Mitral Regurgitation Information
What is Mitral Regurgitation (Mitral Valve Regurgitation)
Mitral regurgitation may result from many processes. Rheumatic disease is associated with a thickened valve with reduced mobility and often a mixed picture of stenosis and regurgitation. In developed countries, more common causes of mitral regurgitation include myxomatous degeneration (eg, mitral valve prolapse with or without connective tissue diseases such as Marfan's syndrome), infective endocarditis, and subvalvular dysfunction (due to papillary muscle dysfunction or ruptured chordae tendineae). Cardiac tumors, chiefly left atrial myxoma, are a rare cause of mitral regurgitation.
Clinical Findings of Mitral Regurgitation
Symptoms and Signs of Mild Mitral Regurgitation
During left ventricular systole, the mitral leaflets do not close normally, and blood is ejected into the left atrium as well as through the aortic valve. The net effect is an increased volume load on the left ventricle, and the presentation depends on the rapidity with which the lesion develops. In acute regurgitation, left atrial pressure rises abruptly, leading to pulmonary edema if severe. When it is chronic, the left atrium enlarges progressively, but the pressure in pulmonary veins and capillaries rises only transiently during exertion. Exertional dyspnea and fatigue progress gradually over many years.
Mitral regurgitation leads to left atrial enlargement and may cause subsequent atrial fibrillation. Systemic embolization is relatively unusual compared with other conditions causing atrial fibrillation. Mitral regurgitation may predispose to infective endocarditis.
Clinically, mitral regurgitation is characterized by a pansystolic murmur maximal at the apex, radiating to the axilla and occasionally to the base; a hyperdynamic left ventricular impulse and a brisk carotid upstroke; and a prominent third heart sound. Left atrial enlargement is usually considerable in chronic mitral regurgitation; the degree of left ventricular enlargement usually reflects the severity of regurgitation. Calcification of the mitral valve is less common than in pure mitral stenosis. Hemodynamically, left ventricular volume overload may ultimately lead to left ventricular failure and reduced cardiac output, but for many years the left ventricular end-diastolic pressure and the cardiac output may be normal at rest, even with considerable increase in left ventricular volume.
Nonrheumatic mitral regurgitation may develop abruptly, such as with papillary muscle dysfunction following myocardial infarction, valve perforation in infective endocarditis, or ruptured chordae tendineae in mitral valve prolapse. In acute mitral regurgitation, patients are in sinus rhythm rather than atrial fibrillation and have little or no enlargement of the left atrium, no calcification of the mitral valve, no associated mitral stenosis, and in many cases little left ventricular dilation.