Valvular heart disease

Mitral Stenosis

Etiology Primarily a result of rheumatic fever

(~ 99% of MV’s @ surgery show rheumatic damage )

Scarring & fusion of valve apparatus Rarely congenital Pure or predominant MS occurs in

approximately 40% of all patients with rheumatic heart disease

Two-thirds of all patients with MS are female.

patophysiology Symptoms Fatigue Palpitations Cough SOB Left sided failureo Orthopnea o PND

Palpitation Systemic embolism Pulmonary infection Hemoptysis Right sided failureo Hepatic Congestiono Edema

Worsened by conditions that cardiac output.o Exertion,fever, anemia, tachycardia, ,

pregnancy, thyrotoxicosis

Recognizing Mitral Stenosis Complications Atrial dysrrhythmias Systemic embolization (10-25%)o Risk of embolization is related to, age, presence of atrial fibrillation, previous embolic events Congestive heart failure Pulmonary infarcts (result of severe CHF) Hemoptysis o Massive: 20 to ruptured bronchial veins (pulm HTN)o Streaking/pink froth: pulmonary edema, or infection Endocarditis Pulmonary infections

Palpation: Small volume pulse Tapping apex-palpable

S1 +/- palpable opening

snap (OS) RV lift Palpable S2 ECG: LAE, AFIB, RVH, RAD

Auscultation: Loud S1- as loud as S2 in

aortic area A2 to OS interval inversely

proportional to severity Diastolic rumble: length

proportional to severity In severe MS with low

flow- S1, OS & rumble may be inaudible

Right Heart Failure:Hepatic Congestion

JVDTricuspid

RegurgitationRA Enlargement

Pulmonary HTNPulmonary Congestion

LA EnlargementAtrial Fib

LA Thrombi LA Pressure

RV Pressure OverloadRVH

RV FailureLV Filling

Physical Exam Common Murmurs Auscultation-Timing of A2 to OS Interval First heart sound (S1) is accentuated and

snapping Opening snap (OS) after aortic valve closure Low pitch diastolic rumble at the apex Pre-systolic accentuation (esp. if in sinus rhythm)

Systolic Murmurs Aortic stenosis Mitral insufficiency Mitral valve

prolapse Tricuspid

insufficiency

Diastolic Murmurs Aortic

insufficiency Mitral stenosis

Width of A2-OS inversely correlates with severity

The more severe the MS the higher the LAP the earlirthe LV pressure falls below LAP and the MV opens

EKG Role of Echocardiography

LAE RVH Premature contractions Atrial flutter and/or fibrillationo freq. in pts with mod-severe MS for several yearso A fib develops in » 30% to 40% of pts w/symptoms

Diagnosis of Mitral Stenosis

Assessment of hemodynamic severity o mean gradient,

mitral valve area, pulmonary artery pressure

Assessment of right ventricular size and function.

Assessment of valve morphology to determine

suitability for percutaneous mitral balloon valvuloplasty

Diagnosis and assessment of concomitant valvular lesions

Reevaluation of patients with known MS with changing symptoms or signs.

F/U of asymptomatic patients with mod-severe MS

Recommendations for Mitral Valve Repair for Mitral Stenosis

ACC/AHA Class I• Patients with NYHA functional Class III-IV

symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology favorable for repair if percutaneous mitral balloon valvotomy is not available

• Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology favorable for repair if a left atrial thrombus is present despite anticoagulation

• Patients with NYHA functional Class III-IV symptoms, moderate or severe MS (mitral valve area <1.5 cm 2 ),* and a non-pliable or calcified valve with the decision to proceed with either repair or replacement made at the time of the operation.

Therapy MedicaloDiuretics for LHF/RHFoDigitalis/Beta blockers/CCB: Rate control

in A FiboAnticoagulation: In A FiboEndocarditis prophylaxis

Balloon valvuloplasty o Effective long term improvement

SurgicaloMitral commissurotomy oMitral Valve Replacement

Mechanical Bioprosthetic

ACC/AHA Class IIB o Patients in NYHA functional Class I, moderate or

severe MS (mitral valve area <1.5 cm 2 ),* and valve morphology favorable for repair who have had recurrent episodes of embolic events on adequate anticoagulation.

ACC/AHA Class IIIo Patients with NYHA functional Class I-IV symptoms

and mild MS.

