Right atrial–right ventricular coupling drives decongestion and residual regurgitation after transcatheter tricuspid repair

Objectives Right atrial–right ventricular (RA–RV) coupling may represent the central mechanism linking atrial remodeling, ventricular adaptation, and systemic congestion in severe functional tricuspid regurgitation (TR). We investigated the longitudinal behavior and clinical significance of RA–RV coupling after transcatheter tricuspid edge-to-edge repair (T-TEER). Background Clinical recovery after T-TEER is heterogeneous and incompletely explained by residual TR severity or right ventricular–pulmonary arterial (RV–PA) coupling, suggesting that post-repair physiology extends beyond ventriculo-arterial interaction alone. Methods In 131 consecutive patients undergoing T-TEER (median age 77 years; 61% women), comprehensive echocardiography was obtained at baseline, pre-discharge, 6 months, and 12 months. RA–RV coupling was quantified by RV systolic function normalized to right-atrial size (primary: RV strain/RAVImax). RV–PA coupling served as comparator. Longitudinal mixed-effects models, ordinal regression for residual TR, and decongestion phenotyping were applied. Results RA–RV coupling exhibited a biphasic trajectory with early deterioration after repair followed by partial recovery, whereas RV–PA coupling showed weaker and less consistent dynamics. RA–RV indices demonstrated greater patient-level stability than RV–PA metrics. In multivariable longitudinal models, RA strain and RA–RV coupling independently tracked NT-proBNP trajectories, whereas RV–PA coupling did not. Impaired baseline RA–RV coupling predicted higher residual TR at 6 months and lower probability of combined biological and symptomatic decongestion. At 12 months, RA strain emerged as the dominant correlate of residual TR severity, consistent with progressive atrial substrate influence. Conclusions After T-TEER, recovery is governed predominantly by atrioventricular mechanical efficiency rather than ventriculo-arterial interaction alone. RA–RV coupling integrates atrial remodeling, ventricular adaptation, and systemic congestion, providing a mechanistic framework for phenotyping and risk stratification beyond TR reduction.