Key result
Severe tricuspid regurgitation in ARVC is linked to ~3.1-fold higher risk of sustained ventricular arrhythmias.
Why the study?
Although right ventricular remodelling is common in arrhythmogenic right ventricular cardiomyopathy (ARVC), the prevalence, mechanisms, and prognostic role of tricuspid regurgitation and tricuspid annular dilatation remain poorly defined.
Does tricuspid regurgitation severity and tricuspid annulus dilatation predict sustained ventricular arrhythmia and death in patients with definite arrhythmogenic right ventricular cardiomyopathy?
Cohort (n=514)
Yes
Does tricuspid regurgitation severity and tricuspid annulus dilatation predict sustained ventricular arrhythmia and death in patients with definite arrhythmogenic right ventricular cardiomyopathy?
In patients with definite ARVC, tricuspid regurgitation severity and tricuspid annulus dilatation are independent predictors of sustained ventricular arrhythmia and death, identifying high-risk patients even in the primary prevention setting.
Severe TR may refine arrhythmia risk stratification in ARVC; leaves open whether tricuspid interventions alter outcomes.
Background/Introduction Tricuspid regurgitation (TR) is associated with adverse outcomes. Although right ventricular remodelling is common in arrhythmogenic right ventricular cardiomyopathy (ARVC), the role of TR remains hardly defined. Purpose This study aimed to evaluate the prevalence, mechanisms, and prognostic significance of TR and tricuspid annular dilatation in patients with ARVC. Methods In this international cohort study the phenotype of definite ARVC patients was characterized by echocardiography, sustained ventricular arrhythmia (VA) and death were considered as outcomes, and Cox or logistic regression models were used for analysis. Results The study included 514 patients (mean age 46 years, 45% women), with 58% showing none/trivial, 29% mild, and 13% moderate/severe TR. TR mostly (89%) exhibited ventricular-secondary origin. Tricuspid annulus dilatation was an independent determinant of TR (OR 2.22, 95% CI: 1.83–2.75). During follow-up 5.1 years, 146 patients experienced VA and 42 died. TR severity and tricuspid annulus dilatation were independently associated with increased risk of either outcome (severe TR HR for VA 3.15, 95% CI 1.87–5.32; HR for death 21.81, 95% CI 9.67–49.23). Primary prevention patients (i.e. without prior VA) with moderate/severe TR or tricuspid annulus dilatation had VA-free survival similar to secondary prevention patients. Tricuspid annulus dilatation predicted VA or death independent of genotype, previous VA, TR severity, and RV or left ventricular strain. Its discriminatory power for VA in primary prevention patients tended to exceed that of RV strain (time-dependent ROC AUC 0.741, 95% CI 0.629–0.852; RV free-wall strain AUC 0.575, 95% CI 0.433–0.716). Conclusion TR occurs frequently in ARVC showing ventricular-secondary origin due to dilated tricuspid annulus. TR severity and annulus dilatation identify patients at higher risk irrespective of genotype, history of prior VA and right or left ventricular strain, with similar VA-free survival in primary and secondary prevention patients.figure_1figure_2
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Donati et al. (2026) conducted a cohort in Arrhythmogenic right ventricular cardiomyopathy (ARVC) (n=514). Severe tricuspid regurgitation and tricuspid annulus dilatation vs. None/trivial tricuspid regurgitation was evaluated on Sustained ventricular arrhythmia (VA) and death (HR 3.15, 95% CI 1.87-5.32). Severe tricuspid regurgitation in ARVC was independently associated with increased risk of sustained ventricular arrhythmia (HR 3.15; 95% CI 1.87-5.32) and death (HR 21.81; 95% CI 9.67-49.23).
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