the heart 16th march 13

7/28/2019 The Heart 16th March 13

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DR KANWAL ZAHRA

16th March 2013

The Heart


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OVERVIEW

The right side receivesdeoxygenated blood fromthe body and tissues andthen pumps it to the lungsfor oxygenenationIts left side receivesoxygenated blood returningfrom the lungs and pumpsthis blood throughout the

body to supply oxygen andnutrients to the body tissues


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simplified

Cone shaped muscle

Four chambers

Two atria, two ventricles

Two circulations

Systemiccircuit: blood vessels that transport

blood to and from all the body tissues

Pulmonarycircuit: blood vessels that carry blood

to and from the lungs


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simplified

Heart weight:

250 300 g in females

300 350 g in males

0.4 0.5 % of body wt.

Right ventricular wall thickness is 0.3 0.5 cm

1.3 1.5 cm for left ventricle

Cardiomegaley above 500 g is associated with

ischemic changes and termed as cor bovium.


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Coverings of the heart: pericardium

Fibrous pericardium

Serous pericardium (a) Parietal layer (b) Visceral layer = epicardium:

part of heart wall

(Between the layers is pericardial cavity)


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Layers of pericardium and heart wall


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Myocardium


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Cardiac Valves

Tricuspid valve

RA to RV

Pulmonary valve

RV to pulmonary trunk

Mitral (bicuspid) valve

LA to LV

Aortic valve

LV to aorta


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AV (Mitral and tricuspid) valves are composed of:

Annulus, leaflets, chordae tendineae and papillary

muscles


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Semilunar valves (aortic and pulmonic) are

composed of: 3 cusps each with a sinus

3 commissures (corpora arantii)


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Valves are relatively avascular.

ATRIAL SIDE:

Lined by endothelial cells on a thin layer of

collagen and elastin. VENTRICULAR SIDE:

A thicker layer of dense collagen.

Loose myxoid C.T (zona spongiosa) in b/w.

Fibrous and spongiotic regions are of equalthickness.


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Function of AV valves

f l l


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Function of semilunar valves

(Aortic and pulmonary valves)


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Conduction system

SA node (sinoatrial)In wall of RASets basic rate: 70-80

Impulse from SA to atriaImpulse also to AV node via internodalpathwayAV node (In interatrial septum)

AV node through AV bundle(bundle of His)

Into interventricular septumDivide R and L bundle branches

subendocardial branches become(Purkinje fibers)

Contraction begins at apexComposed of specialized myocyteswith fewer interclated discs sndhigher glycogen content


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Blood supply to the heart(theres a lot of variation)

Coronary arteries:

Epicardial coronary arteries

Intramural arteries

Capillary network

Major epicardial coronary arteries are:

Left ant. Descending(LAD)

Left circumflex(LCX)

Both arises from left (main) coronary artery

Right coronary artery


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GROSS EXAMINATION AND TISSUE

HANDLING

ENDOMYOCARDIAL BIOPSIES: taken via Rt. Sidedcardiac catheter

Indications: To moniter heart transplant rejection

Tissue fragments are measured and countedduring gross exam.

Minimum of three preferably four samples ofmyocardium are recommended.

Examination of at least three levels arerecommended. An adequate biopsy must containat least 50% myocardium excluding previousbiopsy sites.


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CARDIAC VALVES: Removed because of

Calcific degeneration or perforation as sequel of

bacterial endocarditis. Mostly received in fragments, if present description of

vegetations and presence and absence of non-surgery

related leaflet destruction should included.

In calcific degeneration, acid decalcification is

required, sections from free edge to annulus.


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For mechanical heart valves, only vegetations

are submitted if present.

For bioprosthetic valves, the valve cusps are also

submitted.

MYOMECTOMY SPECIMENS:

From ventricular aneurysm repair or septal

myomectomy procedures.

Measured, weighed and sectioned at 3mm

intervals perpendicular to endocardial

surface.

All layers of heart should be described.


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HEART EXPLANT SPECIMENS:

Should be weighed

Valves and walls (circumference and diameter)

should be measured

Septal and ventricular configuration

(ventricular hypertrophy etc) should be

described.

Fragments of donor tissue (inflow tract) to

match with recipients anatomy are usually

present in same container.


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CONDUCTING AN AUTOPSY

Examination of the heart includes removing the chest

plate then taking the heart out of the pericardial sac The outside surfaces are examined first and the blood

vessels (coronary arteries) are dissected.

