Passive electrical remodeling following myocardial infarction (MI) is well established. These changes can alter electrotonic loading and trigger the remodeling of repolarization currents, a potential mechanism for ventricular fibrillation (VF). However, little is known about the role of passive electrical markers as tools to identify VF-susceptibility post-MI. This study investigated electrotonic remodeling in the post-MI ventricle, as measured by myocardial electrical impedance (MEI), in animals prone to and resistant to VF. MI was induced in dogs by a two-stage left-anterior descending (LAD) coronary artery ligation. Before infarction, MEI electrodes were placed in remote (left-circumflex, LCX) and infarcted (LAD) myocardium. MEI was measured in awake animals 1, 2, 7, and 21 days post-MI. Subsequently, VF-susceptibility was tested by a 2-min LCX occlusion during exercise; 12 animals developed VF (susceptible, S) and 12 did not (resistant, R). The healing infarct had lower MEI than the normal myocardium. This difference was stable by day 2 post-MI (287 ± 32 vs. 425 ± 62, P<0.05). Significant differences were observed between resistant and susceptible animals 7 days post-MI: susceptible dogs had a wider electrotonic gradient between remote and infarcted myocardium (R: 89 ± 60 vs. S: 180 ± 37). This difference increased over time in susceptible animals (252 ± 53 at 21-days), due to post-MI impedance changes on the remote myocardium. These data suggest that early electrotonic changes post-MI could be used to assess later arrhythmia susceptibility. In addition, passive-electrical changes could be a mechanism driving active-electrical remodeling post-MI, thereby, facilitating the induction of arrhythmias.