Mitral Stenosis

Abnormal narrowing of the mitral valve orifice.

Mitral stenosis is usually identified before patients reach old age. Most patients with severe mitral stenosis have surgery or die before reaching the age of 65; thus, elderly patients with mitral stenosis have a mild to moderate form of disease that has become severe because the valve has become heavily calcified in late life.

Mitral stenosis is due almost exclusively to rheumatic heart disease. Rheumatic fever, although its incidence has markedly decreased in the USA, was still prevalent when the elderly were children or adolescents. Also, in developing countries, the incidence of rheumatic heart disease is still high. A much less common cause of mitral stenosis is progressive extension of mitral annular calcification, which results in moderate mitral stenosis. One third of patients > 70 have calcium deposits in the mitral or aortic valve.

Pathophysiology

Acute rheumatic fever results in commissural fusion and fibrosis. Later, the chordae tendineae fuse and the valve calcifies. Some degree of mitral regurgitation often coexists.

As the mitral orifice narrows to < 2 cm² during diastole, blood flow through the valve is progressively obstructed, resulting in an increase in left atrial pressure and a diastolic gradient across the mitral valve. As left atrial pressure increases, pulmonary capillary pressure increases and right ventricular and pulmonary artery systolic pressures passively increase, leading to pulmonary hypertension. In 10 to 15% of patients, pulmonary arteriolar vasoconstriction is marked, pulmonary vascular resistance is greatly increased, and pulmonary hypertension is severe. Because afterload on the right ventricle is increased, right ventricular hypertrophy, dilation, and failure develop.

Increased pulmonary venous pressure results in collateral runoff to the bronchial veins; if they rupture, hemoptysis results. Dilation of the left atrium results in early atrial fibrillation and stasis of blood. Atrial fibrillation results in thromboembolic events and may cause heart failure.

Symptoms, Signs, and Diagnosis

Most elderly patients with mild to moderate mitral stenosis have few or no symptoms and are in sinus rhythm. If mitral stenosis is moderate (especially if atrial fibrillation develops) or is severe, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema can occur. Later, with the development of pulmonary hypertension, right ventricular failure supervenes.

Clinical features, comparable to those in younger patients, include a loud first heart sound, an apical diastolic rumble with presystolic accentuation, and an opening snap. The first heart sound and opening snap may soften or disappear if valvular calcification is present. The diastolic murmur may become softer, especially when stroke volume is decreased (as in heart failure) and when dilation of the right ventricle pushes the left ventricle away from the chest wall. A right ventricular parasternal impulse is often palpable, and venous pressure may be elevated. Atrial fibrillation and arterial embolism are more common among elderly patients. Atrial fibrillation often precipitates clinical deterioration; it sometimes causes pulmonary edema, peripheral arterial embolism, and stroke.

Left atrial enlargement is often seen on chest x-ray. ECG evidence of right ventricular hypertrophy is common when the stenosis is severe. Doppler echocardiography can document mitral stenosis and help estimate its severity. Left atrial myxoma, which may mimic mitral stenosis, can be differentiated by echocardiography.

Treatment

Most elderly patients with mild to moderate mitral stenosis respond well to medical therapy. If atrial fibrillation develops, digoxin, verapamil, or a -blocker can slow the ventricular response rate and reduce symptoms. Pharmacologic or electrical cardioversion to sinus rhythm may relieve symptoms, especially if the patient can be maintained in sinus rhythm by antiarrhythmic drugs.

Although elderly patients are at increased risk of bleeding, anticoagulants are recommended. The risk of peripheral arterial embolism and of embolic stroke is much higher than the risk of complications from anticoagulant therapy. Prolongation of the international normalized ratio (INR) to 2 to 3 is optimal.

Valve replacement is warranted for symptomatic patients with progressively severe mitral stenosis, because the calcified valve is rarely amenable to commissurotomy. Embolization without symptomatic hemodynamically severe mitral stenosis is not an indication for valve replacement. For the few patients who have uncalcified or minimally calcified valves, flexible valve leaflets, and mild mitral regurgitation, percutaneous balloon valvuloplasty is the procedure of choice.