Valvular Heart Disease

Aortic Stenosis (AS)


• Calcific: predominant cause in Pts '70 y; risk factors include HTN and T chol.

• Congenital heart disease (ie. bicuspid AoV): cause in 50% of Pts - 70 y

• Rheumatic heart disease (AS usually accompanied by Al and usually w/ MV disease)

• AS mimickers: hypertrophic obstructive CMP; subAo membrane

Clinical manifestations (usually indicates AVA < 1 cm2 or concomitant CAD)

• Angina: T O2 demand (hypertrophy) + i Oi supply (i cor perfusion pressure) • CAD

• Syncope (exertional): peripheral vasodil. wI fixed CO — i MAP 1 cerebral perfusion

• Heart failure: dyspnea due to pulmonary edema; can be precip. by AF (loss of LV filling)

• Acquired von Willebrand disease ( 20% of sev. AS): destruction of vWF (NEJM 2003 349:343) Physical examination

• High-pitched, mid-systolic crescendo-decrescendo murmur at RUSB

radiates to sternal notch, carotids, apex (often holosystolic Gallavardin effect) t w/ passive leg raise, i wI standing & Valsalva, but not specific

• In contrast, dynamic outflow obstruction i w/ passive leg raise & ' w/ standing & Valsalva

• Ejection click sometimes heard with bicuspid AoV

• Signs of severity: kite-peaking murmur, paradoxically split Sj or inaudible A2. small and delayed carotid pulse ("pulsus parvus et tardus"). LV heave. © S< (occasionally palpable) Diagnostic studies

• CXR: cardiomegaly. post-stenotic dilation of Ao. AoV calcif.. pulmonary congestion

• Echo: valve morphology, estimated pressure gradient (V). calculated AVA. EF

• Cardiac catheterization: V from simultaneous LV & Ao pressures, calculated AVA.

but primarily to rlo concomitant CAD (seen in 50% of calcific AS)

• Dobutamine challenge during echo or cath if low EF and V <30 to differentiate:

afterlood mismatch (T SV & t V; implies good contractile reserve & T EF post-AVR) vs. pseudostenosis (T SV. no change in V. i AVA; implies low AVA artifact of LV dysfxn) vs. fixed CMP (no change in SV. V. or AVA; implies EF prob. will not improve w/ AVR)

Classification of Aortic Stenosis


Mean Gradient (mmHg)

Jet Vet. (m/s)

AVA (cm')

















Severe, compensated





Severe, decompensated





Treatment {JACC 2006:48 d)

• AVR: symptomatic AS (almost invariably severe; if not look for another causc of sx)

asx sev. AS + EF <50%; also consider if asx sev. AS and AVA <0.6 cm2, mean gradient >60 mmHg, aortic jet >5 m/s,. BP w/ exercise (can carefully exercise asx AS to uncover sx. do not exercise sx AS), or high likelihood of rapid prog, asymptomatic mod.-sev. AS and undergoing CABG. valvular or aortic surgery

• Medical therapy: used in symptomatic Pts who are not operative candidates careful diuresis, control HTN. maint. SR; dig; ? statin <n£/m 2005:3S2 2389;/acc 2007.49 554) avoid venodilators (nitrates) and inotropes (Ji-blockers & CCB) in severe AS nitroprusside if sev. AS. EF - 35%. CHF w/ CI <2.2. but normotensive (NE/m 2003:3481756)

• IABP: stabilization, bridge to surgery

• Balloon valvuloplasty: 50% t in AVA & 50% i peak V. but 50% restenosis by 6-12 mos &

risk of peri-PAV stroke (NejM 1988.319125). use as bridge to AVR or if not surgical cand.

• Percutaneous AVR remains under study (Ore 2006:1141616)

• Endocarditis prophylaxis: avoid vigorous physical exertion once AS moderate-severe

Natural history (Cxculaoon 1968:38(Suppl.V):61)

• Usually slowly progressive until symptoms develop

• Echo q1-2 y if mod.. q3-5 y if mild, or if A sx

• AVA i -0.1 cm2 per y (Oft 1997:95:2262). but marked interindividual variability

• Angina 5 y mean survival; syncope 3 y mean survival; CHF 2 y mean survival

Aortic Insufficiency (Al)


• Valve disease rheumatic heart disease (usually mixed AS/AI and concomitant MV disease) bicuspid AoV: natural hx: 1/3 -» normal. 1/3 -»AS. 1/6 Al. 1/6 — endocarditis — Al infective endocarditis valvulitis: RA. SLE

amphet. & DA agonists that stimulate 5-HT receptors (NEJM 1998:339:719 & 2007:356:29.39)

aortic aneurysm or dissection, annuloaortic ectasia. Marfan syndrome aortic inflammation: giant cell.Takayasu's. ankylosing spond.. reactive arthritis, syphilis

