Background: Na channel blockade has a long history used for the treatment of symptomatic ventricular premature contractions and tachycardia. However, the Cardiac Arrhythmia Suppression Trial (CAST) in patients with old myocardial infarction showed that class-I antiarrhythmic drugs have proarrhythmic effects, resulting in poor prognoses. So far, the arrhythmogenic mechanisms by the Na channel blockade are not well-known. Methods: To clarify this issue, we conducted simulations of action potential propagation in a myofiber model incorporating the electric field mechanism (taking into account the intercellular cleft potentials). Since it is recently reported that Na channels are confined to intercalated discs of surviving myocytes (lack of Na channels in lateral cell membrane) in the ischemic border zone, we incorporated the intracellular remodeling of Na channels into the model. Results: We found that the intracellular remodeling of Na channels in myocytes located at ischemic border zone contributed to conduction slowing. In addition, conduction block tended to occur in the ischemic border zone when numerically administered Na channel blockade to the myofiber model, but this was not the case when the Na channels were distributed over the entire cell membrane. Conclusion: Ischemia-induced intracellular remodeling of Na channels might be partly responsible for the proarrhythmic effects of Na channel blockade in patients with old myocardial infarction.