Genetics of acquired long QT syndrome
Dan M. Roden, Prakash C. Viswanathan
Dan M. Roden, Prakash C. Viswanathan
Published August 1, 2005
Citation Information: J Clin Invest. 2005;115(8):2025-2032. https://doi.org/10.1172/JCI25539.
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Review Series

Genetics of acquired long QT syndrome

Abstract

The QT interval is the electrocardiographic manifestation of ventricular repolarization, is variable under physiologic conditions, and is measurably prolonged by many drugs. Rarely, however, individuals with normal base-line intervals may display exaggerated QT interval prolongation, and the potentially fatal polymorphic ventricular tachycardia torsade de pointes, with drugs or other environmental stressors such as heart block or heart failure. This review summarizes the molecular and cellular mechanisms underlying this acquired or drug-induced form of long QT syndrome, describes approaches to the analysis of a role for DNA variants in the mediation of individual susceptibility, and proposes that these concepts may be generalizable to common acquired arrhythmias.

Authors

Dan M. Roden, Prakash C. Viswanathan

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Figure 5

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Mechanisms of sudden death with HERG blockade. Drug blockade of the HERG...
Mechanisms of sudden death with HERG blockade. Drug blockade of the HERG channel (left) produces prolongation (blue) and an EAD (red) in the cardiac action potential. These changes, which are heterogeneous across the ventricular wall, generate QT interval prolongation and, through mechanisms described further in the text, torsade de pointes (right; upper panel). In this example, the arrhythmia degenerates to ventricular fibrillation (VF).