(TTE) can accurately diagnose the presenceof an ASD but transesophageal echo-cardiography (TEE) is necessary to assess thepulmonary venous connections, determinewhether defects are single or multiple andwhether they are suitable for device closure.

Ventricular septal defects

Most defects of the IVS (approximately70%), are located beneath the posteriorright and noncoronary cusps of the aorticvalve in the region of the interventricularportion of the membranous septum (Figure12.11). Perimembranous ventricular septaldefects (VSDs) are usually small, solitary andrestrictive. The high velocity jet across thistype of defect can cause a Venturi effect thatsucks the right or noncoronary cusp intothe defect causing aortic regurgitation.Perimembranous VSDs often close sponta-neously during early childhood by incorpo-ration of TV tissue into the defect.

Muscular VSDs are entirely surrounded byventricular myocardium and are subclassi-fied by their location, as defects in the inlet(between the RV and LV inflow tracts (RVITand LVIT)), trabecular (usually in the vicin-ity of the moderator band) or outlet(between the infundibulum and LVOT) por-tions of the IVS. Muscular VSDs may bemultiple and located in different parts ofthe muscular septum. Subarterial or doublycommitted VSDs result from a deficiency ofthe infundibular septum and are boundsuperiorly by the semilunar valves.

Flow across a restrictive VSD can be read-ily appreciated by color Doppler imaging.By carefully aligning the ultrasound beam

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RV

RA LA

L

LIPV

RIPV

LV

IVS

P

Figure 12.10 A diagram of normal atrial and atrial septalanatomy in apical four-chamber orientation. The arrowpoints to the flap of the fossa ovalis (P, primum atrialseptum; L, limbus; RIPV, right inferior pulmonary vein;LIPV, left inferior pulmonary vein; RV, right ventricle; LV,left ventricle; RA, right atrium; LA, left atrium).

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with the jet, which often requires off-axis,non-standard transducer positions, CWDoppler will yield the velocity of the inter-ventricular flow from which the trans-septalpressure gradient can be calculated by themodified Bournoulli equation. Subtractingthe trans-septal gradient from the cuff sys-tolic blood pressure yields an estimate ofthe RV systolic pressure, which should be inagreement with estimate obtained from themaximum TR velocity and RA pressure.Qp:Qs and pulmonary artery pressuresmust be carefully evaluated in all cases ofleft-to-right shunt.

Nonrestrictive VSDs are large and the pul-monary circulation is exposed to systemicpressure in the absence of pulmonic steno-sis (Figure 12.12) and these patients usuallyrequire surgery in infancy. Restricting bandsused to be placed around the PA to pro-tect the pulmonary vasculature in infantswith nonrestrictive VSDs who were notcandidates for definitive surgical repair.

Tetralogy of Fallot

Embryologic malalignment of theinfundibular septum with the rest of themuscular septum causing a large, non-restrictive, perimembranous VSD is thecardinal feature of tetralogy of Fallot (TOF),which is the most common cause of cyan-otic heart disease (Table 12.1). Anteriordeviation of the infundibulur septum nar-rows the RVOT (Figure 12.13) and causesthe aorta to override the muscular IVS(Figure 12.14). The pulmonary valve annu-lus is small and the pulmonic valve isusually stenotic, often with a bicuspid orunicuspid morphology. RVH and musclebundles in the infundibular wall may con-tribute to the RVOT obstruction, which issufficient to prevent pulmonary hyperten-sion in TOF. Symptoms and exercise toler-ance vary with the degree of pulmonarystenosis (PS). Patients with TOF and severePS or TOF with pulmonary atresia present inearly infancy with cyanosis and hypoxemia


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Figure 12.11 Color flow Doppler in the parasternal long axis (left panel) and parasternal short axis (right panel) showingsystolic flow through a perimembranous interventricular septum (RV, right ventricle; LV, left ventricle; RA, right atrium; LA, leftatrium; AO, aorta; LVOT, LV outflow tract).

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upon closure of the PDA as the pulmonarycirculation is largely supplied by retrogradeflow from the aorta through the duct.

