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Stenosis means narrowing of an opening, such as a heart valve. Stenosis of the mitral valve limits the forward flow of blood from the left atrium to the left ventricle. This may cause a back-up of blood and fluid in the lungs. Mitral stenosis most commonly develops many years after a person has had rheumatic fever, although many patients diagnosed with mitral stenosis don't recall ever having the illness.
Causes: Diagnosed with mitral stenosis don’t recall ever having the illness. During rheumatic fever, the valve becomes Mitral stenosis most commonly develops many years after a person has had rheumatic fever, although many patients inflamed. Over time, the leaflets of the inflamed valve stick together and become scarred, rigid and thickened, limiting its ability to open completely.
Symptoms: Many of the symptoms of mitral stenosis, such as shortness of breath and fatigue, result from a back-up of blood in the lungs. Other symptoms of mitral stenosis may include quick weight gain; weakness; dizziness; swelling in the ankles, feet and/or abdomen (edema); and/or heart palpitations (irregular heartbeat).
Treatment: A balloon valvotomy is the preferred treatment for mitral valve stenosis. It is a procedure that widens the mitral valve so that blood flows more easily through the heart. A balloon valvotomy is a minimally invasive procedure. A doctor uses a thin flexible tube (catheter) that is inserted through an artery in the groin or arm and threaded into the heart. When the tube reaches the narrowed mitral valve, a balloon device located on the tip of the catheter is quickly inflated. The narrowed or fused mitral valve leaflets are separated and stretched open as the balloon presses against them. This process increases the size of the mitral valve opening and allows more blood to flow from the left atrium into the left ventricle.
Statistics: In a 27-member family, 8 individuals had mitral valve prolapse (MVP) by echocardiography. Four of them suffered a total of eight cerebral ischemic events in the first four decades of life. In none of these patients could risk factors for stroke, other than MVP, be found. Stroke did not occur in individuals free of MVP. This report draws attention to a previously unrecognized cause of familial stroke which strengthens the relationship between MVP and premature stroke. This group of 26 patients (21 females, five males, with mean age of 46 years), had the syndrome identified as idiopathic mitral valve prolapse (IMVP), which was characterized by a systolic click-murmur, clinical symptoms that were highly variable in duration and intensity, angiographically-documented mitral prolapse, and no obvious associated systemic or cardiovascular disease. Mitral regurgitation was of moderate degree in four, mild in 14, and absent in eight. The left ventricular (LV) end-diastolic volume index was elevated in ten of 25 (40%), the LV mass index was elevated in six of 17 (35%), but the LV anterior wall thickness was increase in only one of 17. Three major patterns of ventricular contraction were identified: 1) normal in seven; 2) abnormal, usually an inferior deformity and/or anterior asynergy, in eight; and 3) hyperkinetic in 11. Normal resting left ventricular function, assessed as an ejection fraction greater than 55%, was present in 17 of 25 (68%). Selective coronary arteriography was essentially normal in all 25 patients studied. An ischemic ECG response was detected during only one of 12 maximal treadmill exercise tests and in none of ten atrial pacing stress tests (AP).
