Subthreshold delayed afterdepolarizations provide an important arrhythmogenic substrate in the border zone of infarcted hearts

Sudden cardiac arrest resulting from myocardial infarction (MI) is most often due to ventricular tachycardia (VT). In the infarcted heart, VT has been shown to originate at the periphery of the scar1. Such tissue is often termed the infarct border zone (BZ) and is comprised of a heterogeneous admixture of fibrosis and surviving cardiomyocytes2. Extended regions of BZ tissue that penetrate through non-conducting necrotic core scar can give rise to anatomical isthmuses which provide slow conducting re-entrant pathways that can help sustain VT circuits3.