Regional differences in the right ventricular activation and repolarization patterns between Brugada patients and controls

Abstract Background Brugada Syndrome (BrS) is an electrophysiological disorder affecting the right ventricular outflow tract (RVOT). The two leading theories of BrS pathophysiology suggest that arrhythmogenesis arises from either repolarization or depolarization dispersion within the RVOT. Currently, there are few studies characterizing the electrophysiological substrate of BrS in detail, particularly those that compare findings with control groups. Recent studies utilizing endocardial high-density electroanatomical mapping (HDEAM) have identified potential risk markers by analyzing activation time (AT), activation-recovery interval (ARI), and low-voltage mapping. Purpose This study retrospectively analyzed data from endocardial HDEAM to quantify repolarization and depolarization dispersion between the RVOT and right ventricular free wall (FW) in a cohort of BrS patients with spontaneous type-1 ECG pattern, comparing these findings to a control cohort of healthy individuals. Methods Both patients and control subjects underwent RV endocardial HDEAM using the CARTO 3 system (Biosense Webster Inc.), with a linear multipolar DecaNav catheter. Six controls and eight patients were selected for analysis. Patient data were exported in MATLAB using openEP and processed off-line using in-house code. Unipolar signals were filtered at 80 Hz and discarded if their amplitude was below common voltage criteria (4mV for unipolar, 1.5mV for Bipolar). For each subject, the RV anterior wall was divided into RVOT and FW using the location of the tricuspid valve as reference (see Fig. 1). Electrograms were then grouped by recording site and used to evaluate the median AT and ARI in the respective region. The dispersion of AT and ARI was quantified as the difference of the median values in the RVOT minus FW (ΔAT and ΔARI, respectively). Results In 12 out of 14 subjects, ARI was significantly shorter in the RVOT than in the FW, while in 13 out of 14 subjects, AT was significantly longer in the RVOT than in the FW. No significant difference was found between patients and controls for median AT or ARI in either the FW (3.5 vs -6 ms, p = 0.15 for AT; 351 vs 322 ms, p = 0.32 for ARI) or the RVOT (25 vs 24.5 ms, p = 0.72 for AT; 292 vs 279 ms, p = 0.57 for ARI). However, BrS patients exhibited a significantly greater ΔAT compared to controls (29 vs 24 ms, p=0.04), while ΔARI showed no significant difference ( -50 vs -48 ms, p = 0.88), refer to Fig. 2. Conclusion Our findings indicate a significant dispersion of activation time (AT) between the RVOT and FW in BrS patients with spontaneous pattern compared to controls, with no significant difference observed in ARI. Further investigation may reveal additional HDEAM features that could enhance understanding of the electrophysiological substrates in BrS.Figure 1:division of maps into regions Figure 2:dispersion of ARI and AT