Patients with aortic valve insufficiency can remain clinically asymptomatic for an extended period of time, but cardiac function often tends to decline. Once patients with aortic valve insufficiency develop significant clinical symptoms, the condition deteriorates dramatically and heart failure rapidly develops, with the ejection fraction of the heart falling to 30％ to 40％ in most patients, or even losing the opportunity for surgical treatment in more severe cases. Aortic valve insufficiency often arises from rheumatic heart disease combined with other valve pathologies, degenerative changes in the aortic valve, congenital aortic valve malformations, aortic valve pathologies combined with other congenital heart diseases, and infective endocarditis. Mitral valve insufficiency can also be caused by mitral valve annular relaxation due to left ventricular enlargement. Because of the long duration of the disease and slow progression of the lesion, these patients usually have no clinical symptoms and often seek medical attention because of rapid deterioration of cardiac function due to triggers such as colds, fatigue, and strenuous activity. Therefore, regardless of the long course of chronic aortic valve insufficiency or the acute onset of chronic aortic valve insufficiency, it is difficult to determine a good timing for surgery until significant clinical symptoms appear. Only when finally the aortic valve insufficiency reaches a very severe level, when the cardiac aspect shows significant clinical symptoms, when the left ventricular pressure and volume exceed the load producing a significant progressive left ventricular dilatation, resulting in an enlarged left ventricle and a significant decrease in cardiac output, the patient has to undergo surgery, which poses a great risk for surgical treatment and postoperative recovery. In these cases, the end-diastolic volume of the left ventricle can be greater than 300 ml, and the ejection fraction fluctuates from 0.3 to 0.4, which puts the patient in the category of “critical valve disease” and makes surgical intervention extremely risky. It has been demonstrated that these patients should undergo surgery with satisfactory results, probably due to their increased left ventricular end-diastolic volume. Although the patient’s postoperative ejection fraction values are also only between 0.3 and 0.48, the per-pulse volume of the giant left ventricle secures the blood supply to the vital organs of the body, especially the liver and kidneys. In particular, aortic valve replacement and mitral valvuloplasty resulted in good closure of the aortic and mitral valves, which in turn led to a decrease in pulmonary artery systolic pressure to some extent, and patients felt very satisfied with the improvement of their clinical symptoms. The combined mitral valve insufficiency is mostly caused by enlargement of the mitral annulus. In determining the surgical principle, on the one hand, considering that the patient needs the integrity of the left ventricular subvalvular structures to support the huge left ventricle, and on the other hand, the mitral valve annulus enlargement resulting in insufficiency of closure has the possibility of shaping, valvuloplasty and implantation of mitral valve shaping ring should be performed, and those with aortic valve closure insufficiency combined with mitral valve closure insufficiency receive aortic valve replacement and mitral valve shaping with very satisfactory results. In conclusion, for those with simple aortic valve closure insufficiency, if the left ventricle is significantly enlarged or progressively enlarged within a short period of time, or if the ejection fraction is low, active surgery should be performed even if there are no clinical symptoms; and for those with clinical symptoms of aortic valve closure insufficiency, active surgery should be performed even if the ejection fraction is low. Otherwise, once congestive heart failure occurs, it is difficult to save the patient and the mortality rate is extremely high.