Key result
Mitral annular disjunction acts as an arrhythmogenic substrate predisposing patients to ventricular arrhythmias.
Recognizing MAD may inform arrhythmia risk assessment in MVP; leaves open causal role and management implications pending prospective data.
Mitral annular disjunction (MAD) is increasingly recognized as an arrhythmogenic substrate associated with malignant ventricular arrhythmias and sudden cardiac death (SCD) (1,2). MAD commonly co-exists with mitral valve prolapse (MVP) but can also occur in isolation. Structural separation between the mitral annulus and left ventricular myocardium may promote mechanical stretch, myocardial fibrosis, and electrical instability, predisposing patients to premature ventricular complexes (PVCs), ventricular tachycardia (VT), and ventricular fibrillation (VF) (3).
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Ezzeddine et al. (2026) conducted a review in Mitral annular disjunction. Long-term continuous rhythm monitoring was evaluated. Mitral annular disjunction is recognized as an arrhythmogenic substrate predisposing patients to premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation.
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