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 <.01). This increase inverted the APD gradient between RV and LV. By contrast, the increase in RT was significantly higher in the LV than in the RV (3.37 ± 1.84 vs. 2.80 ± 2.11ms, p <0.05). According to our results, Flecainide leads to inhomogeneous modification of electrophysiological properties of the heart and may therefore produce heterogeneities likely to initiate and/or maintain a fibrillatory process.