The heart is opened to reveal the internal surfaces

and structures, including the valves and heart muscle

(myocardium).

The muscle is then cut to reveal the surface color,

textures and other features. Finally, tissue sections are prepared to examine under

the microscope.


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Tricuspid and Mitral valves


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Aortic and Pulmonary valves


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PATHOPHYSIOLOGY OF HEART

DISEASES

Failure of pump

Obstruction to flow

Regurgitant flow Shunted flow

Disorders of cardiac conduction

Rupture of heart or a major blood vessel


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HEART FAILURE Often called CHF, when heart unable to pump blood

at a rate sufficient to meet metabolic demands. Compensatory mechanisms which maintain arterial

pressure and perfusion of vital organs include

1- Frank- Starling mechanism: inc filling vol. dilates theheart and inc functional cross bridges formation,enhancing contractility

2- Myocardial adaptations, hypertrophy

3- Activation of neurohumoral systems: Release ofnorepinephrine, activation of renin- angiotensin-aldosterone system , atrial natriuretic peptide,adjust filling vol. and pressure.


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LEFT-SIDED HEART FAILURE

Etiology: IHD, HTN, aortic and mitral valvular

disease, myocardial disease

Morphology: findings depend upon disease

process.

Gross: gross structural abnormalities e.g

myocardial infarcts, deformed, stenotic or

regurgitant valves may be present. Lt. ventricle

is usually hypertrophied often dilated.

M/E: non sp. Mainly myocyte hypertrophy and

varying degree of interstitial fibrosis.


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RIGHT-SIDED HEART FAILURE

Etiology: Lt. sided heart failure, pure Rt. Heartfailure is infrequent, associated with lungdisease so referred as Cor pulmonale (Latincor, heart;pulmnle, of the lungs)

Morphology: varies with cause. Rarelystructural defects(valvular abn, endocardialfibrosis) may be seen. In contrast to Lt. sidedfailure pulm. Congestion is minimal but portaland systemic venous systems may be engorged.

The only finding may be Rt. Atrial or ventriculardilatation.


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CONGENITAL HEART DISEASE

Cardiac development


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CONGENITAL HEART DISEASE

The structural anomalies in CHD fall into three

major categories:

1- Left-to-right shunt

2- Right-to-left shunt 3- Obstruction

LEFT-TO-RIGHT SHUNT:

Most commonly encountered shunts includeASDs, VSDs, Patent ductus arteriosus and

atrioventricular septal defects.


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1- Atrial septal defects (ASDs): classified according to their


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1 Atrial septal defects (ASDs): classified according to theirlocation as:

1- Secundum ASDs: 90% of all, may be single, multiple orfenestrated, near centre of atrial septum.

2- Primum ASDs: 5% of all, adjacent to AV valve. 3- Sinus venosus: 5%, near entrance of sup. vena cava, may be

associated with pulm. Venous return to Rt. atrium.

2-Ventricular septal defects (VSDs):

1- Membranous VSDs: 90% of all, involves the region ofmembranous interventricular septum

2- Infundibular VSDs: Lie below the pulm. Valve


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3- Within muscular septum

Most VSDs are single but those in muscular

septum may be multiple so called Swisscheese septum.

3 P ( i ) d i (PDA)


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3- Patent (persistent) ductus arteriosus (PDA):

Occur if ductus arteriosus remain open after birth, infetal circulation it shunts the blood from pulm.

artery to aorta so bypass the lungs. Produce characteristic harsh murmer described as

machinery like murmer

4- Atrioventricular septal defect (AVSD): results fromfailure of sup. and inf. endocardial cushions of AVcanal to fuse adequately.

Partial AVSD: consisting of primum ASD and cleft ofant. Mitral leaflet, causing mitral insufficiency


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Complete AVSD: large combined AV septal

defect and large common AV valve (hole in

centre of heart). All chambers freelycommunicate inducing vol. hypertrophy.


