The main pathophysiological alteration of mitral regurgitation is to increase the diastolic load of the left atrium, which in turn also increases the diastolic load of the left ventricle. This is because during left ventricular systole, blood flow is simultaneously injected from the left ventricle into the higher pressure aorta (whose pressure corresponds to the systolic pressure, i.e., the high pressure when blood pressure is measured, which normally has 90-140 mm Hg) and the less resistant left atrium (which normally has a pressure of only a few mm Hg). This pressure contrast makes the left atrium a pressure-suspended, absolute low-pressure cavity, the place of runoff. So even if there is only a tiny little gap in the mitral valve, blood will enter the left atrium as a result. The amount of blood that regurgitates into the left atrium can vary, and the return flow into the left atrium can be more than half of the total blood discharge from the left ventricle. The left atrium receives blood from the left ventricle in addition to the blood that would normally return from the four pulmonary veins. Therefore, there is an increase in pressure in the left atrium, which in turn causes an increase in pressure in the pulmonary veins and pulmonary capillaries, causing them to dilate and stagnate, an increase in the diastolic volume load of the left ventricle, a series of pathological changes such as enlargement of the left ventricle and pulmonary hypertension, leading to clinical manifestations of heart failure and arrhythmias.