Mitral regurgitation

Etiology MR Pathophysiology MR SymptomsValvular-leaflets• Myxomatous MV

Disease• Rheumatic• Endocarditis • Congenital-clefts

Chordae • Fused/

inflammatory• trauma • Degenerative • IE

Annulus• Calcification, IE

(abcess) Papillary Muscles

• CAD (Ischemia, Infarction, Rupture)

• HCM• Infiltrative disorders

LV dilatation & functional regurgitation

Chronic LV volume overload -» compensatory LVE initially maintaining cardiac output

Decompensation (increased LV wall tension) -»CHF

LVE – » annulus dilation – » increased MR Backflow – » LAE, Afib, Pulmonary HTN

Similar to MS Dyspnea, Orthopnea, PND Fatigue Pulmonary HTN, right sided failure Hemoptysis Systemic embolization in A Fib

Chronic Mitral Regurgitation Acute Severe Mitral Regurgitation Pulse: • brisk, low volume

Apex: • hyperdynamic • laterally displaced• palpable S3 +/- thrill• late parasternal lift 2°

to LA filling S 1 soft or normal S 2 wide split (early

A2) unless LBBB

Murmer-Fixed MR:• pansystolic • loudest apex to axilla • no post extra-systolic

accentuation Murmer-Dynamic

MR(MVP) • mid systolic• +/- click• upright

S 3 / flow rumble if severe

Acute severe dyspnea, CHF & hypotension

LV size normal LV may/may not be

hyperdynamic Loud S1 Systolic murmur

may/may not be pan-systolic

Inflow/rumble S3 present-may be

only abnormality

RV lift TTE/TEE for diagnosis

• Chordal or papilllary muscle rupture/tear

• Infarction with papillary muscle ischaemia or tear

• Infectious endocarditis with leaflet perforation or disruption or chordal tear

• Flail MV segment

Assessing Severity of Chronic Mitral Regurgitation Recognizing Mitral Regurgitation Echocardiography

Measure the Impact on the LV: Apical displacement and size Palpable S3 Longer/louder MR murmer (chronic MR) S3 intensity/ length of diastolic flow rumble Wider split S2 (earlier A2) unless HPT narrows the

split

ECG:• LA enlargement• Afib • LVH (50% pts. With

severe MR)• RVH (15%)• Combined

hypertrophy (5%)

CXR:• LV• LA• pulmonary vascularity • CHF• Ca++ MV/MAC

Etiology: • flail leaflets (chord/pap rupture)• thick (RHD)• post mvt of leaflets (MVP)• vegetations(IE)

Severity: • regurgitant volume/fraction/orifice area• LV systolic function • increased LV/LA size, EF

MR Stages Echo Indicators for Valve Replacement in Asymptomatic Aortic & Mitral Regurgitation

LV size and function defined by echo Stage 1-compensated:

• End-diastolic dimension less 63mm, ESD less 42mm• EF more than 60

Stage 2-transitional • EDD 65-68mm, ESD 44-45mm, EF 53-57

Stage 3-decompensated • EDD more than 70mm, ESD more than 45mm, EF less than 50

Type of Regurgitation

LVESD mm EF % FS

Aortic > 55 < 55 < 0.27Mitral > 45 < 60 < 0.32

RECOMMENDED FREQUENCY OF ECHOCARDIOGRAPHY IN PATIENTS WITH CHRONIC MITRAL REGURGITATION AND PRIMARY MITRAL-VALVE DISEASE.

Mitral Valve Surgery

SEVERITY OFMITRALREGURGITATION

LEFT VENTRICULAR FUNCTION*

FREQUENCY OFECHOCARDIOGRA-PHIC FOLLOW-UP

Mild Normal ESD and EF Every 5 yr

Moderate Normal ESD and EF Every 1 –2 yr

Moderate ESD >40 mm or EF <0.65

Annually

Severe Normal ESD and EF Annually

Severe ESD >40 mm or EF <0.65

Every 6 mo

Only effective treatment is valve repair/replacement

Optimal timing determined:•Presence/absence of symptoms •Functional state of ventricle •Feasability of valve repair •Presence of Afib/PHTN•Preference/expectations of patient

Surgical Therapy – Timing Surgery reduces morbidity and mortality from

severe MR but exposes patient to risk of surgery and prosthetic valve

Surgery should be performed before onset of severe symptoms or development of LV contractile dysfunction

