Reversed septal motion in congenital corrected transposition of the great arteries: A potential mechanism for tricuspid regurgitation.

Pang, Kunjing; Xing, Jiayi; Xu, Nan; Zhang, Li; Zhang, Tingting; Liu, Rui; Wang, Rong; Li, Shoujun · J Thorac Cardiovasc Surg · 2025

retrospective_cohort · Level III

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Abstract

The mechanisms underlying anatomic tricuspid regurgitation in congenitally corrected transposition of the great arteries remain unclear. This study investigated the association between interventricular septal motion and tricuspid regurgitation severity. Echocardiographic data from 406 patients with congenitally corrected transposition of the great arteries were retrospectively analyzed and stratified by tricuspid regurgitation grade (≥3 vs ≤2) at the initial evaluation. Interventricular septal motion was categorized as normal, reversed, or bidirectional. Patients who underwent pulmonary artery banding and those with tricuspid regurgitation grade 2 or less without prior surgery were analyzed as separate subgroups. Among 109 patients with tricuspid regurgitation grade 3 or greater, 91 (83.49%) had reversed interventricular septal motion, significantly higher than in the 2 or less group (6/297, 2.02%). In the pulmonary artery banding subgroup (n = 79), tricuspid regurgitation severity significantly decreased postprocedure (P < .001), accompanied by a shift in interventricular septal motion from reversed to normal (P < .001). In the no surgery group (n = 136), 14 patients (10.29%) developed progressive tricuspid regurgitation and right ventricular dilation secondary to the reversal of interventricular septal motion. Reversed interventricular septal motion was a strong predictor of severe tricuspid regurgitation (area under the curve, 0.77; P = .001) and independently associated with its development (hazard ratio, 28.35; P < .001). Reversed interventricular septal motion is significantly associated with severe tricuspid regurgitation in congenitally corrected transposition of the great arteries and may act as both a mechanistic contributor and a predictive marker of disease progression.

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