The incidence of late tricuspid valve insufficiency after left heart valve (mitral and aortic valve) replacement is common. The incidence of late tricuspid valve insufficiency after left heart valve replacement is about 27%, and a recent study at our hospital showed that it is 31%. Repeat surgery has a high perioperative and late mortality rate, so prevention of late tricuspid valve insufficiency after left heart valve surgery is clinically important. In view of this, understanding the risk factors for the development of late tricuspid valve insufficiency at the time of the first left valve replacement surgery is valuable in making surgical treatment decisions to prevent its occurrence. The pathogenesis of tricuspid valve insufficiency in mitral valve disease is complex and multifactorial. Tricuspid valve insufficiency is often functional and results primarily from right ventricular dilatation and dysfunction and from dilatation of the tricuspid annulus. Mitral valve pathology leads to left atrial enlargement and left atrial pressure increase followed by atrial fibrillation, which leads to right atrial enlargement and tricuspid annulus dilation; mitral valve pathology leads to left atrial pressure increase, which leads to pulmonary hypertension, which leads to right ventricular dysfunction and dilation and leads to tricuspid annulus dilation and papillary muscle displacement. After left valve replacement surgery with the release of mitral valve lesions, pulmonary artery pressure decreases, theoretically the right ventricular afterload decreases, the right ventricle remodels, the tricuspid annulus does not continue to expand, and tricuspid valve closure insufficiency should be reduced or disappear. However, the incidence of late tricuspid valve closure insufficiency or exacerbation of the original tricuspid valve closure insufficiency after left heart valve surgery is still high, and the mechanism may be as follows: 1. The enlarged tricuspid annulus and right ventricular insufficiency are more closely related to functional tricuspid valve closure insufficiency, and once the tricuspid annulus is enlarged, the tricuspid annulus cannot automatically return to normal size after left heart valve replacement, and the tricuspid annulus continues to expand, resulting in an Tricuspid valve closure insufficiency is aggravated. When left valve replacement is performed, tricuspid annulus diameter exceeding 33 mm significantly increases tricuspid insufficiency after left valve replacement [16]. In such patients, tricuspid valvuloplasty should be performed at the same time as left heart valve replacement. 2, Atrial fibrillation is a risk factor for late tricuspid valve closure insufficiency after left valve replacement. The cases in our present study were all combined with atrial fibrillation, and the study showed that atrial fibrillation with rapid ventricular rate significantly increased the incidence of late tricuspid valve closure insufficiency after left valve replacement. The reasons for this may be the loss of atrial contraction in late diastole; completely irregular ventricular rhythm too fast and too short cardiac cycles that limit ventricular filling; in addition, rapid atrial fibrillation can cause cardiomyopathy. 3, Late tricuspid valve closure insufficiency is significantly higher in those with mitral valve plus aortic valve replacement than in those with mitral valve replacement alone. The specific reason for this phenomenon is unclear, and it may be that the prosthetic valve implanted after left heart valve replacement affects the cardiac fibrous skeleton geometry, and that the effect on the cardiac fibrous skeleton is greater after double valve replacement than in those with mitral valve replacement alone. In conclusion, left heart valve replacement in patients with atrial fibrillation and double valve replacement is a risk factor for advanced tricuspid valve closure insufficiency. In patients presenting with advanced tricuspid valve closure insufficiency, the ventricular rate of atrial fibrillation was significantly faster in the postoperative period of 3 months. Therefore, ventricular rate control and improvement of cardiac function in cases with atrial fibrillation after left valve replacement should be the primary postoperative treatment.