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Harrison’s Manual of Medicine



Mitral Stenosis (MS)
Mitral Regurgitation (MR)
Mitral Valve Prolapse (MVP)
Aortic Stenosis (AS)
Aortic Regurgitation (AR)
Tricuspid Stenosis (TS)
Tricuspid Regurgitation (TR)
ETIOLOGY   Most commonly rheumatic, although history of acute rheumatic fever is now uncommon; congenital MS is an uncommon cause, observed primarily in infants.
HISTORY   Symptoms most commonly begin in the fourth decade, but MS often causes severe disability by age 20 in economically deprived areas. Principal symptoms are dyspnea and pulmonary edema precipitated by exertion, excitement, fever, anemia, paroxysmal tachycardia, pregnancy, sexual intercourse, etc.
PHYSICAL EXAMINATION   Right ventricular lift; palpable S1; opening snap (OS) follows A2 by 0.06 to 0.12 s; OS–A2 interval inversely proportional to severity of obstruction. Diastolic rumbling murmur with presystolic accentuation in sinus rhythm. Duration of murmur correlates with severity of obstruction.
COMPLICATIONS   Hemoptysis, pulmonary embolism, pulmonary infection, systemic embolization; endocarditis is uncommon in pure MS.
LABORATORY   ECG Typically shows atrial fibrillation (AF) or left atrial (LA) enlargement when sinus rhythm is present. Right-axis deviation and RV hypertrophy in the presence of pulmonary hypertension.
CXR   Shows LA and RV enlargement and Kerley B lines.
ECHOCARDIOGRAM   Most useful noninvasive test; shows inadequate separation, calcification and thickening of valve leaflets, and LA enlargement. Doppler echocardiogram allows estimation of transvalvular gradient and mitral valve area (Chap. 113).

(See Fig. 118-1) Pts should receive prophylaxis for rheumatic fever (penicillin) and infective endocarditis (Chap. 80). In the presence of dyspnea, medical therapy for heart failure; digitalis, beta blockers, or verapamil to slow ventricular rate in AF; diuretics, and sodium restriction. Anticoagulants for pts with AF and/or history of systemic and pulmonic emboli. Mitral valvotomy in the presence of symptoms and mitral orifice £ approximately 1.6 cm2. In uncomplicated MS, percutaneous balloon valvuloplasty is the procedure of choice; if not feasible, then open surgical valvotomy.

FIGURE 118-1. Management of mitral stenosis.

ETIOLOGY   Rheumatic heart disease in approximately 33%. Other causes: mitral valve prolapse, ischemic heart disease with papillary muscle dysfunction, LV dilatation of any cause, mitral annular calcification, hypertrophic cardiomyopathy, infective endocarditis, congenital.
CLINICAL MANIFESTATIONS   Fatigue, weakness, and exertional dyspnea. Physical examination: sharp upstroke of arterial pulse, LV lift, S1 diminished: wide splitting of S2; S3; loud holosystolic murmur and often a brief early-mid-diastolic murmur.
ECHOCARDIOGRAM   Enlarged LA, hyperdynamic LV; Doppler echocardiogram helpful in diagnosing and assessing severity of MR.

(See Fig. 118-2) As for heart failure (Chap. 116), including diuretics and digoxin. Afterload reduction (ACE inhibitors, hydralazine, or IV nitroprusside) decreases the degree of regurgitation, increases forward cardiac output, and improves symptomatology. Endocarditis prophylaxis is indicated, as is anticoagulation in the presence of atrial fibrillation. Surgical treatment, either valve repair or replacement, is indicated in the presence of symptoms or evidence of progressive LV dysfunction (LVEF < 60% or end-systolic LV diameter by echo >45 mm/m2). Operation should be carried out before development of severe chronic heart failure.

FIGURE 118-2. Management of advanced mitral regurgitation. *Including class II; ACEI, angiotensin converting-enzyme inhibitors; ESD, end-systolic diameter.

