Introduction: Shock-induced vulnerability and defibrillation have been mostly studied in structurally normal hearts. However, defibrillation therapy is normally applied to patients with diseased hearts, frequently those with prior myocardial infarction (MI). Shock-induced vulnerability and defibrillation have not been well studied under this condition. We sought to examine the mechanisms of shock-induced arrhythmogenesis and arrhythmia maintenance in a rabbit model of healed MI (4 weeks or more post-infarction). Methods and Results: Ligation of the left circumflex artery midway between the apex and the base of the ventricle was performed 53 ± 21 days before acute experiments. Shock-induced vulnerability was assessed in the infarcted (n=8) and structurally normal (n=8) hearts by delivering internal monophasic shocks at different shock strengths and delivery phases. Electrical activities from the anterior epicardium during shock application and during shock-induced arrhythmias were optically recorded and quantitatively analyzed. Ligation resulted in a transmural left ventricular free wall infarction mainly located at the apical region with a consistent endocardial border zone (BZ) as confirmed by histologic studies. There were significant increases in the incidence, severity and duration of shock-induced arrhythmias in the infarcted hearts versus controls due to: 1) Post-shock break-excitation wavefronts that frequently originated near the infarction BZ; 2) The existence of an infarction BZ that created an anatomic reentry pathway and facilitated arrhythmia maintenance. Conclusions: Infarction BZ contributes to both increased shock-induced arrhythmogenesis and arrhythmia maintenance in the rabbit model of healed MI.