Background—We sought to identify preoperative predictors of clinical outcomes after surgery in patients with severe tricuspid regurgitation.

Methods and Results—We prospectively enrolled 61 consecutive patients (54 women, aged 57±9 years) with isolated severe tricuspid regurgitation undergoing corrective surgery. Twenty-one patients (34%) were in New York Heart Association functional class II, 35 (57%) in class III, and 5 (9%) in class IV. Fifty-seven patients (93%) had previous history of left-sided valve surgery. Preoperative echocardiography revealed pulmonary artery systolic pressure of 41.5±8.7 mm Hg, right ventricular (RV) end-diastolic area of 35.1±9.0 cm², and RV fractional area change of 41.3±8.4%. The median follow-up duration after surgery was 32 months (range, 12 to 70). Six of the 61 patients died before discharge; thus, operative mortality was 10%. Three of the 55 patients who survived surgery died during follow-up, and 6 patients required readmission because of cardiovascular problems. Thus, 46 patients (75%) remained event free at the end of follow-up. In the 54 patients who underwent 6-month clinical and echocardiographic follow-up, RV end-diastolic area decreased by 29%, with a corresponding 26% reduction in RV fractional area change. Thirty-three patients (61%) showed improved functional capacity after surgery. On multivariable Cox regression analysis, preoperative hemoglobin level (P<0.001) and RV end-systolic area (P<0.001) emerged as independent determinants of clinical outcomes. On receiver operating characteristic curve analysis, we found that RV end-systolic area <20 cm² predicted event-free survival with a sensitivity of 73% and a specificity of 67%, and a hemoglobin level >11.3 g/dL predicted event-free survival with a sensitivity of 73% and a specificity of 83%.

Conclusions—Timely correction of severe tricuspid regurgitation carries an acceptable risk and improves functional capacity. Surgery should be considered before the development of advanced RV systolic dysfunction and before the development of anemia.