Essential elements of the echocardio-graphic evaluation of a patient with TOFinclude determination of the site and sever-ity of RVOT obstruction; the magnitude anddirection of trans-septal flow; estimation ofRV and PA pressures and assessment of pul-monary regurgitation. The RVOT is visual-ized from the parasternal short axis andparasternal long axis views of the RVOT butthese views do not always permit alignmentof the CW Doppler beam with flow whenthe obstruction is at the infundibular level.This is better achieved from the apicalview when the transducer is angled anteri-orly past the LVOT and from the subcostalshort axis at the base of the heart. Trans-septal flow will usually be low velocityreflecting nearly equal RV and LV systolic

pressure. The RV systolic pressure can beestimated by the CW signal of TR as usual.PA systolic pressure is obtained by subtract-ing the RVOT gradient from the RV systolic

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Figure 12.12 Apical four-chamber view from a patient with a nonrestrictive ventricular septal defect (VSD) (RV, rightventricle; LV, left ventricle; RA, right atrium; LA, left atrium).

Right ventricular hypertrophyPulmonic stenosisVentricular septal defectOverriding aorta

Table 12.1 Tetrology of FallotFigure 12.13 In tetralogy of Fallot anterior deviation ofthe infundibular septum (arrow) narrows the RV outflowtract and causes the ventricular septal defect (*) with anoverriding aorta (RV, right ventricle; RA, right atrium; LA,left atrium).

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pressure. TOF is often associated with a rightaortic arch.

Surgical repair of TOF consists of a patchclosure of the VSD and alleviation of theRVOT obstruction. The RVOT may beenlarged with a patch across the PV annu-lus, and this is often associated with signifi-cant pulmonary insufficiency. Surgical scarsin the vicinity of the RVOT are a substratefor arrhythmias.

Double outlet right ventricle

Double outlet RV (DORV) may be consideredto be an exaggerated form of TOF in whichthe aorta is to the right of the IVS, althoughsome authors insist that for the diagnosisof DORV, the aorta and mitral valves mustnot be in continuity but separated by aninfundibulum. In DORV all oxygenatedblood must pass through the VSD, whichmust therefore be large and this exposes thepulmonary vasculature to systemic pressureunless there is also subpulmonic obstruc-tion. With PS, symptoms will resemble TOF,without PS the symptoms will be those of anonrestrictive VSD. The aorta sits adjacentto the VSD and preferentially receives oxy-genated blood. In the Taussig–Bing type ofDORV the great vessels are transposed, the

PA is on the left and the aorta on the right.This type of DORV mimics complete trans-position of the great arteries and cyanosis ispredominant.

OBSTRUCTIVE LESIONS

Congenital valvular abnormalities are dis-cussed in Chapter 8.

Cor triatriatum

In cor triatriatum the pulmonary veinsenter an accessory chamber that is sepa-rated from the LA by a membrane (Figure12.15). It is often an incidental findingwithout hemodynamic significance but ifthe opening in the membrane is small,symptoms will mimic those seen in mitralstenosis. An imperforate cor triatriatummembrane will be associated with totalanomalous pulmonary venous return(TAPVR). Pulmonary venous return to theheart will be to the RA by way of an ascend-ing vertical vein to the brachiocephalicvein and SVC, to the RA via subdiaphrag-matic connection of a vertical vein to theIVC (scimitar syndrome) or the pulmonary


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Figure 12.14 This parasternal long axis view demonstrates the ventricular septal defect (*) and overriding aorta in tetralogyof Fallot (RV, right ventricle; LV, left ventricle; LA, left atrium; AO, aorta).

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veins will remain at the level of the heartand drain into the RA, SVC, or coronarysinus individually or in combinations.Generally, TAPVR is to the RA so that anASD is obligatory.

Coarctation of the aorta

Coarctation of the aorta is a narrowing orcomplete interruption of the aorta in theregion of the ligamentum arteriosum thatis usually discrete but may be a tubularnarrowing affecting a variable length ofthe aorta (Figure 12.16). Coarctation is fourtimes more common in males and oftenassociated with a bicuspid aortic valve. Insevere cases presenting in infancy, flow tothe distal aorta may be predominatelythrough a PDA and peripheral but not cen-

tral cyanosis will be present. Coarctation ofthe aorta is usually only visualized fromthe suprasternal notch (SSN), which alsoenables CW Doppler assessment of the pres-sure gradient across the obstruction, whichif high, persists through diastole (Figure12.17). The distal thoracic and abdominalaorta are diminished in size in proportionto the degree of obstruction.

173

Figure 12.15 A non-obstructing membrane is seen in theleft atrium (LA) (arrow) in this apical four-chamber view inthis patient with cor triatriatum (RV, right ventricle; LV, leftventricle).

Figure 12.16 Suprasternal notch view in a patient withcoarctation of the aorta (Tao, transverse aorta; Dao,descending aorta).