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RIGHT-TO-LEFT SHUNTS

Cyanosis early in postnatal life (cyanotic heartdiseases) includes:

Tetralogy of Fallot

Transposition of Great Arteries

Persistent Truncus Arteriosus

Tricuspid Atresia

Total Anomalous Pulmonary venous connection

l f ll ( )


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Tetrology of Fallot (TOF) Four cardinal features include:

1- VSD

2- Obstruction to right ventricular outflow tract (subpulmonary

stenosis)

3- An aorta that overrides the VSD

4- Right ventricular hypertrophy


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Morphology: Heart is enlarged and may be

boot-shaped as a result of marked ventricular

hypertrophy,in apical region VSD is usually large, aortic valve usually form

the sup. Border so override the defect and both

ventricular chambers.

Obstruction to Rt. Ventricular outflow is due to

subpulmonic stenosis which can be

accompanied by pulm. Valvular stenosis

Sometimes an aortic valve insufficiency or an

ASD may also be present.


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Transposition of great arteries (TGA)

Produces ventriculoarterial discordance, aorta

arises from Rt. Ventricle and lies ant. To and to

the Rt. of pulm. Artery which originates from Lt.

ventricle


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Condition is incompatible with postnatal life

unless a shunt exists for blood mixing.

The infants out look depends on degree ofblood mixing. Pts with TGA and VSD may have

stable shunts(35%) while those with patent

foramen ovale or PDA have unstable shunts.


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Persistant Truncus Arteriosus Failure of seperation of embryologic TA into aorta and

pulm. Artery. Results in single great artery that receive blood from

both ventricles, give rise to systemic, pulm and coronary

circurlation

T i id A i


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Tricuspid Atresia Complete occlusion of tricuspid valve orifice

Mitral valve is larger than normal and hypoplasia of Rt.Ventricle, Circulation is maintained by RT. to LT. shunt

thru ASD, PFO and a VSD. Inc mortality rate in 1st few wks

or months of life

T l l l


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Total anomalous pulmonary venous

connection

Pulmonary veins fails to join the Lt. atrium Results when common pulmonary vein fails to

develop or become atretic

Fetal development is made possible by primitive

venous channels that drain from lungs into Lt.innominate vein or coronary sinus

PFO or ASD is always present, allowing venous blood

to enter Lt. atrium. Vol. and pressure hypt of Rt. side of heart, dilation of

pulm. trunck. Lt. atrium is hypoplastic but Lt.ventricle is normal in size

Ob i i l li


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Obstructive congenital anomalies Obstruction occur at the level of heart valves or

within a great vessel includes: Stenosis or atresia of aortic or pulmonary valves

Coarctation of the Aorta

Obstruction can also occur within a chamber aswith subpulmonary stenosis in TOF.

Coarctation of the Aorta

2 classic forms are 1- Infantile form 2- Adult form In infantile form there is tubular hypoplasia of

aortic arch proximal to PDA often symptomaticin early childhood

I d lt f th i id lik i f ldi f t j t it


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In adult form there is a ridge like infolding of aorta just oppositeto closed ligamentum arteriosum

It may occur solitary but in 50% of cases accompanied by bicuspidaortic valve and also be associated with aortic stenosis, ASD, VSD,

mitral regurgitation, or berry aneurysms of the circle of Willis inthe brain.

There is cardiomegaly due to left ventricular pressure-overload hypertrophy.

P l St i d At i


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Pulmonary Stenosis and Atresia

obstruction at the pulmonary valve, which may be mild to

severe. Can be isolated or part of a more complex anomaly-either

TOF or TGA.

Right ventricular hypertrophy, poststenotic dilation of thepulmonary artery due to injury of the wall by "jetting"

blood. Subpulmonary stenosis (TOF), the high ventricularpressure is not transmitted to the valve, and thepulmonary trunk is not dilated and may in fact behypoplastic.

When the valve is entirely atretic, there is nocommunication between the right ventricle and lungs. Insuch cases the anomaly is associated with a hypoplasticright ventricle and an ASD; blood reaches the lungsthrough a PDA.

Aortic Stenosis and Atresia


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Aortic Stenosis and Atresia Congenital narrowing and obstruction of the

aortic valve can occur at three locations: valvular, subvalvular, and supravalvular.

valvular aortic stenosis: cusps may be hypoplastic, dysplastic, or abnormal in number.

underdevelopment (hypoplasia) of the leftventricle and ascending aorta, sometimesaccompanied by dense, porcelain-like left

ventricular endocardial fibroelastosis. This iscalled the hypoplastic left heart syndrome, isnearly always fatal in the first week of life, whenthe ductus closes


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Subaortic stenosis : caused by a thickened ring(discrete type) or collar (tunnel type) of dense

endocardial fibrous tissue below the level of thecusps

Supravalvular aortic stenosis: inherited form ofaortic dysplasia. In some cases it results from

deletions on chromosome 7 that include thegene for elastin. Ch. delation cause disruption ofelastin-smooth muscle cell interactions.

