open access

Vol 15, No 2 (2008)
Review paper
Published online: 2008-02-21
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Drug-induced spatial dispersion of repolarization

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

open access

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

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)

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)
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Keywords

LQT syndrome; Brugada syndrome; spatial dispersion of repolarization; channelopathies

About this article
Title

Drug-induced spatial dispersion of repolarization

Journal

Cardiology Journal

Issue

Vol 15, No 2 (2008)

Article type

Review paper

Pages

100-121

Published online

2008-02-21

Bibliographic record

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

Keywords

LQT syndrome
Brugada syndrome
spatial dispersion of repolarization
channelopathies

Authors

Charles Antzelevitch

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