Figure 12.17 Continuous wave Doppler through thecoarctation shown in Figure 12.16. The pressure gradientpersists through diastole.

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COMPLEX CONGENITAL CARDIACMALFORMATIONS

An exhaustive treatment of the subject ofcomplex congenital cardiac abnormalities isbeyond the scope of this text. The followingexamples are chosen because, althoughrare, they are encountered in the adultpopulation.

Ebstein anomaly

In Ebstein anomaly the TV leaflets do notseparate adequately from the RV endo-cardium but remain attached at variablepoints. The coaptation point is apically dis-placed and the portion of the RV proximal tothe coaptation point is ‘atrialized’, forming acommon chamber with the RA and not con-tributing to RV systolic contraction (Figure12.18). The TV tissue is markedly redundantand dysplastic, the anterior leaflet is elon-gated and sail-like and may cause RVOTobstruction. TR is almost universally presentand often severe but the velocity is low. TheTR originates at the coaptation point and theextent of its displacement can be readilyrecognized with color Doppler (Figure12.19). Right-to-left shunting at the atrial


174

Figure 12.18 Apical four-chamber view in a patient with Ebstein anomaly. The point of tricuspid valve closure is displacedtoward the apex. A large portion of the right ventricle (RV) is ‘atrialized’ (LV, left ventricle; RA, right atrium; LA, left atrium).

Figure 12.19 This patient has moderate tricuspidregurgitation (TR) by color flow Doppler. The TR signaloriginates from the point of coaptation of the tricuspidleaflets, which is displaced toward the apex.

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level from ASDs or stretched PFOs is com-mon and can cause cyanosis. Doppler/echocardiography is used to evaluate theextent and location of valve tethering and

dysplasia, degree of RV atrialization, thedegree of TR, and the magnitude of atrialshunting.

Endocardial cushion defects

ECD or atrioventricular canal defects resultfrom failure in the development of theendocardial cushions, from which isderived the tissue that divides the embry-ologic common AV canal into separatetricuspid and mitral orifices (Figure 12.20).These may be partial or complete andcommonly affect patients with trisomy 21(Down syndrome), complete defects morecommonly than partial. Echocardiographicfindings in partial ECD consist of a primumASD, AV septal defect, cleft anterior MVleaflet and coplanar attachments of theanterior MV and septal TV leaflets. A defecton the upper ventricular septum is almostinvariably present in complete ECD andthere is one common AV annulus with fiveleaflets (Figure 12.21), which may havechordal attachments to the contralateralventricle through the VSD or to the superiorIVS. Surgery is generally required before theage of 2 years for complete ECD. A transi-tional type of ECD consists of a primumASD with a common AV valve but in this

175

Figure 12.20 Parasternal short axis view in a patient withan endocardial cushion defect. There is a primum atrialseptal defect (*) and a ventricular septal defect (arrow)(RV, right ventricle; RA, right atrium; LA, left atrium).

Figure 12.21 Subcostal short axis view in a patient with complete endocardial cushion defect. There is a commonatrioventricular valve with five leaflets (RV, right ventricle; LV, left ventricle).

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176

Figure 12.22 Parasternal long axis in a patient with D-loop transposition of the great vessels. The aorta (AO)arises from the right ventricle (RV) and the pulmonaryartery (PA) from the left ventricle (LV). The semilunar valvesare coplanar.

To increase pulmonary artery blood flow as in tetralogy of FallotBlalock–Taussig Subclavian artery to PA anastomosisGlenn shunt SVC to RPA anastomosis Waterston shunt Ascending AO to RPA anastomosis Potts shunt Descending AO to PA anastomosis

For D-looped transpositionRashkind Balloon atrial septostomy to increase the mixing of systemic and pulmonary venous return

in D-looped transposition of the great vesselsBlalock–Hanlon Operative atrial septostomy to increase the mixing of systemic and pulmonary venous

return in D-looped transposition of the great vesselsMustard or Senning procedure Creates an intra-atrial baffle to direct pulmonary venous return to the RV and systemic

venous return to the LV. The baffle is made of prosthetic material or pericardium in theMustard procedure and flaps of atrial tissue in the Senning procedure

Rastelli For D-transposition with a malalignment VSD. The aorta is connected to the LV through theVSD. The PV is sewn shut and a valved conduit used to connect the RV to the PA

Jatene Arterial switch with reimplantation of the coronaries for complete transposition of thegreat vessels

