Key result
Diverse large animal TR models highlight the need for leaflet-preserving approaches to reproduce functional phenotypes.
This review highlights the limitations of current large animal models of tricuspid regurgitation and emphasizes the need for models that better replicate the pathophysiology of secondary TR for translational research.
Existing TR models overlook secondary forms from right heart remodeling; leaves open development of remodeling-based large animal models for translational research.
Despite growing interest in tricuspid regurgitation (TR), evidence remains insufficient to define the optimal timing of intervention and therapeutic strategies, highlighting the need for robust experimental models. Existing large animal models of TR use diverse approaches and can be grouped into two categories: direct valvular interventions targeting the tricuspid leaflets, annulus, or chordae, and indirect induction through mechanisms such as increased right ventricular loading, pulmonary hypertension, or pacing-induced tachycardia. Although direct valvular interventions can reproducibly induce TR and are well suited for modeling primary TR, clinically prevalent secondary TR is driven by annular dilation, leaflet tethering, and right-sided chamber remodeling rather than intrinsic valvular injury. This gap represents a major limitation in the field. In this review, we compare large animal models of TR and outline key considerations to guide model selection, with a focus on approaches that more faithfully reproduce the pathophysiology of TR for mechanistic and translational research.
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Sukienik et al. (2026) conducted a review in Tricuspid regurgitation. Large animal models was evaluated. Existing large animal models of tricuspid regurgitation use diverse approaches, highlighting a need for leaflet-preserving models that better reproduce ventricular and atrial functional phenotypes.
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