Clinical manifestations

• Acute: sudden i forward SV and * LVEDP (noncompliant ventricle) — pulmonary edema

~ hypotension and cardiogenic shock

• Chronic: clinically silent while LV dilates (i compliance to keep LVEDP low) chronic volume overload LV decompensation CHF

Physical examination

• Early diastolic decrescendo murmur at LUSB (RUSB if dilated aortic root)

t with sitting forward, expiration, handgrip severity of Al proportional to duration of murmur (except in acute and severe late) Austin Flint murmur: diastolic rumble at apex (Al jet interfering w/ mitral inflow)

• Wide pulse pressure due to t stroke volume — many of classic signs (see table)

(pulse pressure narrows in late Al with I LV function)

• PMI diffuse and laterally displaced; soft Si. (early closure of MV); © Sj (* i EF in Al)

• Bisferiens (twice-beating) arterial pulse

Classic Eponymous Signs in Chronic Al



Corrigan's pulse

"water hammer" pulse (ie. rapid rise and fall or collapsing)

Hills sign

(popliteal SBP - brachial SBP) 60 mmHg

Duroziez's sign

gradual pressure over femoral artery systolic and diastolic bruits

Traube's sound

double sound heard at femoral artery when compressed distally

de Musset's sign

head-bobbing with each heartbeat (low Se)

Müllers sign

systolic pulsations of the uvula

Quincke's pulses

subungual capillary pulsations (low Sp)

(Soulhtrn Mcdxol Journal 1981:74:459) Diagnostic studies

• ECG: LVH. LAD; CXR: cardiomegaly * aortic dilatation

• Echocardiogram: severity of Al (severe Al » width of regurgitant jet >65% LVOT or presence of flow reversal in descending aorta) and LV size & fxn

• Cardiac MRI (severity of Al. aortic root size. LV size & fxn); aortography (severity of Al)

Treatment (NEJM 2004:351:1539; JACC 2006;48:c1)

symptomatic severe Al (if Al not severe, unlikely to be cause of sx) asx severe Al and EF <50% or LV dilation (sysL diam. >55 mm or diasL diam. >75 mm) or undergoing cardiac surgery

• Medical therapy: vasodilators (nifedipine. ACEI. hydralazine) if severe Al w/ sx or LV

dysfxn & Pt not operative cand.; benefit in asx severe Al w/ nl LV fxn controversial (NEJM 1994:331:689 & 2005:353:1342); diuretics and digoxin if CHF

• Acute decompensation (consider ischemia and endocarditis as possible précipitants)

IV afterload reduction (nitroprusside) and inotropic support (dobutamine) • chronotropic support (î HR 1 diastole — 1 time for regurgitation) pure vasoconstrictors and IABP contraindicated surgery usually needed for acute severe Al which is poorly tolerated by LV Natural history

• Variable progression (unlike AS. can be fast or slow)

• Once decompensation begins, prognosis poor w/o AVR (mortality -10%/y)

Mitral Stenosis (MS)


• Rheumatic heart disease (RHD): fusion of the commissures -»"fish mouth" valve due to autoimmune rxn to beta strep infxn; seen largely in developing world today

• Functional MS due to severe mitral annular calcific. (MAC) — encroachment upon leaflets

• Congenital, myxoma, thrombus, large endocarditis lesions

• Valvulitis (eg. SLE. amyloid, carcinoid) or infiltration (eg. mucopolysaccharidoses)

Clinical manifestations

• Dyspnea and pulmonary edema (if due to RHD. sx usually begin in 30s)

précipitants: tachycardia, volume overload (incl. pregnancy). AF. fever, anemia

• Atrial fibrillation: often precipitates heart failure in Pts w/ MS

• Embolic events (especially in atrial fibrillation or endocarditis)

• Pulmonary symptoms: hemoptysis, frequent bronchitis (due to congestion). PHT

Physical examination

• Low-pitched mid-diastolic rumble at apex w/ presystolic accentuation (if not in AF)

appreciated best when Pt in left lateral decubitus position, î w I exercise severity of MS proportional to duration of murmur (not intensity)

• Opening snap (high-pitched early diastolic sound at left sternal border and apex)

MVA proportional to S2-OS interval (tighter valve » Î LA pressure — shorter interval)