For univentricular atrioventricular connectionFontan procedure The RA is connected to the RPA either directly or with the interposition of a valved conduit

and the ASD and VSD are closedDamas–Kaye–Stansel Modification of the Fontan procedure for univentricular AV connection to a morphologic

LV with transposition and subaortic stenosis or restrictive VSD. The PA is severed. Theproximal PA is anastomosed to the AO and the RA connected to the distal PA

PA, pulmonary artery; SVC, superior vena cava; RPA, right PA; AO, aorta; RV right ventricle, LV, left ventricle; VSD, ventricular septal

defect; PV, pulmonic valve; ASD, atrial septal defect; RA, right atrium

Table 12.2 Surgery for congenital heart defects

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type, the VSD is closed by abnormal AVvalve tissue.

Transposition of the great vessels

Transposition of the great vessels (TGV) isthe most common form of cyanotic heartdisease presenting in infancy. In completeTGV (D-loop transposition) there is AV con-cordance and ventriculoarterial (VA) discor-dance. The aorta arises from a normallypositioned RV anterior and to the rightof the PA. The PA does not curve aroundthe aorta, the great vessels are parallel andthe semilunar valves are usually coplanar(Figure 12.22). Systemic venous return is tothe aorta and pulmonary venous return isto the PA and this is incompatible with lifewithout a large intracardiac shunt. VSDscoexist in a third of cases but a balloonatrial septostomy (Rashkind procedure) isoften required to create or enlarge an ASDas a palliative procedure in early infancy.The Jatene procedure or arterial switch with

reimplantation of the coronary arteriescompletely corrects the defect. Prior to thedevelopment of the arterial switch tech-nique an atrial switch (Mustard or Senning)procedure (Table 12.2) was performed forcomplete transposition and a large numberof patients have survived to adulthoodbecause of these procedures (Figure 12.23).An intra-atrial baffle is created to routesystemic venous return to the LV andpulmonary venous return to the rightventricle. The RV is the systemic ventricleand late RV failure and TR are common.Echocardiographic evaluation of patientswith Mustard or Senning procedures mustinclude examination of the baffle for leaksand obstruction and a careful assessment ofthe size and function of the RV and the pres-ence of TR, which reflects systemic pressureand is the reason for the RV hypertrophy.The LV is usually hyperdynamic.

In congenitally corrected or L-loopedtransposition both the AV and VA connec-tions are discordant such that the ventricles

177

Figure 12.23 Apical four-chamber view in a patient with D-loop transposition of the great vessels with an intra-atrial switchrepair (Mustard procedure). The left panel shows the communication between the pulmonary veins and the right ventricle (RV).The right panel shows the communication between the systemic venous return and the left ventricle (LV) (RA, right atrium; LA,left atrium).

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178

Figure 12.25 Off-axis apical ‘four-chamber’ view in a patient with univentricular atrioventricular connection to amorphologic right ventricle (RV). This patient had dextrocardia and this image was recorded with the transducer at the rightmid-clavicular line in the seventh intercostal space. Both atrioventricular valves are seen entering a common chamber, whichis identified as a morphologic RV by the prominent apical trabeculations. The left ventricle (LV) was hypoplastic and posteriorto the RV. Both great vessels came off the RV and the pulmonary vasculature was shielded by a stenosed pulmonic valve(LA, left atrium).

Figure 12.24 Apical four-chamber view in a patient withL-loop transposition of the great vessels. The ventricles areinverted. The right ventricle (RV) is identified by themoderator band (arrow) and by the more apical insertionof the septal leaflet of the tricuspid valve (LV, leftventricle; RA, right atrium; LA, left atrium).

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are inverted (Figure 12.24). Patients mayremain asymptomatic for decades but asin patients with intra-atrial baffles, late RVfailure is common.

Univentricular atrioventricular connection

In univentricular AV connection bothsystemic and pulmonary venous drainageis to one ventricle, which is referred to asthe dominant ventricle, while the otherventricle is hypoplastic. Univentricular AVconnection results from tricuspid atresia ormitral atresia in which ASDs are obligatoryand from double inlet right or left ventricles(Figure 12.25). When the combined venousreturn is to a morphologic RV, the LV is ahypoplastic slit on the diaphragmatic aspectof the heart posterior to the RV and usually

has neither inflow nor outflow. Both greatvessels arise either from the RV (DORV) orthere may be PA atresia. When combinedvenous return is to a morphological LV, theRV consists of a small outflow chamberanterior and superior to the LV connectedto it by a VSD. The hypoplastic RV givesoff at least one great vessel. Patients with TVatresia usually have diminished pulmonaryblood flow either from pulmonary valvularstenosis or a flow limiting VSD. The Fontanprocedure was originally used for patientswith tricuspid atresia. The RA is connectedto the right PA either directly or with theinterposition of a valved conduit and theASD and VSD are closed. Alternatively,bicaval to PA or RA to RV infundibularconnections are made, the latter with thehope that the hypoplastic RV can contributeto systolic flow.

