More than 90% of sudden cardiac deaths (SCD) is caused by coronary artery disease (CAD) with arterial stenosis greater than 75%. The pathophysiology bases of SCD - often the first manifestation of CAD – are malignant arrhythmias (ventricular tachycardia and ventricular fibrillation). Until 10 years ago, the investigation of ventricular arrhythmogenesis, in order to predict the arrhythmogenic potential and prevent SCD, was focused to QT and QTc (corrected QT intervals) and QT and QTc (corrected QT) dispersion (QTd, QTcd). (1-3) In this context, the prolonged QT interval was accepted as an indicator of extended repolarization time, and increased QT dispersion was considered a reflection of spatial differences in myocardial repolarization. Recently, research of ventricular arrhythmogenesis has been increasingly focused on two newer electrocardiographic (ECG) indicators: Tp-e (T peak-to-end) interval and Tp-e/QT ratio. According to the latest findings, these ECG indicators are the reflection of transmural heterogenicity of repolarization, i.e. the differences in voltage between the individual layers of the same segment of the ventricle wall. Their changes are accepted as a promising indicator of arrhythmogenic potential in patients with several cardiovascular diseases, such as prolonged (congenital or acquired) QT syndrome, short QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy, acute coronary syndrome and chronic stable CAD. This presentation will provide basic insights into the electrophysiological background of the Tp-e interval and the Tp-e/QT ratio with particular attention to their changes in CAD patients in which restoration of blood supply normalizes exercise-induced repolarization abnormalities, suggesting that revascularization of a previously ischemic myocardium lowers its arrhythmogenic potential.