ETIOLOGY   Most commonly idiopathic; ?familial; may accompany rheumatic fever, ischemic heart disease, atrial septal defect, the Marfan syndrome.
PATHOLOGY   Redundant mitral valve tissue with myxedematous degeneration and elongated chordae tendineae.
CLINICAL MANIFESTATIONS   More common in females. Most pts are asymptomatic and remain so. Most common symptoms are atypical chest pain and a variety of supraventricular and ventricular arrhythmias. Most important complication is severe MR resulting in LV failure. Rarely, systemic emboli from platelet-fibrin deposits on valve. Sudden death is a very rare complication.
PHYSICAL EXAMINATION   Mid or late systolic click(s) followed by late systolic murmur; exaggeration by Valsalva maneuver, reduced by squatting and isometric exercise (Chap. 112).
ECHOCARDIOGRAM   Shows posterior displacement of posterior (occasionally anterior) mitral leaflet late in systole.

Asymptomatic pts should be reassured, but if systolic murmur is present and/ or typical echocardiographic findings with significant MR, prophylaxis for infective endocarditis is indicated. Valve repair or replacement for pts with severe mitral regurgitation; anticoagulants for pts with history of embolization.

ETIOLOGY   Often congenital; rheumatic AS is usually associated with rheumatic mitral valve disease. Idiopathic, calcific AS is a degenerative disorder common in the elderly and usually mild.
SYMPTOMS   Dyspnea, angina, and syncope are cardinal symptoms; they occur late, after years of obstruction.
PHYSICAL EXAMINATION   Weak and delayed arterial pulses with carotid thrill. Double apical impulse; A2 soft or absent; S4 common. Diamond- shaped systolic murmur ³grade 3/6, often with systolic thrill.
LABORATORY   ECG and CXR   Often show LV hypertrophy, but not useful for predicting gradient.
ECHOCARDIOGRAM   Shows thickening of LV wall, calcification and thickening of aortic valve cusps. Dilatation and reduced contraction of LV indicate poor prognosis. Doppler useful for estimating gradient and calculating valve area.

Avoid strenuous activity in severe AS, even in asymptomatic phase. Treat heart failure in standard fashion (Chap. 116), but avoid afterload reduction. Valve replacement is indicated in adults with symptoms resulting from AS and hemodynamic evidence of severe obstruction. Operation should be carried out before frank failure has developed.

ETIOLOGY   Rheumatic in 70%; also may be due to infective endocarditis, syphilis, aortic dissection, or aortic dilatation due to cystic medial necrosis; three-fourths of pts are males.
CLINICAL MANIFESTATIONS   Exertional dyspnea and awareness of heart beat, angina pectoris, and signs of LV failure. Wide pulse pressure, waterhammer pulse, capillary pulsations (Quincke’s sign), A2 soft or absent, S3 common. Blowing, decrescendo diastolic murmur along left sternal border (along right sternal border with aortic dilatation). May be accompanied by systolic murmur of augmented blood flow.
LABORATORY   ECG and CXR   LV enlargement.
ECHOCARDIOGRAM   Increased excursion of posterior LV wall, LA enlargement, LV enlargement, high-frequency diastolic fluttering of mitral valve. Doppler studies useful in detection and quantification of AR.

Standard therapy for LV failure (Chap. 116). Surgical valve replacement should be carried out in pts with severe AR when symptoms develop or in asymptomatic pts with LV dysfunction (LV ejection fraction <55%, LV end- systolic volume >55 mL/m2, or end-systolic diameter >55 mm) by echocardiography.

ETIOLOGY   Usually rheumatic; most common in females; almost invariably associated with MS.
CLINICAL MANIFESTATIONS   Hepatomegaly, ascites, edema, jaundice, jugular venous distention with slow g descent (Chap. 112). Diastolic rumbling murmur along left sternal border increased by inspiration with loud presystolic component. Right atrial and superior vena caval enlargement on x-ray.

In severe TS, surgical relief is indicated and usually requires valve replacement.

ETIOLOGY   Usually functional and secondary to marked RV dilatation of any cause and often associated with pulmonary hypertension.
CLINICAL MANIFESTATIONS   Severe RV failure, with edema, hepatomegaly, and prominent v waves in jugular venous pulse with rapid y descent (Chap. 112). Systolic murmur along sternal edge is increased by inspiration.

Intensive diuretic therapy. In severe cases (in absence of severe pulmonary hypertension), surgical treatment consists of tricuspid annuloplasty or valve replacement.


For a more detailed discussion, see Braunwald E: Valvular Heart Disease, Chap. 236, p. 1343, in HPIM-15.


One comment on “118 VALVULAR HEART DISEASE

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