The mortality rate of surgical treatment depends on the patient’s hemodynamic and clinical condition, especially the left ventricular function as well as the liver, kidney and lung function and the proficiency of the surgical team. In most medical research centers, the mortality rate for mitral valve replacement in patients with predominantly mitral valve closure alone is between 2% and 7%, and the mortality rate for repair is even lower, at 1% to 2%. Most patients can have improved clinical symptoms and quality of life after surgery, with reduced pulmonary hypertension, reduced heart size and left ventricular weight, and significantly improved survival compared with medical therapy, but in patients with a long preoperative history and poor cardiac function, the postoperative improvement in cardiac function is less satisfactory than after mitral stenosis and aortic valve replacement. In conclusion, patients who underwent surgery for mitral regurgitation had a lower survival rate than those who underwent surgery for mitral stenosis. However, observational studies have found that undergoing surgical treatment at any time improves long-term survival. Notably, survival rates were not only higher in patients with class I and II cardiac function at the time of surgery than in those with severe preoperative symptoms, but also did not differ from the survival rates expected for the corresponding age and sex in the total population. The most common cause of death after surgical correction of mitral regurgitation is abnormal left ventricular function due to long-term irreversible myocardial damage. The incidence of postoperative congestive heart failure increases with time (38% at year 10 in postoperative survivors), and most (2/3) are often postoperative residual left ventricular functional abnormalities. Valvular or surgical functional abnormalities explain heart failure in nearly one-third of patients. Postoperative congestive heart failure has a poor prognosis and should be prevented whenever possible, including early correction of mitral regurgitation. In the majority of patients who have undergone successful valve replacement, the decline in EF may be due to a combination of several factors: preoperative myocardial damage due to volume overload; persistent myocardial damage that sometimes occurs intraoperatively; and postoperative changes in load status, with a reduced afterload of left ventricular ejection in mitral valve insufficiency, which increases after surgery compared with the original, and a significantly lower preload after surgery compared with the preoperative In addition, the change of papillary muscle annular connection after removal of subvalvular device during valve replacement also affects the improvement of left ventricular function, and the application of vasodilators is effective in improving cardiac function and increasing EF. Foreign studies on the relationship between pre- and postoperative LV function and between pre-operative LV function and postoperative survival suggest that EF may be reduced by nearly 10% in the early postoperative period after valve replacement. However, there are significant individual differences, and a greater reduction in postoperative EF may also be seen in those patients with significantly increased LV end-systolic diameter, volume, or wall stress, or those with severe symptoms, prolonged mitral regurgitation, or concomitant coronary artery disease. The best surgical results are seen in patients who are asymptomatic or minimally symptomatic and whose EF is not less than 60%. A significant reduction in preoperative EF (<50%) is associated with higher mortality in the late postoperative period, and even EFs at critical status (50% to 60%) are accompanied by increased mortality in the late period. Thus, preoperative EF is a useful independent predictor of postoperative and survival. Nevertheless, surgical treatment of these patients is advocated, as surgical treatment will still provide a better prognosis than pharmacological treatment.