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181

acoustic impedance 1acoustic matching layer 3acute chest pain, echocardiographic evaluation

66–7acute infarction complications, coronary artery

disease 67–74acute pulmonary embolism 48–50afterload 35alcoholic cardiomyopathy 120aliasing 6–7amyloid heart disease 131–3anatomy 13aneurysms

aortic atherosclerotic disease 148–50coronary artery disease 67–9

angiosarcomas, cardiac masses 160anthracycline cardiomyopathy 121–2aorta 147–53

anatomy 147–8aortic dissection 150–3atherosclerotic disease 148–50

aortic dissection 150–3classification 150echocardiography 150–3Marfan syndrome 151

aortic regurgitation (AR) 94–100acute severe 99–100assessment 95Doppler 96–9M-mode 95two-dimensional echo 95–6

aortic stenosis (AS) 89–94congenital 89Doppler echo 91–4Doppler-echocardiography 90–4M-mode 90rheumatic 89senile calcific 89subvalvular 89–90supravalvular 90symptoms 90two-dimensional echo 90–1

aortic valve

anatomy 87AS 89–94bicuspid aortic valve (BAV) 87–9valvular heart disease 87–100

apical four-chamber view, coronary arterydisease 62–4, 66, 68, 69, 70, 72, 73

apical long axis view 26apical short axis view 27–8

coronary artery disease 70apical three-chamber view, coronary artery

disease 65apical two-chamber view 27, 28

coronary artery disease 68, 71apical window 22–8

apical long axis view 26apical short axis view 27–8apical two-chamber view 27, 28MR 22–6

AR see aortic regurgitationarrhythmogenic RV dysplasia (ARVD) 134AS see aortic stenosisASDs see atrial septal defectsatherosclerotic disease, aorta 148–50atrial septal defects (ASDs)

congenital cardiac malformations 167–9ostium primum ASDs 167–8ostium secundum ASDs 167sinus venosus ASDs 167–8, 169

atrioventricular canal defects, congenitalcardiac malformations 175–7

attenuation 1, 2axial resolution 2

B-mode 3bacterial pericarditis 145BAV see bicuspid aortic valveBecker muscular dystrophy, cardiomyopathies

123bicuspid aortic valve (BAV) 87–9Blalock–Hanlon surgical technique, congenital

cardiac malformations 176Blalock–Taussig surgical technique, congenital

cardiac malformations 176

Index

Note: bold denotes figures, where separate from text reference

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182

INDEX

carcinoid heart disease 103cardiac masses 155–61

angiosarcomas 160fibromas 158hemangiomas 159lipomas 159myxomas 158papillary fibroelastomas 158–9primary benign cardiac tumors 158–9primary cardiac lymphomas 161rhabdomyomas 158rhabdomyosarcomas 160–1secondary cardiac tumors 156–8

cardiac rupture, coronary artery disease 69–71cardiomyopathies (CM) 117–34

alcoholic cardiomyopathy 120anthracycline cardiomyopathy 121–2Chagas’ disease 122–3dilated cardiomyopathy (DCM) 118–24hypertrophic cardiomyopathy (HCM) 124–30HIV/AIDS cardiomyopathy 121muscular dystrophies 123noncompaction 124peripartum cardiomyopathy 121prolonged tachyarrhythmias 123restrictive cardiomyopathies (RCM) 130–4

Chagas’ disease 122–3chest pain, echocardiographic evaluation

66–7CM see cardiomyopathiescoarctation of the aorta, congenital cardiac

malformations 173color Doppler flow mapping, MR 84–5complex congenital cardiac malformations

174–9compression algorithms 4, 5congenital cardiac malformations 163–79

ASDs 167–9atrioventricular canal defects 175–7coarctation of the aorta 173complex congenital cardiac malformations

