Tricuspid regurgitation is closely related to functional ischemic mitral regurgitation. Up to 30% of patients with ischemic mitral regurgitation who underwent mitral valve repair developed significant tricuspid regurgitation, and 57% of these patients underwent mitral valve surgery to explore the tricuspid valve. Follow-up of 50% of patients who underwent mitral valve repair for functional mitral regurgitation revealed that significant tricuspid regurgitation occurred in 25% within 1 year, 53% between 1-3 years, and 74% over 3 years. The cause was mainly due to the altered geometry of the right and left ventricles accompanied by enlargement of the tricuspid annulus due to remodeling of the ischemic myocardium. Right ventricular pressure overload secondary to preexisting mitral valve disease can cause these pathophysiologic changes in right ventricular geometry and eventual tricuspid annular enlargement. Myocardial ischemia contributes to the development of tricuspid regurgitation; however, 16% of patients without ischemic mitral regurgitation who undergo mitral valve repair are still found to have 3+-4+ tricuspid regurgitation at 8-year follow-up. The incidence of tricuspid regurgitation in patients with functional mitral regurgitation who underwent mitral valve repair was not influenced by preoperative pulmonary hypertension or postoperative residual mitral regurgitation. On the other hand, preoperative tricuspid annular enlargement can be a predictor of late tricuspid regurgitation, and preoperative and postoperative follow-up has shown that patients with late tricuspid regurgitation have significantly enlarged tricuspid annular diameters. These patients are usually older and have chronic right ventricular pressure overload. In patients undergoing percutaneous transluminal balloon mitral valvuloplasty, the presence of preexisting tricuspid regurgitation is associated with a poor clinical outcome and poor prognosis, regardless of the success of the procedure. Excluding preexisting tricuspid regurgitation, late functional tricuspid regurgitation remains the most common incidental phenomenon after mitral stenosis. In patients undergoing mitral valve replacement for rheumatic mitral stenosis, the degree of tricuspid regurgitation is associated with the degree of mitral valve disease, pulmonary hypertension, the degree of preoperative tricuspid regurgitation, and signs of right heart failure. Wang et al studied the incidence of late tricuspid regurgitation after left heart valve surgery and found that 30% of patients had progressive tricuspid regurgitation (25.1% had significant tricuspid regurgitation), which can lead to increased morbidity and mortality in the early and late postoperative periods, and that pulmonary hypertension and tricuspid annular enlargement were significant risk factors for late tricuspid regurgitation. In addition, a significant number of clinical conditions are associated with the development of late secondary tricuspid regurgitation as independent risk factors, with the cycle of left heart valve disease from onset to surgical treatment being a standard risk factor, and left atrial enlargement with decreased systolic force suggesting increased right ventricular afterload and right ventricular remodeling. Atrial fibrillation, as a manifestation of atrial systolic dysfunction, can also lead to an increase in right ventricular afterload. These hemodynamic alterations in the right ventricle, together with structural and electrophysiological remodeling of both atria, contribute to the progression of right ventricular remodeling and tricuspid regurgitation. kim et al demonstrated that MAZE surgery combined with left heart valve surgery reduced the incidence and severity of tricuspid regurgitation. On the other hand, Song et al examined the relationship between atrial fibrillation and late tricuspid regurgitation based on previous studies and found that MAZE surgery was not associated with prognosis. The higher incidence of late tricuspid regurgitation in female patients may be due to their higher incidence of rheumatic mitral valve disease. As left heart valve damage leads to altered hemodynamics, rheumatic fever can lead to allodynia, and the right ventricle is prone to subclinical damage, malfunction, and altered geometry. De Bonis et al studied the progression of tricuspid regurgitation after mitral valve replacement in patients with functional mitral regurgitation, particularly dilated cardiomyopathy, and found that 18% of patients with preoperative TR ≤ 2+ who did not undergo intraoperative tricuspid valvuloplasty had progression of tricuspid regurgitation ≥ grade 2 at postoperative follow-up. Tricuspid regurgitation was more severe if preoperative tricuspid regurgitation and right ventricular dyskinesia were more severe. Consistent with previous studies, they noted enlargement of the tricuspid annulus as a potential mechanism and also found significant tricuspid leaflet strain due to right ventricular enlargement with closure depth >0.5 cm. natural history of dilated cardiomyopathy, right and left ventricular malfunction with heart failure, increased right ventricular afterload due to pulmonary hypertension, recurrence after functional mitral regurgitation repair, ICD and pacing lead implantation, and postoperative reversible remodeling reduction are all potential risk factors for tricuspid regurgitation.