Repolarization Heterogeneity and Ventricular Arrhythmias in Ischemia– Reperfusion

Abstract:

Augmented spatial heterogeneity of ventricular repolarization is considered to constitute an arrhythmogenic substrate that predisposes to malignant ventricular arrhythmias. Since acute myocardial infarction is inherently accompanied by increased repolarization dispersion, understanding the role of repolarization heterogeneity in arrhythmogenesis has clinical significance. This review aims to summarize experimental evidence on the genesis and electrocardiographic manifestations of repolarization dispersion, focusing specifically on electrophysiological markers associated with ventricular tachyarrhythmias in animal models of ischemia–reperfusion. Although the transmural repolarization gradient, along with apicobasal and interventricular gradients, was documented in intact hearts, its magnitude was significantly smaller than that of the inter-regional gradients, suggesting only a minor contribution to T wave genesis. Experimentally induced local myocardial ischemia increased global, apicobasal, and ischemia–border zone repolarization dispersions and was associated with prolongation of the Tpeak–Tend and corrected QT intervals, as well as increased T-wave amplitude dispersion. However, ventricular tachyarrhythmias were associated with increased duration of repolarization in the nonischemic zone rather than with repolarization dispersion, and this repolarization prolongation was reflected in the electrocardiogram as terminal T-wave inversion. In conclusion, ventricular arrhythmogenesis in ischemia–reperfusion is determined not only by spatial dispersion of repolarization but also by region-specific alterations in repolarization duration. ECG-derived markers, including morphological features, provide a noninvasive assessment of both repolarization dispersion and local repolarization duration abnormalities and therefore have the potential to improve risk stratification for malignant ventricular arrhythmias.