Other features of the syndrome include

hypercalcemia, cognitive abnormalities, andhallmark facial anomalies (Williams-Beurensyndrome).

I h i H t Di (IHD)


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Ischemic Heart Disease (IHD)

leading cause of death worldwide for both men

and women (7 million total per year)

results from myocardial ischemia. In 90% of

cases, the cause of myocardial ischemia is

reduced blood flow due to obstructiveatheroscleotic lesions in the coronary arteries.

so termed as coronary artery disease (CAD) or

coronary heart disease. IHD usually presents as one or more of the

following clinical syndromes:


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Myocardial infarction

Angina pectoris

Chronic IHD with heart failure.

Sudden cardiac death.

In addition to atherosclerosis, MI may be caused

by coronary emboli, blockage of small

myocardial blood vessels, and lowered systemic

blood pressure.

Pathogenesis of IHD


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MYOCARDIAL INFARCTION (MI)


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MYOCARDIAL INFARCTION (MI) MI, also known as "heart attack," is the death of cardiac

muscle due to prolonged severe ischemia.FEATURES TIME

Onset of ATP depletion Seconds

Loss of contractility 1 hr


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Evolution of Morphologic Changes in Myocardial Infarction


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Time Gross Features Light Microscope

Electron

Microscope

REVERSIBLE

INJURY0- hr None None Ralaxation of

myofibrils;

glycogen loss;

mitochondrial

swelling

IRREVERSIBL

EINJURY

-4 hr None Usually none; variable

waviness of fibers at border

Sarcolemmal

disruption;mitochondrial

amorphous

densities

4-12 hr Dark mottling (occasional) Early coagulation necrosis;

edema; hemorrhage

Time Gross Features Light Microscope


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12-24 hr Dark mottling Ongoing coagulation necrosis; pyknosis of

nuclei; myocyte hypereosinophilia; marginal

contraction band necrosis; early neutrophilic

infiltrate1-3 days Mottling with yellow-tan infarct

center

Coagulation necrosis, with loss of nuclei and

striations; brisk interstitial infiltrate of

neutrophils

3-7 days Hyperemic border; central

yellow-tan softening

Beginning disintegration of dead myofibers,

with dying neutrophils; early phagocytosis of

dead cells by macrophages at infarct border

7-10 days Maximally yellow-tan and soft,

with depressed red-tan

margins

Well-developed phagocytosis of dead cells;

early formation of fibrovascular granulation

tissue at margins

10-14 days Red-gray depressed infarct

borders

Well-established granulation tissue with new

blood vessels and collagen deposition

2-8 wk Gray-white scar, progressive

from border toward core of

infarct

Increased collagen deposition, with decreased

cellularity

>2 mo Scarring complete Dense collagenous scar


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complications following acute MI


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complications following acute MI

Hypertensive Heart Disease (HHD)


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Hypertensive Heart Disease (HHD) SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE:

HTN induces Lt. ventricular hypertrophy, initially withoutventricular dilation. The thickness of the left ventricular wallmay exceed 2.0 cm, and the heart weight may exceed 500gm.

M/E the earliest change of systemic HHD is an increase in

the transverse diameter of myocytes. Enlargement oftenaccompanied by interstitial fibrosis.

PULMONARY (RIGHT-SIDED) HYPERTENSIVE HEART DISEASE(COR PULMONALE):

In acute cor pulmonale there is marked dilation of the rightventricle without hypertrophy.

In chronic cor pulmonale the right ventricular wall thickens,sometimes up to 1.0 cm or more.


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More subtle right ventricular hypertrophy may

take the form of thickening of the muscle

bundles in the outflow tract, immediately belowthe pulmonary valve.

Valvular Heart Disease


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Valvular Heart Disease Valvular abnormalities may be congenital or

acquired. Acquired stenoses of the aortic andmitral valves account for approximately two

thirds of all cases.

most frequent abnormalities are: Aortic stenosis: associated with calcification

Aortic insufficiency: usually related to

hypertension and aging. Mitral stenosis: rheumatic heart disease

Mitral insufficiency: myxomatous degeneration

VALVULAR DEGENERATION ASSOCIATED


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WITH CALCIFICATION Calcific Aortic Stenosis:

most common of all, usually the consequence ofage-associated "wear and tear"

Morphology: hallmark of nonrheumatic, calcificaortic stenosis is heaped-up calcified masses within

the aortic cusps, free edges of the cusps are usuallynot involved.