Ejection Fraction (LVEF) Mitral Regurgitation ACC/AHA recommendations

Indications for Surgery Isolated,Severe Chronic MR

Strongest predictor of outcome following surgery Should be assessed quantitatively Surgery indicated if LVEF is below normal (60%) If EF normal, follow every 6 to 12 months If EF <30%, medical management (valve repair

experimental in this setting)

Surgery Recommended in patients who areSymptomaticAsymptomatic with

• Any LV dysfunction• Atrial fibrillation• Pulmonary hypertension• Reparable valves•Recurrent VT

Definite (major criteria):• NYHA Class III or IV heart failure (any duration)• EF <60%• EF >60% but decreasing on serial measurements

Emerging (minor criteria):• Any symptoms of heart failure

or sub optimal exercise tolerance test• Flail mitral leaflet• Left atrial diameter >45mm• Paroxysmal atrial fibrillation• Abnormal exercise end-systolic volume index or

ejection fraction

MV Repair vs. Replacement Lower operative mortality Better late outcome Curative Avoids anticoagulation unless atrial fibrillation Open Afib ablation

Valve replacement:o Mortality 2-7%o Anti-coagulationo Decreased LVEF

Tissue prosthetic valve degeneration Mechanical prosthetic valve dysfunction/

thrombosis

Valve repairo Mortality 2-3%o No anticoagulation (unless Afib)o Preservation of LVEF

Valve repair always preferableo Feasible in 70-90% of patients

Aortic stenosis

Etiology Asymptomatic Young patient think

congenital• Bicuspid

2% population 3:1 male:female

distribution Co-existing

coarctation 6% of patients

Rarely• Unicuspid valve• Sub-aortic stenosis o Discreteo Diffuse (Tunnel)

Middle aged patient(4&5th decades) think bicuspid or rheumatic disease

Old patient think degenerative (6,7,8th decades)

Normal bicuspid Ao V

“normal” greatric calcific valve

Common in asymptomatic adults Characterized by

• Grade I – II @ LSB• Systolic ejection pattern

S1 S2– Normal intensity & splitting of second sound (S2)– No other abnormal sounds or murmurs– No evidence of LVH, and no with Valsalva

Symptoms Physical Findings Recognizing Aortic Stenosis Cardinal Symptoms

• Chest pain (angina)o Reduced coronary flow reserveo Increased demand-high afterload

• Syncope/Dizziness (exertional pre-syncope)o Fixed cardiac outputo Vasodepressor response

• Dyspnea on exertion & rest• Impaired exercise tolerance

Other signs of LV failure • Diastolic & systolic dysfunction

Intensity DOES NOT predict severity Presence of thrill DOES NOT predict severity “Diamond” shaped, harsh, systolic crescendo-decrescendo Decreased, delay & prolongation of pulse amplitude Paradoxical S2 S3 (with left ventricular failure)

sign Correlation wi severityJVP-prominent A wave NoCarotid-delayed,anacrotc Yes A2 audible over carotid If A2 transmitted to carotids

mean AV gradient <50mmHgApex-sustained, atrial kick

Yes

Enlarge, displaced Yes Thrill NoCardiomegaly YesSoft S1 Yes Paradoxical S2 Yes S3, S4 YesSEM –intensity -late peak

No Yes

ECG- LAE, LVH Yes

Severity of Stenosis Echocardiogram Normal aortic valve area 2.5-3.5 cm2

Mild stenosis 1.5-2.5 cm2 Moderate stenosis 1.0-1.5 cm2 Severe stenosis < 1.0 cm2 Onset of symptoms

~ 0.9 cm2 with CAD~ 0.7 cm2 without CAD

Etiology Valve gradient and area LVH Systolic LV function Diastolic LV function LA size Concomitant regional wall motion abnormalities Coarctation associated with bicuspid AV

S1 S2

Prognosis Natural History Operative mortality of AVR in the elderly

Symptom/Sign Live expectancyAngina 5 yearsSyncope 2-3 yearsCongestive Heart Failure

1-2 years

Therapy: Valve replacement for severe aortic stenosis Operative mortality (elderly) ~ 4-24%/Morbidity ~ 3-11%Event rate in asymptomatic severe AS ~ 1%/year

