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Updated: Jul 4, 2026

Chronic Ovine Model of Right Ventricular Failure and Functional Tricuspid Regurgitation
Published on: March 17, 2023
Severe tricuspid regurgitation is a congestion-driven cardiorenal disease: A longitudinal study defining a right
Layal Mansour1, Prayuth Rasmeehirun1, Guillaume L'Official1
1Université de Rennes, CHU Rennes, Service de Cardiologie Inserm, LTSI - UMR 1099, Rennes, France.
Background:
Severe tricuspid regurgitation (TR) is increasingly recognized as a major determinant of outcomes, yet its mechanistic trajectory under contemporary medical therapy remains insufficiently defined.
Objectives:
To characterize the longitudinal evolution of severe TR managed conservatively and to define a reproducible congestion-right ventricle-renal phenotype associated with clinical outcomes.
Methods:
We conducted a longitudinal observational cohort including 40 consecutive patients with at least severe TR. Serial assessments at baseline and 6, 12, 18, and 24 months included clinical status, echocardiography, biomarkers, and treatment data. The primary endpoint was a composite of heart failure hospitalization or all-cause death. Associations between right ventricular (RV) function, NT-proBNP, diuretic intensity, and renal function were evaluated.
Results:
Patients were elderly (78.5 ± 5.5 years), predominantly female, with atrial functional TR (95%) and atrial fibrillation (93%). Persistent congestion was observed throughout follow-up, with sustained high-dose diuretic use (≥80 mg/day in 57.5% at baseline, remaining stable over time). Renal function declined progressively (eGFR 50.2 ± 10 to 43.5 ± 11 mL/min/1.73 m2; p < 0.01), while NT-proBNP increased significantly (median ∼ 1700 to >3000 pg/mL; p < 0.01). During longitudinal follow-up, recurrent heart failure events and progressive renal impairment were frequently observed. Renal impairment and diuretic intensity were independently associated with adverse outcomes. Strong correlations linked RV dysfunction, biomarker activation, diuretic burden, and renal decline.
Conclusions:
Severe TR follows a structured, congestion-driven trajectory linking venous congestion, RV dysfunction, renal impairment, and clinical events. This study defines a reproducible cardiorenal phenotype and supports earlier, mechanism-based intervention strategies.
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