Calcification of the aortic valve restricts the activity of the valve cusps due to calcium deposition at the base of the valve, causing stenosis of the aortic valve orifice, resulting in dyspnea, angina, fainting and other hazards. 1. Dyspnea: aortic stenosis leads to progressive elevation of left ventricular end-diastolic pressure, which increases left atrial afterload. Long-term increase in left atrial load will lead to successive increase in pulmonary venous pressure, pulmonary capillary mold pressure and pulmonary artery pressure, resulting in exertional dyspnea, and paroxysmal nocturnal dyspnea, sedentary respiration, and even acute pulmonary edema with the development of the disease. 2. Angina pectoris: aortic stenosis, resulting in thickening of the left ventricular wall, elevated ventricular systolic pressure and prolonged ejection time, increasing myocardial oxygen consumption; diastolic intracavitary pressure increases, compression of the subendocardial coronary artery, resulting in myocardial underperfusion, angina pectoris caused by the above reasons, often induced by exercise, can be relieved by resting and nitroglycerin intake. 3. syncope: aortic stenosis, decreased cardiac output, insufficient cerebral blood supply, syncope. The occurrence of aortic valve calcification is related to hypertension, dyslipidemia, diabetes mellitus and smoking, etc. If you have any of the above high-risk factors, it is recommended that you have regular review of your cardiac ultrasound to detect the problem early and intervene at an early stage.