Heart failure reduces life expectancy to less than 2 years

Angina and syncope reduce life expectancy between 2 and 5 years

Rate of progression ¯ @ 0.1 cm2/year

~ 4-24%/year Risk factors for

operative mortality• Functional class• Lack of sinus

rhythm• HTN• Pre-existing LV

dysfunction

• Aortic regurgitation• Concomitant surgical

procedures:CABG/MV surgery

• Previous bypass• Emergency surgery• CAD• Female gender

Prosthetic Valves

MECHANICAL•Durable•Large orifice•High thromboembolic potential•Best in Left Side•Chronic warfarin therapy

BIO-PROSTHETIC• Not durable• Smaller orifice/functional stenosis • Low thromboembolic potential• Consider in elderly• Best in tricuspid position

Aortic regurgitation

Etiology Symptoms Central Signs of Severe Aortic RegurgitationAny conditions

resulting in incompetent aortic leaflets

Congenital•Bicuspid valve

Aortopathy • Cystic medial

necrosis• Collagen

disorders (e.g. Marfan’s)

• Ehler-Danlos • Osteogenesis

imperfecta • Pseudoxanthom

a elasticum

Acquired• Rheumatic heart

disease• Dilated aorta (e.g.

hypertension..)• Degenerative• Connective tissue

disorders o E.g. ankylosing

spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-cell arteritis )

• Syphilis (chronic aortitis)

Acute AI: aortic dissection, infective endocarditis, trauma

Dyspnea, orthopnea, PND Chest pain.

• Nocturnal angina >> exertional angina • (¯ diastolic aortic pressure and increased

LVEDP thus ¯ coronary artery diastolic flow)

With extreme reductions in diastolic pressures (e.g. < 40) may see angina

Apex:• Enlarged• Displaced• Hyper-dynamic• Palpable S3 • Austin-Flint murmur

Aortic diastolic murmur• length correlates with

severity (chronic AR)• in acute AR murmur

shortens as Aortic DP=LVEDP

• in acute AR - mitral pre-closurePeripheral Signs of Severe Aortic

Regurgitation Physical Exam Quincke’s sign:

capillary pulsation Corrigan’s sign:

water hammer pulse

Bisferiens pulse (AS/AR > AR)

De Musset’s sign: systolic head bobbing

Mueller’s sign: systolic pulsation of uvula.

Durosier’s sign: femoral retrograde bruits

Traube’s sign: pistol shot femorals

Hill’s sign:BP Lower extremity >BP Upper extremity by o > 20 mm Hg -

mild ARo > 40 mm Hg –

mod ARo > 60 mm Hg –

severe AR

Widened pulse pressure • Systolic – diastolic = pulse pressure

High pitched, blowing, decrescendo diastolic murmur at LSB

Best heard at end-expiration & leaning forwardHands & Knee position

Assessing Severity of AR Echo Indications for Valve Replacement in Asymptomatic AR & MR

Natural History

Assess severity by impact on peripheral signs and LV• peripheral signs = severity• LV = severity• S3• Austin -Flint• LVH• radiological cardiomegaly

Type of Regurgitation

LVESD (mm)

EF (%) FS

Aortic > 55 < 55 < 0.27mitral > 45 < 60 < 0.32

Asymptomatic %/YNormal LV function (~good prognosis)

•Progression to symptoms or LV dysfunction < 6•Progression to asymptomatic LV dysfunction < 3.5•75% 5-year survival•Sudden death < 0.2

Abnormal LV function•Progression to cardiac symptoms 25

Symptomatic (Poor prognosis) Mortality > 10 TX: Medical ® Surgery BEFORE LV dysfunction

S1 S2 S1

Indication for Valve Replacement in Aortic Regurgitation ACC/AHA Class I

• Symptomatic patients with preserved LVF (LVEF >50%)• Asymptomatic patients with mild to moderate LV

dysfunction (EF 25-49%)• Patients undergoing CABG, aortic or other valvular

surgery ACC/AHA Class II a

• Asymptomatic patients with preserved LVEF but severe LV dilatation (EDD>75 mm or ESD > 55mm)

ACC/AHA Class II b• Patients with severe LV dysfunction (EF < 25%)• Asymptomatic patients with normal systolic func-tion

at rest (EF >0.50) and progressi ve LV dilata-tion when the degree of dilatation is moderatelysevere (EDD 70 to 75 mm, ESD 50 to 55 mm).

ACC/AHA Class III • Asymptomatic patients with normal systolicf unction

at rest (EF >0.50) and LV dilatation when the degree of dilatation is not severe (EDD <70 mm, ESD <50 mm).