Inhomogeneous Modification of Cardiac Electrophysiological Properties due to Flecainide Administration

Brugada syndrome is characterized by a genetic mutation that leads to a reduction in sodium inward current in phase 0 of the cardiac action potential. However, electrophysiological abnormalities that underlie the phenotypical presentation of this disease remain unclear. The objective of this study was to characterize the spatial electrophysiological changes produced by a reduction in sodium current. Epicardial transmembrane voltage optical maps of 10 Wistar rat hearts isolated and perfused in a Langendorff system were analyzed. For each heart, mean transmembrane action potential duration (APD50) and action potential up-stroke rise time (RT) were measured in the right ventricle (RV) right ventricular outflow tract (RVOT) and left ventricle (LV). Measurements were obtained at baseline and after injection of Flecainide 10uM, a potent sodium channel blocker. Flecainide injection produced a significant increase in APD duration and in the RT at each region with respect to basal conditions. However, the increase in the duration of the APD was higher in the RV compared to the LV (17.34 ± 6.67ms vs. 7.09 ± 6.39ms, p