174–9cor triatriatum 172–3double outlet RV (DORV) 172Ebstein anomaly 174–5endocardial cushion defect (ECD) 175–7echocardiography 164–6fetal cardiac anatomy 163–4obstructive lesions 172–3ostium primum ASDs 167–8ostium secundum ASDs 167patent ductus arteriosus (PDA) 166–7shunt lesions 166–72sinus venosus ASDs 167–8, 169surgery 176transposition of the great vessels (TGV) 177–9tetrology of Fallot (TOF) 170–2

univentricular atrioventricular connection178, 179

VSDs 169–70, 171congenital complete absence of the parietal

pericardium 146congenital pericardial cysts 145–6constrictive pericarditis (CP) 143–5

vs. restrictive cardiomyopathies 145continuous wave (CW) Doppler 5, 6, 7contrast echocardiography 10–11‘cor pulmonale’ 45, 48cor triatriatum, congenital cardiac

malformations 172–3coronary artery disease 61–74

acute infarction complications 67–74aneurysms 67–9apical four-chamber view 62–4, 66, 68, 69,

70, 72, 73apical short axis view 70apical three-chamber view 65apical two-chamber view 68, 71cardiac rupture 69–71complications, acute infarction 67–74coronary anatomy 61–5echocardiographic evaluation 66–7long axis view 63, 71papillary muscle rupture 74parasternal short axis view 72, 73pseudoaneurysm 71–2right ventricular infarction 74short axis view 64, 70, 72, 73thrombus 69, 70, 71ventricular septal rupture 72–4wall motion abnormalities (WMAs) 62–6

CP see constrictive pericarditisCW Doppler see continuous wave Doppler

damping 2DCM see dilated cardiomyopathydiastolic function 51–60

M-mode 53–4propagation velocity 58–9pulmonary vein Doppler 56–8, 60spectral Doppler 54–60stiffness and relaxation 51–3tissue Doppler imaging (TDI) 59–60transmitral Doppler 54–6two-dimensional imaging 53–4

digital scan converter (DSC) 4dilated cardiomyopathy (DCM) 118–24Doppler 5–11

AR 96–9CW Doppler 5, 6, 7Doppler color flow 8–9high-PRF Doppler 7–8left ventricular (LV) systolic function 39–42power Doppler 9

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INDEX

PS 105PW Doppler 5–7spectral Doppler 6Tei index 39TR 102–3TS 101

Doppler color flow 8–9Doppler echo, AS 91–4Doppler-echocardiography, AS 90–4Doppler findings, mitral stenosis 78–82double outlet RV (DORV), congenital cardiac

malformations 172DSC see digital scan converterDuchenne muscular dystrophy,

cardiomyopathies 123Damas–Kaye–Stansel surgical technique,

congenital cardiac malformations 176

Ebstein anomaly, congenital cardiacmalformations 174–5

ECD see endocardial cushion defectsechocardiographic evaluation

chest pain 66–7coronary artery disease 66–7

EMF see endomyocardial fibrosisendocardial cushion defects (ECD), congenital

cardiac malformations 175–7endocarditis

fungal 109–10nonbacterial thrombotic endocarditis (NBTE)

110TEE vs. TTE 110two-dimensional echo 107–10valvular heart disease 106–10vegetation 107–10

endomyocardial fibrosis (EMF) 130–1eosinophilic endomyocardial disease 131

fast Fourier transformation (FFT) 6fetal cardiac anatomy 163–4FFT see fast Fourier transformationfibroelastomas 110fibromas, cardiac masses 158fibroplastic endocarditis 131focal zone 2Fontan procedure surgical technique,

congenital cardiac malformations 176force and acceleration, left ventricular (LV)

systolic function 39–40frame rate 4Frank–Starling relationship 35–6fungal endocarditis 109–10

Glenn shunt surgical technique, congenitalcardiac malformations 176

HCM see hypertrophic cardiomyopathy

hemangiomas, cardiac masses 159hemochromatosis 133, 134high-PRF Doppler 7–8HIV/AIDS cardiomyopathy 121hypertrophic cardiomyopathy (HCM) 124–30

symptoms 127

interpolation 4

Jatene surgical technique, congenital cardiacmalformations 176

lateral resolution 2–3left ventricular (LV) noncompaction 124left ventricular (LV) systolic function 35–42

apical area/length formula 37Doppler 39–42force and acceleration 39–40LV cavity volume 36–7LV mass/hypertrophy 38M-mode 36–9MR 40shape 37Simpson rule method 37, 38strain and strain rate 42tissue Doppler imaging (TDI) 40–1Tei index 39three-dimensional echocardiography 39two-dimensional echo 36–7

