Baseline Values and Sotalol-Induced Changes of Ventricular Repolarization Duration, Heterogeneity, and Instability in Patients With a History of Drug-Induced Torsades de Pointes

The authors investigated whether computerized parameters quantifying ventricular repolarization delay, heterogeneity, and instability characterize individuals who developed drug‐induced Torsades de Pointes. Assessing an individual's propensity to Torsades de Pointes when exposed to a QT‐prolong...

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Bibliographic Details
Published in:	Journal of clinical pharmacology 2009-01, Vol.49 (1), p.6-16
Main Authors:	Couderc, Jean-Philippe, Kaab, Stefan, Hinterseer, Martin, McNitt, Scott, Xia, Xiaojuan, Fossa, Anthony, Beckmann, Britt M., Polonsky, Slava, Zareba, Wojciech
Format:	Article
Language:	eng
Subjects:	Anti-Arrhythmia Agents - adverse effects electrocardiogram Electrocardiography Female Humans Male Middle Aged QT interval sotalol Sotalol - adverse effects Torsades de Pointes Torsades de Pointes - chemically induced Torsades de Pointes - physiopathology Ventricular Dysfunction - chemically induced Ventricular Dysfunction - physiopathology
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Summary:	The authors investigated whether computerized parameters quantifying ventricular repolarization delay, heterogeneity, and instability characterize individuals who developed drug‐induced Torsades de Pointes. Assessing an individual's propensity to Torsades de Pointes when exposed to a QT‐prolonging drug is challenging because baseline QT prolongation has limited predictive value. Five‐minute digital 12‐lead electrocardiograms were acquired at baseline and after a sotalol challenge in 16 patients who had a history of Torsades de Pointes in the context of a QT‐prolonging drug and 17 patients who did not have such history. Computerized measurements of QTc, T peak to T end intervals (TpTe), TpTe/QTc, and QT variability were implemented, and novel quantifiers of ventricular repolarization heterogeneity from the early (ERD) and late (LRD) part of the T wave were investigated. Compared with electrocardiograms of patients without a history of Torsades de Pointes, the baseline electrocardiograms of patients with a history of Torsades de Pointes had a longer QTc and an increased repolarization heterogeneity of the early part of the T wave (ERD30%: 44 ± 13 vs 35 ± 8 ms, P = .02). On sotalol, the electrocardiograms from individuals with Torsades de Pointes revealed a delay of the terminal part of the T wave that was not present in patients without Torsades de Pointes (TpTe: 27 ± 40 vs −1 ± 21 ms, P = .02; LRD70%: 20 ± 29 vs 2 ± 4 ms, P = .04). Results suggest that the electrocardiogram abnormalities characterizing patients with a history of Torsades de Pointes are (1) an increased repolarization heterogeneity at baseline and (2) a sotalol‐induced prolongation of the terminal part of the T wave.
ISSN:	0091-2700 1552-4604