• Loud Si (unless MV calcified), occasionally palpable Diagnostic studies

• ECG: LAE ("P mitrale"). • atrial fibrillation. • RVH

• CXR: dilated left atrium (straightening of left heart border, double density on right, left mainstem bronchus elevation)

• Echo: estimated pressure gradients (V). RVSP. calculated valve area, valve echo score

(based on leaflet mobility, leaflet thickening, subvalvular thickening, calcification); exercise TTE if discrepancy between sx and severity of MS at resçTEE to assess for LA thrombus before percutaneous valvuloplasty

• Cardiac cath: V from simultaneous PCWP & LV pressures, calculated

MVA (Gorlin formula): LA pressure tall a wave and blunted y descent: I PA pressures

Classification of Mitral Stenosis


Mean gradient (mmHg) MV area (cm )

PA Systolic (mmHg)


0 46



<5 1.5-2

■ 30


5-10 1-1.5



>10 <1


Treatment (Ore 2005:111431 /ACC 2006;48:c1)

• Medical: Na restriction, cautious diuresis, ^-blockers

• Anticoagulation if AF. prior embolism. LA thrombus, or large LA

• Indications for mechanical intervention: heart failure sx w/ MVA 1.5 or heart failure sx w/ MVA >1.5 but T PASP. PCWP. or MV V w/ exercise, or asx Pts w/ MVA s1.5 and PHT (PASP >50 mmHg or 60 mmHg w/ exercise), or ? new onset AF

• Percutaneous mitral valvuloplasty (PMV): preferred Rx if RHD: MVA doubles. V i by

50%: MVR if valve score 8. • mild MR. 0 AF or LA clot (NE/m 1994;331:961:Oc 2002:105:1465)

• Surgical (MV repair if possible, o/w replacement): consider in sx Pts w/ MVA s 1.5

if PMV not available or valve morphology not suitable

Mitral Regurgitation (MR)


• Leaflet abnormalities: myxomatous degeneration (MVP), endocarditis.

rheumatic heart disease, valvulitis (collagen-vascular disease), congenital, trauma

• Ruptured chordae tendinae: myxomatous, spontaneous, endocarditis, trauma

• Papillary muscle dysfunction: ischemia/Ml (usually posteromedial papillary m.

b/c supplied by PDA alone while anterolateral papillary m. supplied by diags. & OMs). displacement due to CMP. infiltration

• Annulus: any cause of LV dilatation: calcific, (typically seen w/ HTN. T chol.. DM. CKD)

• HCMP (see "Cardiomyopathy")

Clinical manifestations

• Acute: pulmonary edema, hypotension, cardiogenic shock (NE/M 2004:351:1627)

• Chronic: typically asx for y. then as LV fails progressive DOE. fatigue. AF. PHT

Physical examination

• High-pitched, blowing, holosystolic murmur at apex; radiates to axilla; r thrill t w/ handgrip (Se 68%. Sp 92%). 1 w/Valsalva (Se 93%) (nejm 1988:3181572) ant. leaflet abnl — post, jet heard at spine; post, leaflet abnl ant jet at sternum

• Lat. displ. hyperdynamic PMI, obscured Si. widely split Sj (Aj early b/c 1 afterload); • Sj

• Carotid upstroke brisk (vs. in AS where it is diminished and delayed)

Diagnostic studies

• CXR: dilated LA. dilated LV. • pulmonary congestion

• Echocardiogram: MV anatomy (ie. cause of MR), degree of MR via jet area (can underestimate eccentric jets), jet width at origin ("vena contracta"), or effective regurgitant orifice (ERO; predicts survival, nejm 2005:352.875). and LV function (EF supranormal in compensated states. EF < 60% with severe MR LV impairment) TEE used if TTE inconclusive or pre/intra-op to assess prob. of repair vs. replacement

• Cardiac cath: prominent PCWP cv waves (not spec, for MR). LVgram for MR severity & EF

Classification of Mitral Regurgitation



Jet Area

Jet width




(% of LA)



(see footnote)






1 +




0 3-0.69









1+ = LA dears w/each beat 2+ : LA docs not clear, faindy opac. after several beats: 3 - = LA & LV opac equal

1+ = LA dears w/each beat 2+ : LA docs not clear, faindy opac. after several beats: 3 - = LA & LV opac equal

Treatment (Cue 2003:1082432. JACC 2006:48*1)

• Surgery (repair preferred over replacement as preserves LV fxn and lower mort.)