left ventricular outflow (LVOT), MR 25–6Libman–Sacks verrucous endocarditis 110lipomas, cardiac masses 159Loffler’s endocarditis 131long axis view

coronary artery disease 63, 71parasternal window 14, 15, 71

LVOT see left ventricular outflow

M-mode 3AR 95AS 90diastolic function 53–4left ventricular (LV) systolic function 36–9mitral stenosis 77MR 84parasternal window 14–15, 16pulmonary embolism (PE) 141pulmonic stenosis (PS) 105tricuspid stenosis (TS) 101

marantic endocarditis 110Marfan syndrome, aortic dissection 151mitral regurgitation (MR) 22–6, 82–7

causes 82–4chronic 82color Doppler flow mapping 84–5ischemic 82–3left ventricular (LV) systolic function 40

183

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mitral regurgitation (MR) (cont.) LVOT 25–6M-mode imaging 84mechanisms 82mitral valve prolapse (MVP) 83–4proximal isovelocity surface area (PISA) 86–7pulmonary vein Doppler 85–7spectral Doppler 85two-dimensional imaging 84

mitral stenosis 76–82Doppler findings 78–82etiology 76–7M-mode echo findings 77proximal isovelocity surface area 80–2two-dimensional echo findings 77–8

mitral valveanatomy 75–6mitral stenosis 76–82valvular heart disease 75–87

mitral valve prolapse (MVP) 83–4MR see mitral regurgitationmuscular dystrophies 123Mustard procedure surgical technique,

congenital cardiac malformations 176MVP see mitral valve prolapsemyxomas, cardiac masses 158

nonbacterial thrombotic endocarditis (NBTE),valvular heart disease 110

Nyquist limit 6

obstructive lesions, congenital cardiacmalformations 172–3

ostium primum ASDs, congenital cardiacmalformations 167–8

ostium secundum ASDs, congenital cardiacmalformations 167

papillary fibroelastomas, cardiac masses 158–9papillary muscle rupture, coronary artery

disease 74‘paraspinal’ imaging 34parasternal window 13–22

long axis view 14, 15, 63, 71M-mode 14–15, 16RA/RV view 15–18RV inflow tract view 15–18short axis view 18–22, 72, 73

patent ductus arteriosus (PDA), congenitalcardiac malformations 166–7

pericardial effusion (PE) 136–9, 140, 141, 142,146

pericardium 135–46anatomy 135bacterial pericarditis 145congenital complete absence of the parietal

pericardium 146

congenital pericardial cysts 145–6constrictive pericarditis 143–5pulmonary embolism (PE) 136–9, 140, 141,

142, 146pericarditis 135–6post-cardiac surgery 145post-infarction pericarditis 145purulent pericarditis 145specific etiologies 145–6tamponade 139–43, 146

peripartum cardiomyopathy 121phased array 4PI see pulmonic insufficiencypiezoelectric crystal 2PISA see proximal isovelocity surface areapost-cardiac surgery 145post-infarction pericarditis 145Potts shunt surgical technique, congenital

cardiac malformations 176power Doppler 9preload 35PRF see pulse repetition frequencyprimary benign cardiac tumors, cardiac masses

158–9primary cardiac lymphomas, cardiac masses 161prolonged tachyarrhythmias 123propagation velocity 1

diastolic function 58–9prosthetic heart valves, valvular heart disease

111–15proximal isovelocity surface area (PISA)

mitral stenosis 80–2MR 86–7

PS see pulmonary stenosispseudoaneurysm, coronary artery disease 71–2pulmonary embolism, acute 48–50pulmonary stenosis (PS) 104–5

assessment 105Doppler 105M-mode 105two-dimensional echo 105

pulmonary vein Dopplerdiastolic function 56–8, 60mitral regurgitation (MR) 85–7

pulmonic insufficiency (PI) 105–6pulmonic valve

anatomy 104pulmonic insufficiency (PI) 105–6pulmonic stenosis (PS) 104–5valvular heart disease 104–6

pulse length 2pulse repetition frequency (PRF) 4pulsed-wave (PW) Doppler 5–7purulent pericarditis 145PW Doppler see pulsed-wave Doppler

