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Numerous advancements in the treatment of acute myocardial infarction (MI), from reperfusion therapy to coronary care units, have markedly reduced 30-day patient mortality. Despite optimal therapy, a significant proportion of patients remain at high risk for sudden cardiac death (SCD), particularly in the first 6 months.1 The absence of herald symptoms and the catastrophic outcomes from arrhythmia-related SCD have led to the investigation of the prophylactic role of implantable cardioverter-defibrillators (ICDs) following acute MI. Two large-scale, randomized clinical trials (DINAMIT, IRIS) of early ICD implantation failed to demonstrate a benefit in all-cause mortality, despite a reduction in arrhythmia-related deaths.2,3 These studies highlight that despite the availability of an effective therapy for the prevention of SCD, we still lack the clinical risk-stratifying tools to identify patients at highest risk who may benefit from ICD therapy.

Unlike other post-infarct complications that are related to the extent of myocardial injury and left ventricular (LV) systolic failure, the development of arrhythmia-related SCD often occurs in patients with medium-to-small infarcts.4 Electrophysiological studies (EPS) have implicated heterogeneity of depolarization and dispersion of repolarization within the border zones of the infarcted myocardium as key substrates in arrhythmia-related SCD.5 It is postulated that these ‘peri-infarct zones’ (PIZs) represent an admixture of fibrotic and viable cardiomyocytes that provide a necessary electrophysiological setting for precipitation of fatal arrhythmias.

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