Symptoms related to<unk>  depend on the degree of stenosis. Most people with mild to moderate<unk>  do not have symptoms. Symptoms usually present in individuals with severe<unk> , though they may also occur in those with mild to moderate<unk> . The three main symptoms of<unk>  are loss of consciousness, anginal chest pain and shortness of breath with activity or other symptoms of heart failure such as shortness of breath while lying flat, episodes of shortness of breath at night, or swollen legs and feet. It may also be accompanied by the characteristic "Dresden china" appearance of pallor with a light flush. Angina Angina in setting of heart failure also increases the risk of death. In people with angina, the 5-year mortality rate is 50% if the aortic valve is not replaced. Angina in the setting of AS occurs due to left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the muscular layer of the left ventricle thickens, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may not receive enough blood supply to meet its oxygen requirement. This ischemia may first be evident during exercise when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of anginal chest pain with exertion. At this stage, a cardiac stress test with imaging may be suggestive of ischemia. Eventually, however, the heart muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of ventricular strain pattern (ST segment depression and T wave inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that is most susceptible to ischemia because it is the most distant from the epicardial coronary arteries. Syncope Syncope (fainting spells) from aortic valve stenosis is usually exertional. In the setting of heart failure it increases the risk of death. In people with syncope, the three-year mortality rate is 50% if the aortic valve is not replaced. It is unclear why<unk>  causes syncope. One theory is that severe AS produces a nearly fixed cardiac output. When a person with<unk>  exercises, their peripheral vascular resistance will decrease as the blood vessels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since people with severe AS cannot increase their cardiac output, the blood pressure falls and the person will faint due to decreased blood perfusion to the brain. A second theory is that during exercise the high pressures generated in the hypertrophied left ventricle cause a vasodepressor response, which causes a secondary peripheral vasodilation that, in turn, causes decreased blood flow to the brain resulting in loss of consciousness. Indeed, in<unk> , because of the fixed obstruction to blood flow out from the heart, it may be impossible for the heart to increase its output to offset peripheral vasodilation. A third mechanism may sometimes be operative. Due to the hypertrophy of the left ventricle in<unk> , including the consequent inability of the coronary arteries to adequately supply blood to the myocardium (see "Angina" below), abnormal heart rhythms may develop. These can lead to syncope. Finally, in calcific<unk>  at least, the calcification in and around the aortic valve can progress and extend to involve the electrical conduction system of the heart. If that occurs, the result may be heart block, a potentially lethal condition of which syncope may be a symptom. Congestive heart failure Congestive heart failure (CHF) carries a grave prognosis in people with AS. People with CHF attributable to AS have a 2-year mortality rate of 50% if the aortic valve is not replaced. CHF in the setting of AS is due to a combination of left ventricular hypertrophy with fibrosis, systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the LV). Associated symptoms In Heyde's syndrome,<unk>  is associated with gastrointestinal bleeding due to angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenotic valve. Complications Notwithstanding the foregoing, the American Heart Association changed its recommendations regarding antibiotic prophylaxis for endocarditis. Specifically, as of 2007 it is recommended that such prophylaxis should be limited only to those with prosthetic heart valves, those with previous episode(s) of endocarditis, and those with certain types of congenital heart disease. Since the stenosed aortic valve may limit the heart's output, people with<unk>  are at risk of syncope and dangerously low blood pressure should they use any of a number of medications for cardiovascular diseases that often coexist with<unk> . Examples include nitroglycerin, nitrates, ACE inhibitors, terazosin (Hytrin), and hydralazine. Note that all of these substances lead to peripheral vasodilation. Under normal circumstances, in the absence of<unk> , the heart is able to increase its output and thereby offset the effect of the dilated blood vessels. In some<unk> es of<unk> , however, due to the obstruction of blood flow out of the heart caused by the stenosed aortic valve, cardiac output cannot be increased. Low blood pressure or syncope may ensue.
Aortic stenosis
Hypertrophic cardiomyopathy
Mitral stenosis
Aortic regurgitation
Tricuspid valve stenosis
Tricuspid regurgitation
Mitral regurgitation
Pulmonary valve stenosis