M/E: the layered architecture of the valve is largelypreserved

In contrast to rheumatic aortic stenosis commissuralfusion is not usually seen. The mitral valve isgenerally normal.


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Mitral Annular Calcification


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Mitral Annular Calcification Degenerative calcific deposits can develop in the

peripheral fibrous ring (annulus) of the mitral valve

Grossly, appear as irregular, stony hard, occasionallyulcerated nodules (2-5 mm in thickness) that liebehind the leaflets.

may lead to (1) regurgitation(2) stenosis (3)

arrhythmias occasionally sudden death by penetration of calcium

deposits to a depth sufficient to impinge on theatrioventricular conduction system.

calcific nodules may also provide a site for thrombithat can embolize, can also be the nidus for infectiveendocarditis.


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MITRAL VALVE PROLAPSE (MYXOMATOUS


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(

DEGENERATION) In mitral valve prolapse (MVP), one or both mitral

valve leaflets are "floppy" andprolapse, into the leftatrium during systole.

Characteristic change in MVP is interchordalballooning (hooding) of the mitral leaflets. The

affected leaflets are often enlarged, redundant,thick, and rubbery.

associated tendinous cords may be elongated,thinned, or even ruptured, and the annulus may bedilated.

M/E : attenuation of the collagenous-fibrosa layer ofthe valve, accompanied by marked thickening of thespongiosa layer with deposition of mucoid(myxomatous) material


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RHEUMATIC HEART DISEASE


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RHEUMATIC HEART DISEASE

Rheumatic fever (RF) is an acute, immunologicallymediated, multisystem inflammatory disease that occurs afew weeks after an episode of group A streptococcalpharyngitis.

It may manifest as acute rheumatic carditis which mayprogress over time to chronic (RHD).

Morphology: During acute RF main lesions occur in theheart, called Aschoff bodies, consist of foci of lymphocytesoccasional plasma cells, and plump activated macrophagescalled Anitschkow cells.

These macrophages have abundant cytoplasm and centralround-to-ovoid nuclei in which the chromatin is disposedin a central, slender, wavy ribbon ("caterpillar cells"), andmay become multinucleated.


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Inflammation results in fibrinoid necrosis within thecusps or along the tendinous cords. Overlying thesenecrotic foci are small (1- to 2-mm) vegetations,

called verrucae, along the lines of closure. Subendocardial lesions, exacerbated by regurgitant

jets, may induce irregular thickeningscalled MacCallum plaques, usually in the left atrium.


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In chronic RHD cardinal features are leafletthickening, commissural fusion and shortening,and thickening and fusion of the tendinous cords,creates a "fish mouth" or "buttonhole" stenoses.

Mitral valve is affected alone in 65% to 70% ofcases, aortic valve in another 25% of cases.Tricuspid and the pulmonary valve involvement isinfrequent


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With tight mitral stenosis, the left atrium progressivelydilates and may harbor mural thrombi in the appendageor along the wall, either of which can embolize.

M/E there is organization of the acute inflammation and

subsequent diffuse fibrosis and neovascularization in themitral leaflets that obliterate the avascular leafletarchitecture.

INFECTIVE ENDOCARDITIS


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INFECTIVE ENDOCARDITIS Infective endocarditis (IE) is characterized by colonization

or invasion of the heart valves or the endocardium by a

microbe, leads to the formation ofvegetations. Morphology: hallmark of IE is the presence of friable,

bulky, vegetations containing fibrin, inflammatory cells,and bacteria or other organisms on the heart valves

The vegetations may be single or multiple and may involvemore than one valve. sometimes erode into theunderlying myocardium and produce an abscess (ringabscess).

Emboli may be shed from them at any time; because theembolic fragments may contain large numbers of virulentorganisms, abscesses often develop at the sites where theemboli lodge.

M/E: vegetations of typical subacute IE often have


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granulation tissue indicative of healing. With time,

fibrosis, calcification, and a chronic inflammatory

infiltrate can develop.

