TRIO score for risk stratification of 12-month mortality after transcatheter tricuspid valve intervention

Background Risk stratification after transcatheter tricuspid valve intervention (TTVI) remains challenging, as prognosis is driven by systemic congestion and multiorgan dysfunction rather than residual regurgitation alone. Biomarkers reflecting systemic stress (GDF-15), hepatorenal dysfunction (MELD-XI), and right-sided hemodynamics (right atrial [RA] pressure) have individually shown prognostic relevance, but have not been integrated into a unified model. Purpose To derive and assess the discriminatory performance of the TRIO Score integrating RA pressure, MELD-XI, and GDF-15 for prediction of 12-month mortality after TTVI. Methods In a prospective single-centre cohort, 131 consecutive patients undergoing TTVI were included. Baseline assessment comprised invasive right heart catheterisation and laboratory testing. The primary endpoint was all-cause mortality at 12 months. The TRIO Score was derived from a multivariable logistic regression model integrating RA pressure, MELD-XI, and GDF-15. Discrimination was assessed by ROC analysis (AUC with 95% confidence intervals). Survival was additionally analysed using Kaplan–Meier estimates across TRIO tertiles. Results Median age was 82 years; 44% were female, and PASCAL was the predominant device used, Table 1. During 12-month follow-up, 22 patients (16.8%) died. The TRIO model demonstrated strong discrimination for 12-month mortality (AUC 0.829, 95% CI 0.726–0.931; p<0.001), Figure 1. Discriminatory performance of the individual components was lower: GDF-15 AUC 0.789 (0.670–0.909; p<0.001), RA pressure AUC 0.708 (0.588–0.828; p=0.005), and MELD-XI AUC 0.665 (0.512–0.819; p=0.021). Mortality increased stepwise across TRIO tertiles, with highest risk observed in the upper tertile (log-rank p<0.001). Conclusion The TRIO Score demonstrated strong discrimination and clinically meaningful risk stratification for 12-month mortality after TTVI, integrating right-sided hemodynamics, organ dysfunction, and systemic stress signalling.