Abstract
Brugada syndrome is an increasingly recognized cause of sudden cardiac arrest, defined by characteristic electrocardiogram (ECG) findings and features suggesting a direct or family history of ventricular tachyarrhythmias.1 However, the mechanisms for arrhythmogenesis remain controversial. Animal studies suggest that the ECG “Brugada sign” reflects loss of action potential dome in the epicardium but not in the endocardium, enabling extra beats (from phase 2 reentry) to interact with transmural repolarization dispersion to initiate reentry.
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