Prolapse refers to a condition of the various four heart valves. With reference to the mitral valve it refers to systolic billowing of one or both mitral leaflets into the left atrium, with or without mitral regurgitation (see fig.115, fig.116, fig.117, fig. 117a). Disease processes involving any one or more of these components may result in dysfunction of the valvular apparatus and prolapse of the mitral leaflets toward the left atrium during systole when left ventricular pressure exceeds left atrial pressure.

Tests for Mitral Valve Prolapse Include:

Electrocardiography,
Echocadiography,
Chest X'ray,
Myocardial Perfusion Scintigraphy,
Cardiac Catheterization and
Electrophysiologic Test.

Echocardiography

Echocardiography is the most useful noninvasive test for defining MVP.The M-mode echocardiograhic definition of MVP include 2 mm or more of posterior displacement of one or both leaflets of holosystolic posterior "hammocking"of more than 3 mm (see Fig.116). On 2-D echocardiography, systolic displacement of one or both mitral leaflets, particularly when they coapt on the LA side of the annular plane, in the parasternal long-axis view indicates a high likelihood of MVP (Fig.116). There is disagreement concerning the reliability of an echocardiographic diagnosis of MVP when observed only in apical four-chamber view. The diagnosis of MPV is even more certain when the leaflet thickness is greater than 5 mm during ventricular diastole. Leaflet redundancy is often associatedh an elongated mitral annulus and elongated chordae. On Doppler velocity recordings, the presence or absence of MR is an important consideration, and MVP is more when the MR is detected as a high-velocity jet midway posterior in the left atrium.
At present, there is no consensus on the 2-D echocardigraphic criteria for MVP. Since echocardiography is a tomographic cross-sectional technique, no single view should be considered diagnostic. The parasternal long-axis view permits visualization of the medial aspect of the anterior mitral leaflet and middle scallop of the posterior leaflet. If findings of prolapse are localized to the lateral scallop of the posterior leaflet, they would be best visualized by the apical four-chamber view. All available echocardiographic views should be used, with the provision that anterior leaflet billowing alone in the four-chamber apical view is not evidence of prolapse; however, a displacement of the posterior leaflet or the coaptation point in any view including the apical views suggests the diagnosis of prolapse. The echocardiographic criteria for MVP should include structural changes such as leaflet thickening, redundancy, annular dilatation, and chordal elongation.
Patients with echocardiographic criteria for MVP but without evidence of thickened/redundant leaflets or definite MR are more difficult to classify. If such patients have auscultatory findings typical of MVP, the echocardiogram confirms the diagnosis. On the other hand, a patient with typical auscultatory findings but a negative echocardiogram likely also has MVP; in the past, as many as 10 percent of patients with MVP have had a nondiagnostic echocardiographic study. Currently, this percentage is lower because of more careful and complete echocardiographic studies. In clinical practice, a false diagnosis of MVP occurs too frequently. The use of echocardiography as a screening test for MVP in patients with and without symptoms who have no systolic click or murmur on serial,carefully performed ausculatory examinations is not recommended, as the likelihood of finding MVP is extremely low.

Among the various causes of mitral valve prolapse (MVP) there is a primary one in which there is a marked proliferation of the spongiosa, the delicate myxomatous connective tissue between the atrialis (a thick layer of collagen and elastic tissue forming the atrial aspects of the leaflet) and the fibrosa or ventricularis, which is composed of dense layers of collagen and forms the basic support of the leaflet. This myxomatous proliferation causes focal disruption of the fibrosa the leaflets become fibrous and the chordae tendineae become thin and elongated (see fig.115, fig.116, fig.117). This particular form of MVP maybe familial, non-familial, and also caused by a disease called Marfan's syndrome and other connective tissue diseases. MVP may also be due to coronary artery disease, rheumatic heart disease, cardiomyopathies, and "flail" mitral valve leaflet(s).

Treatment

The majority of patients with mitral valve prolapse(MVP) are asymptomatic and lack a high risk profile.

These patients with mild or no symptoms and findings of milder forms of prolapse should be reassured of a benign prognosis.A normal life-style and regular exercise is encouraged. It is recommended that antibiotic prophylaxis for the prevention of infective endocarditis while undergoing procedures associated with bacteremia for most patients in whom the diagnosis is definite.

Patients with MVP and palpitations associated with sinus tachycardia or mild tachyarrhythmia and those with chest pain, anxiety, or fatigue often respond to therapy with beta blockers.

In many cases, however, the cessation of catecholamines stimulants such as caffeine, alcohol, cigarettes, and certain drugs may be sufficient to control symptoms.

Orthostatic symptoms (dizziness, fainting) are best treated with volume expansion preferably by liberalizing fluid and salt intake. Mineralocorticoid therapy may be needed in severe cases, and wearing support stockings may be beneficial.

In those with complex arrhythmias, specific therapy should be guided by monitoring techniques, including electrophysiology testing when indicated.

Daily aspirin therapy is recommended for MVP patients with documented focal neurologic deficits,avoiding cigarette smoking and oral contraceptives. Use of anticoagulants may be indicated in those who have suffered a stroke. Restriction from competitive sports is recommended when moderate heart enlargement, left ventricular dysfunction, uncontrolled arrhythmias, unexplained syncope, prolonged QT interval alone or in combination occur.

There is a familial occurrence. There is no contraindication to pregnancy based on the diagnosis of MVP alone.

Patients with severe mitral regurgitation with symptoms and/impaired left ventriclar function require cardiac catheterization and evaluation for mitral valve surgery, including repair or replacement, with a low operative mortality and excellent short term results and less emboli and infection. Asymptomatic patients with no significant mitral regurgitation can be evaluate every 2-3 years.

High risk patients including those with severe regurgitation should be followed more frequently, even if no symptoms are present.