A New ECG Biomarker for Drug Toxicity: a Combined Signal Processing and Computational Modeling Study

Overview

Journal Annu Int Conf IEEE Eng Med Biol Soc

Specialty Biomedical Engineering

Date 2010 Nov 25

PMID 21096447

Citations 4

Authors

Xiao Jie

Blanca Rodriguez

Esther Pueyo

Affiliations

Soon will be listed here.

Abstract

QT prolongation is the only clinically proven, yet insufficient, electrocardiogram (ECG) biomarker for drug-induced cardiac toxicity. The goal of this study is to evaluate whether JT area, i.e., total area of the T-wave, can serve as an ECG biomarker for drug-induced cardiac toxicity using both signal processing and computational modeling approaches. An ECG dataset that contained recordings from patients under control and sotalol condition was analyzed. In order to relate sotalol-induced ECG changes to its effect on ion channel level, i.e., blockade of the rapid component of the delayed rectifier potassium channel (I(Kr)), varied degrees of I(Kr) blockade were simulated in a slab of ventricular tissue. The mean JT area increased by 36.5% following the administration of sotalol in patients. Simulations in the slab tissue showed that sotalol increased action potential duration preferentially in the midmyocardium, which led to increased transmural dispersion of repolarization and JT area. In conclusion, JT area reflects the transmural dispersion of repolarization and may be a potentially useful surrogate/supplemental ECG biomarker to assess drug safety.

Citing Articles

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Torsadogenic Drug-induced Increased Short-term Variability of JT-area.

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