Abstract 4367898: Mechanisms and Anatomical Localization of Left Atrioventricular Valve Regurgitation Following Atrioventricular Canal Defect Repair Using Two- and Three-Dimensional Echocardiography

Abstract

Background: Left atrioventricular valve regurgitation (LAVVR) after atrioventricular canal (AVC) defect repair remains a significant contributor to morbidity and mortality, and often requires reintervention. While previous studies have assessed leaflet morphology and papillary muscle anatomy, limited data exist on the typical mechanisms and anatomic locations of LAVVR in this population. Understanding these factors may inform surgical strategies and improve long-term outcomes. Hypothesis: Two- and three-dimensional echocardiography can characterize the anatomical location and mechanism of significant LAVVR in patients with repaired AVC defects. Methods: Single center, retrospective analysis of patients who underwent echocardiography following AVC repair. 2D and 3D echocardiography were used to evaluate severity, location, and mechanism of LAVVR. LAVVR was characterized as significant if graded as moderate or greater by color Doppler. Anatomic sites and mechanisms were compared between groups. Inter-modality agreement was assessed using Cohen’s Kappa. Results: Echocardiography was performed in 299 patients and 109 (36.4%) demonstrated significant LAVVR. Evaluated patients had complete (76.6%), transitional (9.7%), or incomplete (13.7%) AVC. Based on LAVVR severity, there was no differences in AVC type, Rastelli classification, age or trisomy 21 prevalence. Complete cleft closure and annuloplasty were more frequent in the non-significant LAVVR group. Significant LAVVR more commonly involved the cleft (p<0.001) and region of coaptation between the inferior bridging and mural leaflets (IBL-ML) (p=0.009). Multivariable analysis identified these sites independently increased risk (OR: cleft 3.13, IBL-ML 7.47, p<0.01, Figure 1). Mechanisms of LAVVR were often multifactorial. Restriction or deficiency of neo-anterior and ML, recurrent/residual cleft, dilated LAVV annulus and atrial/ventricular dilation remained significant after adjusting for surgical techniques (Table 1). 2D vs. 3D showed moderate agreement in mechanism identification (κ=0.278–0.629), but lower concordance for location. Conclusion: Clinically significant LAVVR after AVC repair is frequently associated with specific anatomic locations and mechanisms of regurgitation. 3D echocardiography can provide additional insight into these features. Our novel findings enhance the understanding of a significant source of morbidity in this vulnerable patient population.