Cellular basis and mechanism underlying normal and abnormal myocardial repolarization and arrhythmogenesis

Abstract

Regional differences in repolarization characteristics of distinct cell types are responsible for the inscription of the J wave and T wave of the electrocardiogram (ECG). Amplification of these electrical heterogeneities contributes to the development of a variety of cardiac arrhythmias. This brief review examines the ionic and cellular basis for these heterogeneities and their role in the Brugada and long-QT syndromes. Both cases involve an accentuation of transmural dispersion of repolarization (TDR). In the case of the Brugada syndrome. TDR is accentuated as a result of a preferential abbreviation of the right ventricular epicardial action potential, whereas in the long-QT syndrome, accentuation of TDR is secondary to a preferential prolongation of the action potential of the M cell.