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Background: The influence of the etiology of mitral valve (MV) lesion on outcomes of concomitant repair for functional tricuspid regurgitation (TR) is not well studied.Our objectives were to compare long-term survival and TR recurrence after tricuspid valve (TV) repair concomitant with surgery for rheumatic versus degenerative MV disease.Methods: We included 480 patients who had concomitant MV and TV surgery from 2009 to 2019. We grouped the patients into Group 1 (n = 345; rheumatic MV) and Group 2 (n = 135; degenerative MV). Propensity score matching identified 104 matched pairs.Results: There was no significant difference in survival between groups before

Background and Aim of the Study The outcome of mitral valve (MV) repair for chronic ischemic mitral regurgitation (IMR) is suboptimal, due to the high recurrence rate of moderate or severe mitral regurgitation (MR) during follow‐up. The MV adapts to new MR increasing its area to cover the enlarged annular area (mitral plasticity). As this process is often incomplete, we aimed to evaluate if augmenting the anterior leaflet (AL) and cutting the second‐order chords (CC) together with restrictive mitral annuloplasty, a strategy we call “surgical mitral plasticity,” could improve the midterm results of MV repair for IMR. Materials and Methods From November 2017 to October 2019, 22 patients with chronic IMR underwent surgical mitral plasticity. Mean age was 73 ± 7 years and six were female. Mean ejection fraction was 32% ± 11%, IMR grade was moderate in 10 and severe in 12. Mean clinical and echocardiographic follow‐up was 12 ± 6 months. Results There was no early death, and one patient died 6 months after surgery. Ejection fraction improved from 32% ± 15% to 40% ± 6% (P = .031). IMR was absent or mild in all patients, and none showed recurrent moderate or more IMR. Tenting area decreased significantly from 2.5 ± 0.5 to 0.5 ± 0.3 cm² and coaptation length increased from 1.9 ± 0.7 to 7.8 ± 1.6 mm. All patients were in New York Heart Association class I or II. Conclusions Mitral plasticity, if uncomplete, is ineffective in preventing IMR to become significant. Surgical mitral plasticity, by completing incomplete process of MV adaptation, has a strong rationale, which however needs to be validated with longer follow‐up.

Vitamin K antagonist therapy was not superior to antiplatelet therapy to prevent thromboembolic complications after mitral valve repair. Our data suggest that oral anticoagulation may carry a higher bleeding risk compared with antiplatelet therapy, although these results should be confirmed in an adequately powered randomized controlled trial.