Arrhythmias in Brugada: Syndrome Defective Depolarization, Repolarization or Both?

摘要

In the Global EP Rounds of this issue of JACC: Clinical Electrophysiology, Sarcon et al. (1) present a case of Brugada syndrome (BS) as an opportunity for a group of experts to debate the relative merits of the depolarization hypothesis versus the repolarization hypothesis. The depolarization hypothesis posits that structural factors in BS, such as localized fibrosis in the right ventricular (RV) epicardium (and sometimes endo- or mid-myocardium), cause fractionated electrograms (EGs), reflecting slow conduction that predispose the affected areas to re-entry and ventricular fibrillation in BS, especially when inward Na or Ca currents are suppressed. This scenario is supported by the efficacy of targeted radiofrequency ablation of fractionated EGs at suppressing arrhythmias in BS. The repolarization hypothesis, on the other hand, posits that early repolarization in regions of the RV epicardium expressing high densities of the transient outward current (Ito) lead to phase 2 re-entry. When concealed, phase 2 re-entry manifests as fractionated EGs, and when overt, phase 2 re-entry initiates ventricular arrhythmias. The effectiveness of radiofrequency ablation is explained by the extensive ablation of RV epicardial sites to the point that the tissue mass required for Ito-dependent early repolarization to initiate phase 2 re-entry is inadequate.