Abstract 4146885: Association of Structural Remodeling and Mitral Annular Disjunction with Significant Premature Ventricular Contraction Burden in Patients with Mitral Valve Prolapse: A Cardiac Magnetic Resonance Imaging Study

Background: Mitral annular disjunction (MAD) is identified by a displacement of the posterior mitral valve annulus into the left atrial wall and is commonly coexisting with mitral valve prolapse (MVP). MAD and MVP are both associated with a high prevalence of premature ventricular complexes (PVCs); however, the underlying mechanisms of increased PVC burden in these patients are unknown. We sought to determine the association between PVC burden, structural heart changes, and late gadolinium enhancement (LGE) in patients with MVP, with and without MAD. Methods: We analyzed patients with MVP who underwent cardiac magnetic resonance (CMR) imaging and 24-48hr Holter monitoring from 2020 to 2024. Patients with prior myocardial infarction or ischemic pattern LGE were excluded. LGE was characterized dichotomously as present or absent. Multivariate logistic regression was performed to assess significant independent associations with PVC burden > 5%. Results: The study included 107 patients (mean age 53.2 ± 17.6 years old, female (65%), mean LVEDVi 99cc/m 2 , mean LVEF 58±8%, mean mitral regurgitant fraction 23±16%). There were 56 patients with MAD + MVP and 51 with MVP - MAD. PVCs > 5% were noted in 26% of the cohort, and LGE was present in 32%. MAD was present in 52%, and 14% had mitral regurgitant fraction >40%. Multivariate analysis identified MAD and sex-specific LV dilation as independent predictors of significant PVC burden. Mitral regurgitant fraction showed a trend towards significance, while LGE was not significantly associated with PVC burden >5% (Figure 1). Conclusions: PVC burden > 5%, MAD, and LGE were prevalent in patients with MVP referred for CMR evaluation. MAD and left ventricular (LV) dilation were independently associated and more strongly predictive of high PVC burden than LGE. Future studies are needed to investigate further structural mechanisms and potential interactions with myocardial fibrosis impacting electrical activity in patients with MVP.