Vol 15, No 2 (2008)
Review Article
Published online: 2008-02-21

open access

Page views 628
Article views/downloads 1218
Get Citation

Connect on Social Media

Connect on Social Media

Drug-induced spatial dispersion of repolarization

Charles Antzelevitch
Cardiol J 2008;15(2):100-121.

Abstract

Spatial dispersion of repolarization in the form of transmural, trans-septal and apico-basal dispersion of repolarization creates voltage gradients that inscribe the J wave and T wave of the ECG. Amplification of this spatial dispersion of repolarization (SDR) underlies the development of life-threatening ventricular arrhythmias associated with inherited or acquired ion channelopathies giving rise to the long QT, short QT and Brugada syndromes (BrS). This review focuses on the role of spatial dispersion of repolarization in drug-induced arrhythmogenesis associated with the long QT and BrS. In the long QT syndrome, drug-induced amplification of SDR is often secondary to preferential prolongation of the action potential duration (APD) of M cells, whereas in the BrS, it is thought to be due to selective abbreviation of the APD of right ventricular epicardium. Among the challenges ahead is the identification of a means to quantitate SDR non-invasively. This review also discusses the value of the interval between the peak and end of the T wave (Tpeak-Tend, Tp-Te) as an index of SDR and transmural dispersion of repolarization, in particular. (Cardiol J 2008; 15: 100-121)

Article available in PDF format

View PDF Download PDF file