Mitral Regurgitation

The mitral valve is subjected to the highest stresses of the four cardiac valves: it is exposed to the systolic pressure in the left ventricle, at least 120 mm Hg. Its competence is contingent not only on the state and function of its two leaflets but also on the function of the reinforcing auxiliary parts of the mitral-valve apparatus—the chordae tendineae and the papillary muscles of the left ventricle. Consequently, mitral regurgitation may be caused by a variety of mechanisms:

Scarring after rheumatic fever may produce shrinking of the leaflet.

Infective endocarditis may create a hole in a leaflet.

The chordae may stretch, preventing tight closure of the leaflets.

One or more chordae may rupture.

The left ventricular papillary muscle may malfunction and be unable to tighten the chordae.

When the left ventricle dilates, the orifice may become too large for the leaflets to cover it.

The valve may be congenitally deformed.

Mitral regurgitation often develops as a complication of other cardiac diseases. A mild degree of incompetence of this valve has no significant effect on the circulation. Significant mitral regurgitation may also appear as the principal cardiac disease.

Rheumatic mitral regurgitation is most often seen in combination with mitral stenosis, with the latter being the predominant disease. Alone, mitral regurgitation is in some ways similar to mitral stenosis. Although regurgitation in children may be an immediate consequence of rheumatic fever, it is more likely to develop a long time after the attack. Disability tends to appear only in middle age or later. Complications include atrial fibrillation, although embolic episodes are less common than in mitral stenosis. Surgical treatment frequently involves valve replacement, but in some cases the deformed mitral valve can be successfully repaired. In developing countries, where severe recurrent rheumatic fever is prevalent, mitral regurgitation may evolve rapidly, requiring valvular surgery at a young age.

Prolapse of the mitral valve was first identified in the 1960s. Its unique feature is that the volume of blood returning to the left atrium is small and does not increase the workload of the left ventricle. Nevertheless, mitral-valve prolapse has become one of the most widely debated topics in cardiology. The potential complications of this lesion are graver than its direct effect. Mitral-valve prolapse may be associated with the following sequelae:

arrhythmias, both atrial and ventricular

infective endocarditis

embolic stroke (slight but definite risk)

atypical chest pain, which may be mistaken for coronary disease

rupture of some chordae, which can change trivial mitral regurgitation into acute severe mitral regurgitation requiring emergency intervention

In mitral-valve prolapse the leaflets may be larger than normal and stretch the chordae, producing valvular incompetence. Prolapse of the valve means that one leaflet overlaps the other, the most important cause of which is an abnormal structure of the leaflets called mucoid degeneration. This condition is often genetic. Such valves may become progressively larger, with redundant

tissues flapping in the mitral orifice like a parachute. Hereditary degeneration of the mitral valve occurs in young patients, is more common in women than in men, and has a relatively high rate of complications. Yet it accounts for only a small fraction of the cases of prolapse. In general, mitral-valve prolapse is a benign condition most frequently discovered on routine examination and having an excellent prognosis.

A preliminary diagnosis of mitral-valve prolapse may be made simply by listening with the stethoscope (auscultation) for the characteristic heart murmur and an extra sound. The principal test used to establish a firm diagnosis of this disease is the echocardiogram, which shows one leaflet slipping over the other. The echocardiogram may in fact be too sensitive a diagnostic tool: normal mitral valves may have somewhat oversized leaflets, which on the echocardiogram may resemble abnormal prolapse. It is now generally recognized that echocardiographic criteria for diagnosing mitral-valve prolapse have to be critically evaluated to guard against ascribing this valvular disease to healthy young adults.

Patients with mitral-valve prolapse need to be reassured of the favorable prognosis. Some patients require endocarditic prophylaxis. Those with the more pronounced hereditary prolapse are sometimes treated for arrhythmias. In rare cases of severe mitral regurgitation valve replacement may become necessary.

Rupture of the chordae tendineae is one of the causes of acute severe mitral regurgitation. It usually develops as a complication of other cardiac diseases, such as mitral-valve prolapse or infective endocarditis, but may represent a primary mitral-valve disease. Spontaneous rupture of the chords occurs occasionally, especially in older male patients. Chordal rupture may also result from trauma, a nonpenetrating injury to the chest. Mild varieties of chordal rupture usually involve separation of a single chord; it may have a minimal hemodynamic effect and require no treatment. More often, however, rupture involves multiple chords and may create an emergency requiring early valve replacement or repair.

Ischemic mitral regurgitation is a complication of coronary-artery disease, most frequently during or after an acute myocardial infarction. It is caused by damage to one of the two papillary muscles in the left ventricle, which then can no longer pull the chordae

tendineae tight to help make the valve competent. There are two types. (1) Rupture of the papillary muscle or a part of it is a serious, often catastrophic complication of myocardial infarction and usually requires an emergency valvular operation. (2) Malfunction of a papillary muscle may also develop during the course of myocardial infarction but has less serious consequences. Occasionally mitral regurgitation may not be apparent until after recovery from myocardial infarction. The severity of mitral regurgitation due to damage of the papillary muscle varies; furthermore, regurgitation may become progressively more severe. Treatment may be medical or surgical, depending on the severity of the condition and the patient's response to drug therapy. Valve replacement performed because of heart failure produced by mitral regurgitation may be ineffective if serious postinfarction damage to the heart muscle has occurred.

Infective endocarditis may result in new damage to the mitral valve, causing regurgitation in a previously competent valve. This is sometimes the case in patients with mitral stenosis or when the infection develops on a valve with a minor abnormality not affecting its function, such as mitral-valve prolapse. If the infection is seated on an already incompetent valve, the amount of regurgitation may increase, particularly if infection produces perforation of the valve or disrupts the chordae tendineae. Acute mitral regurgitation caused by endocarditis, if severe, may lead to a cardiac emergency requiring immediate valvular surgery.

Rarer varieties of mitral regurgitation include congenital mitral valve clefts (division of one or both leaflets into two parts with a space between them), marked dilatation of the left ventricle in association with heart failure, and cardiac tumors (myxomas of the left atrium), which may interfere with the closure of the valve.