Vol 15, No 2 (2008)
Review Article
Published online: 2008-02-21
Drug-induced spatial dispersion of repolarization
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)
Keywords: LQT syndromeBrugada syndromespatial dispersion of repolarizationchannelopathies