Vol 15, No 2 (2008)
Review Article
Submitted: 2013-01-14
Published online: 2008-02-21
Drug-induced spatial dispersion of repolarization
Charles Antzelevitch
DOI: 10.5603/cj.21614
·
Cardiol J 2008;15(2):100-121.
Vol 15, No 2 (2008)
Review articles
Submitted: 2013-01-14
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)
Keywords
LQT syndrome; Brugada syndrome; spatial dispersion of repolarization; channelopathies
Title
Drug-induced spatial dispersion of repolarization
Journal
Cardiology Journal
Issue
Vol 15, No 2 (2008)
Article type
Review Article
Pages
100-121
Published online
2008-02-21
Page views
567
Article views/downloads
1138
DOI
10.5603/cj.21614
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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