The most significant risk factor in the etiology of aortic valve calcification is aging; followed by osteoporosis and hypertension. Congenital aortic valve lesions may be asymptomatic in early childhood. Early aortic valve calcification does not affect the closing function of the valve and may not cause an increased load on the left ventricle, so it does not cause symptoms of heart failure. In most cases, calcified aortic valve lesions progress slowly and can gradually cause incomplete closure of the aortic valve over several years, resulting in enlargement of the left ventricle and leading to left heart failure, when symptoms such as palpitations after activity, shortness of breath, and discomfort in the precordial region may occur The symptoms may include palpitations after activity, shortness of breath, and anterior heart discomfort. The common symptoms of aortic valve lesions are palpitations, shortness of breath, and angina after exertion. In cases of severe aortic stenosis or aortic valve insufficiency, angina is particularly severe due to a severe shortage of coronary artery blood supply. In severe cases of aortic valve calcification, left anterior branch block and various other degrees of atrioventricular or bundle branch conduction block are seen. Calcification of the valve is one of the main causes of aortic stenosis and is commonly seen in the elderly. Causes of aortic valve calcification There are four main types of aortic valve disease requiring surgical treatment: 1. Congenital aortic valve disease is more commonly known as double leaflet malformation, with clinical manifestations dominated by aortic stenosis and aortic valve systolic transvalvular pressure difference often exceeding 13.3 kPa (100 mmHg). The electrocardiogram shows high voltage in the left ventricle, often with strain, and radiography and ultrasonography often show a small left ventricular cavity and centripetal hypertrophy of the myocardium. Severe aortic stenosis may produce relative mitral valve insufficiency due to high left ventricular systolic pressure. Another common congenital aortic valve lesion is aortic valve leaflet prolapse producing aortic valve insufficiency, a malformation that often occurs in cases of large high ventricular septal defects or aortic sinus aneurysms that break into the right ventricle. In cases of large high ventricular defects, the corresponding leaflet above it loses its septal support and the leaflet prolapses into the right ventricle via the ventricular defect during ventricular diastole. In cases of ruptured sinus tumors, the corresponding aortic valve leaflet prolapses into the left ventricle. About 20% of rheumatic mitral valve disease is combined with aortic valve lesions in rheumatic heart disease, and simple arterial valve lesions are less common. The three aortic valve leaflets have fibrotic thickening, contraction, sclerosis, and even calcification, and the mobility is very poor, so rheumatic aortic valve lesions are often double lesions with stenosis and incomplete closure, and the course of the disease is longer, and the damage to cardiac function is more serious. 3, aortic valve degenerative changes aortic valve leaflets are mucus-like changes, tissue thin and translucent, can not tolerate the diastolic pressure in the aorta and produce closure insufficiency. It is commonly seen in syphilitic aortitis, Marfan’s syndrome, mid-aortic necrosis, senile degenerative changes, and other causes of ascending aortic aneurysms. Because the aortic valve is severely off and the pulse pressure in the peripheral arteries is significantly widened, the left ventricle is hemodynamically heavily volume loaded and therefore enlarged to the left, downward, and backward, and both left ventriculography and echocardiography show a significantly enlarged left ventricular cavity and heavy aortic regurgitation. The contrast agent flows back and forth in the left ventricle and ascending aorta with a long residence time and cannot be emptied rapidly. 4. Bacterial endocarditis leading to aortic valve lesions Bacterial endocarditis often destroys aortic valve leaflet tissue, producing redundancy, perforation, or tearing in the valve leaflet. Therefore, clinically, aortic valve lesions caused by bacterial endocarditis often manifest as aortic valve insufficiency. Because of the short duration of the disease, the hemodynamic changes are rapid, making it difficult for the left ventricle to tolerate the sudden increase in volume load. In addition, the redundant organisms may be dislodged and produce embolism of the arteries of the body circulation.