BACKGROUND: Secondary tricuspid regurgitation (TR) as a result of pulmonary hypertension and/or left-sided heart disease is caused by tricuspid valve (TV) annular dilatation and tethering of the tricuspid leaflet after right ventricular (RV) dilatation. However, the mechanism of isolated TR without significant pulmonary hypertension remains unknown. The present study investigated the RV function and TV deformations in patients with isolated TR to find out the mechanism and etiology of the disease. METHODS AND RESULTS: Twelve patients with isolated, severe TR were included. RV area, volume, ejection fraction (EF), tenting distance and tenting area were measured. These parameters were compared with 12 age-and gender-matched controls and 12 patients with secondary TR. The cause of isolated TR was incomplete coaptation associated with annular dilatation without other problems. Compared with the controls, RV end-diastolic volumes and annular diameters were significantly larger and RVEF was significantly lower in patients with isolated TR. Tenting area and tenting distance were also significantly higher. However, there were no significant differences in these parameters between patients with isolated and secondary TR. CONCLUSIONS: Isolated TR was associated with RV remodeling, systolic dysfunction and resultant annular dilatation and tethering of tricuspid leaflets.
BACKGROUND: Secondary tricuspid regurgitation (TR) as a result of pulmonary hypertension and/or left-sided heart disease is caused by tricuspid valve (TV) annular dilatation and tethering of the tricuspid leaflet after right ventricular (RV) dilatation. However, the mechanism of isolated TR without significant pulmonary hypertension remains unknown. The present study investigated the RV function and TV deformations in patients with isolated TR to find out the mechanism and etiology of the disease. METHODS AND RESULTS: Twelve patients with isolated, severe TR were included. RV area, volume, ejection fraction (EF), tenting distance and tenting area were measured. These parameters were compared with 12 age-and gender-matched controls and 12 patients with secondary TR. The cause of isolated TR was incomplete coaptation associated with annular dilatation without other problems. Compared with the controls, RV end-diastolic volumes and annular diameters were significantly larger and RVEF was significantly lower in patients with isolated TR. Tenting area and tenting distance were also significantly higher. However, there were no significant differences in these parameters between patients with isolated and secondary TR. CONCLUSIONS: Isolated TR was associated with RV remodeling, systolic dysfunction and resultant annular dilatation and tethering of tricuspid leaflets.