Brugada syndrome is characterized by the ECGs with both a right bundle-branch block pattern and ST-segment elevation in the right precordial leads (V1-V3) and by the higher incidence of sudden cardiac death due to ventricular tachycardia/fibrillation. It is commonly believed that the lethal arrhythmias are elicited by the closely coupled premature ventricular contractions via the reflected conduction (i.e., phase-2 reentry) mechanism. Although loss of function mutation in cardiac sodium (Na) channels have been linked to Brugada syndrome, the relation between the loss of function in Na channels and the arrhythmogenic mechanism remains unclear. We have recently reported that the action potential propagation was greatly affected by the subcellular distribution of Na channels in a physiologically-accurate myofiber model where myocytes were electrically coupled with both gap junctions and intercellular cleft conductor (electric field mechanism). Here, we extended the simulation to the initiation of reflected conduction in Brugada syndrome. We conducted computer simulations of action potential propagation in the myofiber model, and investigated the effects of subcellular distributions of Na channels on the development of reflected conduction. We found that the myofiber model with specific subcellular Na channel distribution (all Na channels were distributed only in the intercalated disks and there were no Na channels along the lateral side of each myocyte) resulted in early repolarization followed by reflected conduction. Subcellular Na channel distribution might be responsible for fibrillation induction in Brugada syndrome.