Pulmonary arterial compliance independently predicts mortality after transcatheter tricuspid valve edge-to-edge repair

Background In severe tricuspid regurgitation (TR), right ventricular (RV) dysfunction and pulmonary hypertension (PH) drive adverse outcomes after transcatheter tricuspid valve edge-to-edge repair (T-TEER). RV-pulmonary arterial (RV-PA) coupling is a key prognostic marker; however, pulmonary arterial compliance (PAC) reflects pulsatile RV afterload and integrates pulmonary vascular load with RV–PA interaction and may therefore provide additional prognostic value. Purpose To define the clinical and hemodynamic profile associated with reduced PAC and to evaluate the prognostic value of PAC ≤2.0 mL/mmHg in patients undergoing T-TEER. Methods This retrospective two-center study included 389 patients with significant TR undergoing T-TEER. PAC was invasively calculated as stroke volume divided by pulmonary artery pulse pressure. Patients were stratified according to PAC >2.0 versus ≤2.0 mL/mmHg. Two-year survival was analyzed using Kaplan–Meier estimates and multivariable Cox regression adjusted for age, sex, comorbidities, procedural success, and RV-PA coupling expressed as the ratio of tricuspid annular plane systolic excursion to pulmonary artery systolic pressure (TAPSE/PASP). Results Reduced PAC was present in 191 patients (49%). These patients were older, more frequently female, and had higher NT-proBNP levels. Echocardiography showed higher pulmonary pressures and impaired RV-PA coupling (TAPSE/PASP 0.34 vs. 0.42 mm/mmHg; p<0.001), while left-ventricular function and TR severity were similar. Invasive hemodynamics revealed a distinct adverse profile with higher pulmonary artery pressures, pulmonary vascular resistance (3.3 vs. 1.9 WU), and transpulmonary gradient, together with lower stroke volume (46 vs. 61 mL) and cardiac index (1.9 vs. 2.2 L/min/m²; all p<0.001). Procedural success and residual TR did not differ between groups. During follow-up, 99 deaths occurred; PAC ≤2.0 mL/mmHg was associated with reduced survival (log-rank p=0.001) and predicted mortality (HR 1.69; 95% CI 1.06–2.68; p=0.026), independent of other prognostically relevant covariates, including TAPSE/PASP. Conclusions In patients undergoing T-TEER, reduced PAC identifies a high-risk hemodynamic phenotype characterized by increased pulmonary vascular load and impaired RV-PA interaction. Procedural success after T-TEER is comparable between patients with and without impaired PAC. PAC provides incremental prognostic information beyond RV-PA coupling and may refine risk stratification in this high-risk population.