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ST elevation is a pivotal finding in Brugada syndrome. There has been debate for a long time as to whether the ST elevation results from a depolarization abnormality or a repolarization abnormality.1 According to the repolarization abnormality hypothesis, the pathophysiology of Brugada syndrome is due to a morphologic change of the epicardial action potential and transmural dispersion of the repolarization. On the other hand, according to the depolarization abnormality hypothesis, the ST elevation is due to a voltage gradient induced by delayed epicardial conduction. Delayed potentials, which are a marker of a depolarization abnormality, usually cannot be recorded on the endocardial surface but can be recorded on the ventricular epicardium in patients with Brugada syndrome.2 In 2011, Nademanee and colleagues3 reported that epicardial mapping in patients with frequent ventricular fibrillation (VF) episodes revealed abnormal delayed potentials existing on the epicardial surface of the right ventricular outflow tract (RVOT). Radiofrequency catheter ablation of the area with abnormal potentials eliminated the typical Brugada-type ST elevation and prevented the occurrence of VF.3, 4, 5 The results of ablation have indicated that ST elevation and arrhythmogenicity in high-risk patients are closely associated with epicardial abnormal potentials. Epicardial mapping and ablation are invasive methods and their application is now limited to high-risk patients with recurrent VF episodes.3, 4, 5, 6 However, in asymptomatic patients with Brugada syndrome, the existence and role of delayed potentials in the appearance of a type 1 electrocardiogram (ECG) have not been reported. We here report the results of epicardial mapping in an asymptomatic patient with Brugada syndrome who received enucleation surgery of an intracardiac tumor.

Open chest epicardial mapping in an asymptomatic patient with Brugada syndrome