Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair.
J, S., M, B., M, L., T, K., A, K., V, P., M, N., A, H.F., C, B., & C, E. (2026). Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair.. BMC cardiovascular disorders. https://doi.org/10.1186/s12872-026-06392-6
J S, M B, M L, T K, A K, V P, et al. Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair.. BMC cardiovascular disorders. 2026; doi: 10.1186/s12872-026-06392-6
J S, M B, M L, et al. Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair.[J]. BMC cardiovascular disorders. 2026. DOI: 10.1186/s12872-026-06392-6.
@article{j2026,
author = {Schlegl J and Bannehr M and Lichtenauer M and Kücken T and Krutz A and Paar V and Neuß M and Haase-Fielitz A and Butter C and Edlinger C},
title = {Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair.},
journal = {BMC cardiovascular disorders},
year = {2026},
doi = {10.1186/s12872-026-06392-6},
note = {PMID: 42547888},
}
TY - JOUR AU - Schlegl J AU - Bannehr M AU - Lichtenauer M AU - Kücken T AU - Krutz A AU - Paar V AU - Neuß M AU - Haase-Fielitz A AU - Butter C AU - Edlinger C TI - Biomarkers of systemic disease burden and outcomes after transcatheter tricuspid edge-to-edge repair. T2 - BMC cardiovascular disorders PY - 2026 DO - 10.1186/s12872-026-06392-6 AN - PMID:42547888 ER -
BACKGROUND: Risk stratification after transcatheter tricuspid edge-to-edge repair (T-TEER) remains challenging, particularly in patients with advanced right-sided heart failure and systemic disease burden. Biomarkers reflecting inflammation, stress response and multiorgan dysfunction may provide additional prognostic information in this setting. METHODS: This prospective single-centre cohort study included 84 consecutive patients undergoing T-TEER for severe tricuspid regurgitation using the TriClip or PASCAL system. Baseline concentrations of growth differentiation factor-15 (GDF-15), soluble urokinase plasminogen activator receptor (suPAR), and NT-proBNP were measured prior to intervention. The primary endpoint was all-cause mortality at 12 months. Secondary endpoints included cardiovascular rehospitalisation and a combined cardiovascular endpoint. Prognostic performance was assessed using receiver operating characteristic and tertile-based Kaplan-Meier analyses. Owing to the limited number of events, all analyses were considered exploratory. RESULTS: During 12-month follow-up, all-cause mortality occurred in 10 patients (11.9%), while cardiovascular rehospitalisation was observed in 29 patients (34.5%). GDF-15 demonstrated good discriminative performance for all-cause mortality (AUC 0.823, 95% CI 0.714-0.932, p = 0.001), whereas suPAR showed moderate prognostic discrimination (AUC 0.742, 95% CI 0.605-0.878, p = 0.013). In contrast, NT-proBNP showed no significant discrimination for all-cause mortality (AUC 0.535, 95% CI 0.362-0.709, p = 0.720). Higher tertiles of both GDF-15 and suPAR were associated with reduced overall and rehospitalisation-free survival. CONCLUSION: Baseline GDF-15 and suPAR were associated with adverse outcomes after T-TEER and demonstrated greater prognostic discrimination than NT-proBNP in this exploratory cohort. These exploratory findings support further investigation of systemic stress and inflammation biomarkers for risk stratification in patients with severe tricuspid regurgitation.