RA/RV view, parasternal window 15–18

INDEX

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INDEX

Rashkind surgical technique, congenital cardiacmalformations 176

Rastelli surgical technique, congenital cardiacmalformations 176

RCM see restrictive cardiomyopathiesreject control 3restrictive cardiomyopathies (RCMs) 130–4

amyloid heart disease 131–3arrhythmogenic RV dysplasia (ARVD) 134, 134vs. constrictive pericarditis (CP) 145endomyocardial fibrosis (EMF) 130–1hemochromatosis 133, 134infiltrative diseases 131–4Loffler’s endocarditis 131primary 130–1sarcoidosis 133–4secondary 131–4Uhl’s anomaly 134, 134

rhabdomyomas, cardiac masses 158rhabdomyosarcomas, cardiac masses 160–1right parasternal transducer position 33right ventricular infarction, coronary artery

disease 74right ventricular (RV) function 43–50

acute pulmonary embolism 48–50‘cor pulmonale’ 45, 48RV pressure overload 44–8, 49RV volume overload 44, 46–7tricuspid annular plane systolic excursion

(TAPSE) 43–4RV inflow tract view, parasternal window 15–18

sample volume 6sarcoidosis 133–4secondary cardiac tumors, cardiac masses

156–8Senning procedure surgical technique,

congenital cardiac malformations 176short axis view

coronary artery disease 64, 70, 72, 73parasternal window 18–22, 72, 73

shunt lesions, congenital cardiac malformations166–72

Simpson rule method, left ventricular (LV)systolic function 37, 38

sinus venosus ASDs, congenital cardiacmalformations 167–8, 169

sound 1–2spectral Doppler 6

diastolic function 54–60MR 85

strain and strain rate, left ventricular (LV)systolic function 42

subcostal window 28–31, 32suprasternal notch views 31–3surgery, congenital cardiac malformations

176

surgical treatment, valvular heart disease111–15

tamponade 139–43, 146TAPSE see Tricuspid Annular Plane Systolic

ExcursionTDI see tissue Doppler imagingTEE vs. TTE, endocarditis 110Tei index, left ventricular (LV) systolic function

39tetralogy of Fallot (TOF), congenital cardiac

malformations 170–2TGC see time gain compensationTGV see transposition of the great vesselsthree-dimensional echocardiography 9, 10

left ventricular (LV) systolic function 39thrombus, coronary artery disease 69, 70, 71time gain compensation (TGC) 3tissue characterization 9–10tissue Doppler imaging (TDI)

diastolic function 59–60left ventricular (LV) systolic function 40–1

TOF see tetralogy of FallotTR see tricuspid regurgitationtransducers 2–3, 4transmitral Doppler, diastolic function 54–6transposition of the great vessels (TGV),

congenital cardiac malformations 177–9Tricuspid Annular Plane Systolic Excursion

(TAPSE), right ventricular (RV) function43–4

tricuspid regurgitation (TR) 101–3assessment 102–3Doppler 102–3two-dimensional echo 102

tricuspid stenosis (TS) 100–1Doppler 101M-mode 101two-dimensional echo 101

tricuspid valveanatomy 100tricuspid regurgitation (TR) 101–3tricuspid stenosis (TS) 100–1valvular heart disease 100–3

TS see tricuspid stenosisTTE vs. TEE, endocarditis 110two-dimensional echo

aortic regurgitation (AR) 95–6aortic stenosis (AS) 90–1endocarditis 107–10left ventricular (LV) systolic function 36–7mitral stenosis 77–8pulmonic stenosis (PS) 105tricuspid regurgitation (TR) 102tricuspid stenosis (TS) 101

two-dimensional imaging 3–5diastolic function 53–4

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two-dimensional imaging (cont.) mitral regurgitation (MR) 84

Uhl’s anomaly 134, 134univentricular atrioventricular connection,

congenital cardiac malformations 178,179

valvular heart disease 75–115aortic valve 87–100endocarditis 106–10mitral valve 75–87nonbacterial thrombotic endocarditis (NBTE)

110prosthetic heart valves 111–15

pulmonic valve 104–6surgical treatment 111–15tricuspid valve 100–3

vegetation, endocarditis 107–10ventricular septal defects (VSDs), congenital

cardiac malformations 169–70, 171ventricular septal rupture, coronary artery

disease 72–4VSDs see ventricular septal defects

wall motion abnormalities (WMAs), coronaryartery disease 62–6

Waterston shunt surgical technique, congenitalcardiac malformations 176

WMAs see wall motion abnormalities

INDEX

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the echocardiographers guide

Documents

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vena contracta width

patent ductus arteriosus