Ventricular tachyarrhythmias are the most common cause of sudden cardiac death (SCD); a healed myocardial infarction increases the risk of SCD. We determined the contribution of specific repolarization abnormalities to ventricular tachyarrhythmias in a post-infarction model of SCD. Methods: We used a post- infarction canine model of SCD, where an exercise and ischemia test was used to stratify animals as either susceptible (VF+) or resistant (VF-) to sustained ventricular tachyarrhythmias. Results: No changes in global left ventricular contractility or volumes occurred after infarction. At 8-10 weeks post-MI, myocytes were isolated from the LV mid-myocardial wall and studied. In the VF+ animals, myocyte action potential (AP) prolongation occurred at 50% and 90 % repolarization (p<0.05) and was associated with increased variability of AP duration and afterdepolarizations. Multiple repolarizing K⁺ currents (I_Kr, I_to) and inward I_K1 were also reduced (p<0.05) in myocytes from VF+ animals compared to control, non-infarcted dogs. In contrast, only I_to was reduced in VF- myocytes compared to controls (p<0.05). While afterdepolarizations were not elicited at baseline in myocytes from VF- animals, afterdepolarizations were consistently elicited after the addition of an I_Kr blocker. Conclusions: A loss of repolarization reserve via reductions in multiple repolarizing currents in the VF+ myocytes, leads to action potential prolongation, repolarization instability, and afterdepolarizations in myocytes from animals susceptible to sudden cardiac death. These abnormalities may provide a substrate for initiation of post-MI ventricular tachyarrhythmias.