PATHOLOGICCRITERIA

Microorganisms, demonstrated by culture or histologic examination, in a vegetation, embolus


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g y g g

from a vegetation, or intracardiac abscess

Histologic confirmation of active endocarditis in vegetation or intracardiac abscess

CLINICALCRITERIA

Major

Blood culture(s) positive for a characteristic organism or persistently positive for an unusual

organism

Echocardiographic identification of a valve-related or implant-related mass or abscess, or

partial separation of artificial valve

New valvular regurgitaionMinor

Predisposing heart lesion or intravenous drug use

Fever

Vascular lesions, including arterial petechiae, subungual/splinter hemorrhages, emboli, septic

infarcts, mycotic aneurysm, intracranial hemorrhage, Janeway lesions

Immunological phenomena, including glomerulonephritis, Osler nodes, Roth

spots, rheumatoid factor

Microbiologic evidence, including a single culture positive for an unusual organism

Echocardiographic findings consistent with but not diagnostic of endocarditis, including

worsening or changing of

a preexistent murmur

NONINFECTED VEGETATIONS


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Nonbacterial Thrombotic Endocarditis (NBTE)

encountered in debilitated patients, striking association

with mucinous adenocarcinomas, procoagulant effectsof tumor-derived mucin or tissue factor.

Endocardial trauma, well-recognized predisposingcondition

Deposition of small sterile thrombi on the leaflets of thecardiac valves. 1 mm to 5 mm in size, and occur singly ormultiply along the line of closure of the leaflets.

M/E : composed of bland thrombi that are looselyattached to the underlying valve, do not elicit anyinflammatory reaction. May be the source of systemicemboli that produce infarcts in the brain, heart.


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Endocarditis of SLE (Libman-Sacks Disease)


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( )

small, sterile vegetations (1-4 mm) have a warty (verrucous)

appearance, located on the undersurfaces of the AV valves,

valvular endocardium, chords, or on the mural endocardium ofatria or ventricles.

M/E: Veg consist of finely granular, fibrinous eosinophilic material

that may contain hematoxylin bodies, remnants of nuclei

damaged by anti-nuclear antigen bodies.

Cardiomyopathies


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Cardiomyopathies cardiomyopathy(literally, heart muscle disease)

produce abnormalities in cardiac wall thicknessand chamber size, and mechanical and/or

electrical dysfunction.

Primarycardiomyopathies: predominantlyconfined to the heart muscle.

Secondarycardiomyopathies: have myocardial

involvement as a component of a systemic ormultiorgan disorder.


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Functional Patterns and Causes


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Functio

nal

Pattern

Ejectio

n

Fractio

n

Mechanisms of

Heart Failure

Causes of Phenotype Indirect Myocardial

Dysfunction (Mimicking

Cardiomyopathy)

Dilated


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( )

Morphology: Heart is usually enlarged, heavy (often

weighing two to three times normal), and flabby, due to

dilation of all chambers. Mural thrombi are common

and may be a source of thromboemboli.

M/E: Non specific

HYPERTROPHIC CARDIOMYOPATHY (HCM)


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( )

MORPHOLOGY: The essential feature of HCM ismassive myocardial hypertrophy, usually without

ventricular dilation. The classic pattern is asymmetric septal

hypertrophy.

On cross-section, the ventricular cavity loses its

usual round-to-ovoid shape and compressed into a"banana-like" configuration by bulging of theventricular septum into the lumen.

M/E : (1) extensive myocyte hypertrophy, with

transverse myocyte diameters frequently greaterthan 40 m (normal, 15 m); (2) haphazarddisarray of bundles of myocytes (termed myofiberdisarray); and (3) interstitial fibrosis.


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RESTRICTIVE CARDIOMYOPATHY (RCM)


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characterized by aprimary decrease in ventricularcompliance, resulting in impaired ventricular filling

during diastole. may be idiopathic or associated with, radiation

fibrosis, amyloidosis, sarcoidosis, metastatictumors, or the deposition of metabolites that

accumulate due to inborn errors of metabolism. Morphology. The ventricles are of approximately

normal size or slightly enlarged, the cavities are notdilated, and the myocardium is firm andnoncompliant. Biatrial dilation is commonlyobserved.

M/E, there may be only patchy or diffuse interstitialfibrosis, which can vary from minimal to extensive.