symptomatic severe MR

asx severe MR and EF 30-60% or LV systolic diam. >40 mm. ? AF or PHT

? MV repair (not replacement) for asx severe MR w/ preserved LV fxn or sx severe MR w/ severe LV dysfxn (EF <30% or systolic diam. >55 mm)

• Medical: indicated if Pt not an operative candidate

. preload (i CHF and I amount of MR by i MV orifice): diuretics, nitrates i afterload (ACEI. hydralazine/nitrates): benefits unproven; indicated only if LV dysfxn maintain sinus rhythm

• Percutaneous MV repair: edge-to-edge clip y^CC 2005:46 2134) and annuloplasty band placed in coronary sinus (Ore 2006.113:851) remain under study

• Acute decompensation (consider ischemia and endocarditis as possible precipitants)

IV afterload reduction (nitroprusside), inotropic support (dobutamine). IABP vasoconstrictors contraindicated surgery usually needed for acute severe MR as prognosis is poor w/o MVR Prognosis

• 5-y survival w/ medical therapy 80% if asx. but 45% if sx

Mitral Valve Prolapse (MVP)


• Definition: displacement of any part of either MV leaflet or their coaptation point 2:2 mm above mitral annulus in parasternal long axis echocardiography view

• Myxomatous involvement of the MV apparatus with proliferation of the spongiosa

• Idiopathic, familial, and assoc. w/ connective tissue diseases (eg. Marfan s. Ehlers-Danlos)

• Prevalence 1-2.5% of general population (nejm 1999:341-1)

Clinical manifestations

• Asymptomatic

• MR due to prolapse of the leaflet or ruptured chordae

• Endocarditis; embolic events

• ? Atypical chest pain, arrhythmias

Physical exam

• Midsystolic click * mid-to-late systolic murmur i LV volume (standing, strain phase of Valsalva) click & murmur heard earlier T LV volume or t impedance to LV ejection -» click & murmur heard later & softer


• Endocarditis prophylaxis no longer recommended (Grc 2007.1I5:cpub)

• Aspirin or anticoagulation if prior neurologic event or atrial fibrillation

Prosthetic Heart Valves

Mechanical valves

• Bileaflet-tilting disk (eg. St. Jude Medical); single-tilting disk: caged-ball

• Characteristics: very durable but thrombogenic and .. require anticoagulation consider if age <60-65 y or if already need for anticoagulation


• Heterograft (eg. Carpentier-Edwards) or pericardial

• Characteristics: less durable, but minimally thrombogenic consider if age >60-65 y. lifespan <20 y. or contraindication to anticoagulation

Physical examination

• Normal: crisp sounds. • soft murmur during forward flow (normal to have small V)

• Abnormal: regurgitant murmurs, absent mechanical valve closure sounds

Anticoagulation with Prosthetic Valves




INR 2-3

INR 2.5-3.5

75-100 mg

Mechanical valves

1st 3 mo


After 3 mo

Aortic valve


Aortic valve » risk factor


Mitral valve • risk factor


Bioprosthetic valves

© for all

1st 3 mo

No risk factors

~ ♦

•i Risk factor


After 3 mo

No risk factors

Aortic valve ♦ risk factor


Mitral valve «• risk factor


Risk factors. AF. 1 EF. prior embolic event, hypercoagulable state, mechanical valve other than bileaflet or Medtronic Hall, ? multiple valves


Management of Anticoag. Peri-Procedure in Pts with Mech. Valve

AVR and no risk factors d/c warfarin 48-72 h before surgery restart 24 h after surgery

Risk factors for thromboembolism (ind. mechanical mitral valve)

Preop: d/c warfarin, start UFH when INR -:2

Postop: restart UFH & warfarin ASAP

Procedures include noncarduc surgery, invasiv« procedures, and major dental work (JACC 2006:48 e1)

Procedures include noncarduc surgery, invasiv« procedures, and major dental work (JACC 2006:48 e1)

Endocarditis prophylaxis Complications

• Valve thrombosis: treat w/ surgery (severe sx. L-sided. large dot burden) or lytic or UFH

• Pannus formation (typically forms on inferior surface of valve)

• Embolization (r/o endocarditis); risk of thromboembolism 1-2%/y even w/ warfarin Rx

• Structural failure (r/o endocarditis as cause)

mechanical valves: rare except for Bjork-Shiley bioprosthetic valves: 30% fail rate w/in 10-15 y

• Hemolysis (especially with caged-ball valves)

• Paravalvular leak (r/o endocarditis); small central jet of regurg normal in mechnical valves

• Endocarditis

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  • proserpio
    Are pulmonary vasoconstrictors contraindicated for heart valve problems?
    5 months ago

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