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Valvular Heart Disease

Mitral stenosis and mitral valve obstruction. Although mitral valve obstruction has a variety of potential causes--including atrial myxoma, thrombus, vegetation or thrombotic obstruction of a previously placed mitral valve prosthesis–-classic mitral stenosis in the adult is always rheumatic. You won’t see congenital stenosis in the age population. The majority of patients, particularly these days, who have rheumatic mitral stenosis will have no recollection of that illness in childhood. The latent period, before the first development of symptoms or signs of mitral stenosis, is in excess of a decade. So the symptoms usually appear in mid-life and the rate of progression of stenosis is quite variable. The normal area of the mitral valve is between 4-6 square cm, and as the obstruction progresses and the area is reduced, left atrial hypertension develops resulting in an increased pressure gradient. When the area is reduced to 1.5 square cm there is clinical left atrial hypertension which is translated, of course, into 

With respect to surgery, we do commissurotomies if there is no calcium in the valve and the valve does not leak. Usually these are young patients in sinus rhythm. We think that a commissurotomy will reduce the risk of embolization. Mitral stenosis will occur ordinarily two decades later and then the patient might require mitral valve replacement because by that time calcification of the subvalvular apparatus is extremely likely. Sometimes an

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

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 without cardiac surgical intervention. The pathophysiology here is that there is a chronic left ventricular volume overload. This is ordinarily well tolerated.

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

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

Most of these patients are asymptomatic and they are referred to an internist or cardiologist because of the exculpatory findings. Some patients will complain of atypical chest pain and some patients will have prolapse. It has been my belief for a long time that most patients with these complaints have these complaints having nothing with the exculpatory or echocardiographic findings. Because palpitations and atypical chest pain are prevalent in the worried population and since mitral valve prolapse is easy to detect by physical examination or echocardiography, we have created a large number of patients who worry unnecessarily that symptoms such as these, which might ordinarily be benign, are actually the signs of some severe underlying

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

Aortic stenosis. Aortic stenosis is a common congenital disease. It presents as a bicuspid valve in 1% of the population, so it’s extremely common. If the patient develops significant aortic stenosis young, which I will arbitrarily define as less than 60 years of age - reserving the right to revise the slide as the years go by - then the most common cause is calcification of a congenitally bicuspid valve. If on the other hand the patient develops

Aortic sclerosis is a different entity than aortic stenosis. Aortic sclerosis is merely a sound. You hear a systolic murmur but the patient does not have clinical hemodynamic or echocardiographic or invasively defined hemodynamic evidence of left ventricular outflow obstruction. But keep in mind that, as has recently been discovered, this so-called benign systolic ejection murmur may not be as benign as we used to think it is. Patients who have aortic sclerosis, a murmur along the left sternal border, unassociated with aortic stenosis have a 50% higher risk of cardiovascular death and 

Aortic regurgitation may be due to rheumatic disease, congenital disease, infective endocarditis. A dissecting aneurysm, annular-aortic coarctation, syphilis, or other connective tissue disease that might dilate the root. This entity presents as left ventricular overload in which there is a large stroke volume generated by left ventricular dilatation and left ventricular hypertrophy tends to normalize systolic stress. Unfortunately, dilatation is ordinarily accompanied by an elevation of the diastolic stress of the heart. But at that point may actually be late to repair. The most typical sense 

Tricuspid stenosis is dramatic when significant mitral valve disease or tricuspid stenosis is due to the carcinoid syndrome. These patients have a prominent A-wave and a slow Y descent and a murmur which varies with inspiration. Echocardiogram is diagnostic. Tricuspid regurgitation usually is functional as a consequence of pulmonary hypertension due to left sided heart disease. Either myocardial disease resulting in bi-sided heart failure, pulmonary hypertension, or mitral valve disease resulting in pulmonary hypertension and the tricuspid regurgitation secondarily. The other cause is infective endocarditis, particularly in patients who inject intravenous drugs. These patients have large V-waves with a rapid Y descent, distended neck veins, and they have a loud murmur which varies with inspiration. Ordinarily they have chronic atrial fibrillation. The echo will show paradoxical motion of the septum and is diagnostic of this entity which is ordinarily treated medically.

The pneumonic valve is the one valve that seems not to be affected by rheumatic heart disease.