MYOCARDITIS


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Infectious microorganisms and/or an inflammatory process cause

myocardial injury

INFECTIONSViruses (e.g., coxsackievirus, ECHO, influenza, HIV, cytomegalovirus)

Chlamydiae (e.g., C. psittaci)

Rickettsiae (e.g., R. typhi, typhus fever)

Bacteria (e.g., Corynebacterium diphtheriae, Neisseria meningococcus, Borrelia (Lyme disease)

Fungi (e.g., Candida)

Protozoa (e.g., Trypanosoma cruzi[Chagas disease], toxoplasmosis)

Helminths (e.g. trichinosis)

IMMUNE- MEDIATED REACTIONS

Postviral

Poststreptococcal (rheumatic fever)Systemic lupus erythematosus

Drug hypersensitivity (e.g., methyldopa, sulfonamides)

Transplant rejection

UNKNOWN

Sarcoidosis

Giant cell myocarditis

Morphology: During active phase, heart appear normal


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or dilated, advanced stage the ventricular myocardium is

flabby haveing pale foci or minute hemorrhagic lesions

along with mural thrombi.

M/E: an interstitial mononuclear, predominantly

lymphocytic infiltrate associated with focal myocyte

necrosis, either resolve, leaving no residual changes, or

heal by progressive fibrosis.

Hypersensitivity myocarditis: perivascular infiltrate

composed of lymphocytes, macrophages, and a high

proportion of eosinophils. Giant-cell myocarditis, inflammatory infiltrate containing

multinucleate giant cells interspersed with lymphocytes,

eosinophils, plasma cells, and macrophages

Chagas disease: parasitization of scattered myofibers


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by trypanosomes with an infiltrate of neutrophils,

lymphocytes, macrophages, and occasional eosinophils.

PRIMARY CARDIAC TUMORS

M


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Myxoma

50% of primary tumors, occur in two settings:

Sporadic and familial

Sporadic tumor occurs in middle-aged women

(76%), usually in the left atrium (86%), nearly

always as a single tumor, and without associatedconditions.

familial variety: young people, slightly more

frequent in men, less commonly located in theleft atrium (62%), multicentric, and associated

with extracardiac abnormalities.

Grossly: soft, polypoidal, pale, lobulated masses,


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often attached by a stalk to the septum near the

foramen ovale. A papillary configuration may be

apparent, Calcification may occur, and this seems

to be more common in those located in the right

atrium.


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M/E, round, polygonal, or stellate cells are seen


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surrounded by abundant loose stroma rich in

acid mucopolysaccharides.

Some cells form solid cords and vascular

channels, continuous with the endocardial lining.

Mitoses, pleomorphism, and necrosis are absent

or minimal.

ossification (petrified myxoma), occurrence oftil i ti


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cartilaginous tissue

presence of thymic and foregut remnants,

having well-developed mucin-producing glands.referred as glandular myxoma, can be confusedwith metastatic adenocarcinoma.

development of a thymoma, presumably arisingfrom the thymic remnants.

Other benign tumors and tumorlike

diti


99/105

conditions

Rhabdomyoma and rhabdomyomatosis

Hamartoma of mature cardiac myocytes

Calcified amorphous tumor of the heart (cardiac

CAT) Cystic tumor of the atrioventricular nodal region

Adenomatoid tumor

Papillary fibroelastoma Inflammatory myofibroblastic tumor

Paraganglioma

Primary malignant tumors


100/105

y g

Sarcomas: are exceptionally rare, highly

pleomorphic and unclassifiable.

Of those that can be placed into a specific

category, angiosarcoma is the most common.

Gross: located in the atrium, presents as a largemass


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Metastatic tumors


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Malignant lymphoma is a more common even thanprimary

Any portion of the heart can be involved,conducting system results in heart block.

majority of carcinomas, the primary tumor is in thethoracic cavity or contiguous areas

They reaches the heart by mediastinal lymph nodesand from there extending in a retrograde fashion tothe cardiac lymph vessels.

Tumors spread to the heart by the hematogenousroute are malignant melanoma; carcinomas ofkidney, lung, and breast; choriocarcinomas; andchildhood rhabdomyosarcoma.
http://www.expertconsultbook.com/expertconsult/b/linkTo?type=bookPage&isbn=978-0-323-06969-4&eid=4-u1.0-B978-0-323-06969-4..00005-2--f0100&appID=NGE


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the heart 16th march 13

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