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Mitral Regurgitation and Prolapse  

Mitral regurgitation, the etiology is rheumatic but also there are a variety of other factors which can result in mitral regurgitation; such as prolapse of the valve, ruptured chordae, papillary muscle dysfunction, calcification of the mitral annulus or infective endocarditis will differentiate between chronic and acute mitral regurgitation, because both the presentation and treatment differ. I acute mitral regurgitation there is an acute volume load which immediately results in left ventricular failure. As the large volume is delivered into a left atrium, which is of normal size, this results in marked left atrial hypertension and in pulmonary edema. The causes of this are papillary muscle dysfunction or rupture, usually the consequence of myocardial ischemia due to coronary artery disease, ruptured chordae ordinarily the consequence of the elongation and thinning of the chordae which result from the somatist degeneration of the mitral valve. Infective endocarditis, blunt chest trauma or malfunction of a previously place prosthetic valve, for example a periannular leak which may progress to give huge, severe mitral regurgitation. The history is that of the abrupt heart failure accompanied by the murmur of mitral regurgitation. Ordinarily the ventricle is hyperdynamic. The examination reveals a holosystolic murmur. Keep in mind that this is an unusual situation where the carotids will remain sharp even if the patient is in severe heart failure.

Chronic mitral regurgitation presents quite differently. It is also possible to have chronic rheumatic disease but the most common causes are left ventricular dilatation from coronary disease and prior myocardial infarction, or dilated cardiomyopathies of any cause, calcification of the mitral annulus, a floppy valve, which is to say moderate to severe mitral valve prolapse, or the rare patient who survives acute mitral regurgitation.

So these patients will develop heart failure quite slowly. Examination will reveal cardiomegaly. Echocardiogram ordinarily show atrial fibrillation and may show left ventricle hypertrophy. The chest x-ray will always show cardiomegaly and pulmonary vascular congestion. The echocardiogram will show mitral regurgitation and cardiomegaly and when the patient comes to cardiac catheterization the V-waves are much less impressive than the V-waves that are recorded in patients with acute mitral regurgitation. The cardiac output and the left ventricular ejection fraction are more likely to be depressed. Keep in mind that in an acute mitral regurgitation the left ventricular ejection fraction is usually super-normal.

The treatment is the typical digitalis, diuretics, vasodilator therapies to decompress the left atrium and unload the left ventricle. Surgical therapy is limited to patients - for those situations in which symptoms progress despite therapy, or in which the patient remains asymptomatic but at the expense of high doses of therapy and cardiomegaly continues to progress. Because we regard progressive cardiomegaly as indistinguishable from symptoms in the patient who actually denies symptoms. The same criteria would apply in the choice of prosthesis. Ruptured chordae occur, as I said, as a consequence most commonly of myxomatous degeneration of the mitral valve. It is idiopathic in two-thirds.

Calcification of the mitral annulus applies most notably to this titrimetry of an elderly hypertensive diabetic woman. They have the murmur of mitral regurgitation but the leak is usually not severe enough to be of hemodynamic importance. Also functional mitral stenosis may occur. But again, usually not severe. These patients may have conduction abnormalities, bundle branch blocks and AV block as a consequence of progression of calcification from the annulus of the heart into the conduction system of the heart. These patients are in fact at risk of systemic embolization even without atrial fibrillation.

Mitral prolapse encompasses a very wide spectrum of disease. It has in the past been considered almost to be a normal variant. This depends on how one defines mitral valve prolapse. One can define mitral valve prolapse at a way in which we grade the diagnostic criteria from trivial to mild, to moderate, to severe. And the differentiation of trivial prolapse from no prolapse is really a fine distinction best made by an expert echocardiographer. It is a common entity, particularly if one includes the patients with trivial prolapse. There is a very nice article in the New England Journal that pointed out that if the echocardiographic criteria are typed up so that trivial prolapse is excluded, then mitral valve prolapse in the general population is not nearly as prevalent as your textbooks had previously mentioned. Most of the time, trivial prolapse patients have very few symptoms but severe mitral regurgitation may occur truly as a consequence of mitral valve prolapse.

Some patients with mitral valve prolapse will have skeletal abnormalities, the clicks will be single or multiple, the murmur will be quite variable; which means that if you hear it and the next doctor does not, it does not mean that the second doctor is a fool. It just means that the murmur is evanescent. It is positional and can be made to come and go by a variety of maneuvers. The electrocardiogram is usually normal but may have ST&T-wave

We manage most of these patients by reassurance and generally evaluating these other problems, such as syncope or significant ventricular arrhythmias, on their own grounds. I never raise the issue of sudden death to these patients. I really reassure these patients. If the patient has a murmur and mitral valve prolapse then they do need to take antibiotic prophylaxis for infective endocarditis even though the actual risk of infective endocarditis is vanishingly low. If they get this disease you will be blamed if you donít prescribe the antibiotic, and it is therefore almost mandatory if you hear a murmur and you find a prolapse on an echo, to make such a recommendation. The recent recommendations from the AHA, the prescription of