Christian Besler

Background: Transcatheter tricuspid edge‐to‐edge repair (T‐TEER) has developed as a treatment option for patients experiencing severe tricuspid regurgitation. T‐TEER consistently reduces tricuspid regurgitation, but data on subsequent right heart remodeling remain limited. The aim of this study was to evaluate changes in right heart dimension and function after T‐TEER using extended echocardiographic follow‐up. Methods: The study was based on the international EuroTR (European Registry of Transcatheter Repair for Tricuspid Regurgitation), including patients undergoing T‐TEER between 2016 and 2024 at 18 European centers. Eligible were patients with available baseline and follow‐up (≥90 days postprocedure) echocardiographic assessment. Results: A total of 699 patients (mean age, 78±8 years; 56% women) were included in the analysis. Echocardiographic follow‐up was performed at a median of 407 days (interquartile range, 205–801 days). Right heart dimensions significantly decreased: right ventricular (RV) midventricular diameter from 40.2±8.9 to 37.1±8.4 mm ( P 2 ( P P P <0.001) was observed. Conclusions: In the subset of surviving patients with available echocardiographic follow‐up, treatment with T‐TEER led to favorable long‐term changes with reduced RV dimension, associated with procedural success. RV function modestly decreased, likely reflecting normalization after volume unloading.

BACKGROUND: The impact of proportionality to heart valve regurgitation has been widely investigated in mitral regurgitation, helping to better characterize the best candidates for therapies. However, it has never been studied in tricuspid regurgitation (TR). The aim of the present study is to investigate the impact of the proportionality of TR on outcomes. METHODS: Patients undergoing tricuspid transcatheter edge-to-edge repair were selected from the TRIVALVE registry (International Multisite Transcatheter Tricuspid Valve Therapies Registry). Patients were divided according to the ratio between effective regurgitant orifice area (EROA) and right ventricular (RV) end diastolic diameter (RVEDD) into tertiles: patients with low EROA/RVEDD (RV, dominant); intermediate EROA/RVEDD (RV and TR, RV-TR, codominant), and high EROA/RVEDD (TR, dominant). The primary outcome was all-cause mortality. Median follow-up was 9.7 months (4.2–12.0). RESULTS: A total of 204 patients were included in the present study: 67 for the RV dominant, 68 for the RV-TR codominant, and 69 for the TR dominant group. The 3 groups presented different baseline characteristics. Survival analysis among the 3 groups showed a trend towards worse prognosis for the RV-dominant group, as compared with the RV-TR codominant and TR dominant groups. CONCLUSIONS: The conceptual framework of proportionality is applicable to TR with EROA/RVEDD, defining a higher risk RV-dominant phenotype with a trend towards worse survival after tricuspid transcatheter edge-to-edge repair.

Tricuspid regurgitation (TR) rarely exists as an isolated condition and is most frequently secondary due to heart failure (HF), or atrial fibrillation, with prevalent extracardiac comorbidities. Morphological assessment of the anatomy and severity of TR, together with evaluation of symptoms, currently drives interventional approaches, yet a more holistic integration of causal and contributing comorbid conditions might further improve outcomes. The present review explores such a pathophysiology-driven holistic approach to interpret functional changes and symptomatic burden in patients with TR. It focuses on acknowledging the dynamic nature of TR, but most importantly, the bidirectional crosstalk between TR and HF, as well as other organ systems that might drive symptoms and prognosis, but also TR progression. Assessment of TR is ideally performed after optimizing the treatment of interfering comorbidities and correcting volume overload to isolate the true effects of the TR itself. Invasive haemodynamic assessment, portal vein Doppler, and liver stiffness measurements may offer useful information in clinical decision-making. When TR is identified as the primary driver of disease, or if it is strongly interacting with concomitant diseases, more aggressive therapeutic approaches may be pursued. In contrast, when it is more a consequence of the underlying HF, the right expectations in terms of symptomatic improvement and prognosis should be set. This framework may help to identify patients who are the most likely to benefit from TR interventions, while acknowledging the complexity of their clinical picture in the context of HF.