Spatial Distribution of Repolarization and Depolarization Abnormalities Evaluated by Body Surface Potential Mapping in Patients with Brugada Syndrome

BACKGROUND: Mutations in sodium channel gene, SCN5A, have been identified in Brugada syndrome, but it is still unclear as to how sodium channel dysfunction relates to arrhythmogenesis. We examined spatial distribution of both repolarization and depolarization abnormalities in patients with Brugada syndrome by using 87-leads body surface potential mapping (BSPM). METHODS: BSPM was recorded under baseline condition and after pharmacological interventions in 28 patients with Brugada syndrome (27 males, 49 +/- 14 years). The ST-segment amplitude 20 ms after the end of QRS (ST20), QRS duration, and corrected recovery time (RTc) were measured in all 87-leads, and averaged among 6-leads (D-F, 5-6) reflecting right ventricular outflow tract (RVOT) potentials and the other 81-leads. RESULTS: The ST20 was elevated at baseline, normalized by isoproterenol, and augmented by pilsicainide in only the RVOT. The RTc was longer at baseline and increased by pilsicainide in only the RVOT. On the other hand, the QRS duration was slightly widened at baseline, further increased by pilsicainide, but not changed by isoproterenol in both leads. CONCLUSIONS: The ST-segment elevation and the RTc prolongation were localized and modulated by agents only in the RVOT region, while the slight QRS widening at baseline and further increase by pilsicainide were observed homogeneously. Our data suggest that depolarization abnormalities are distributed homogeneously, whereas repolarization abnormalities are localized in the RVOT.