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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

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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 2

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Computed action potentials, using the Luo-Rudy simulation (94) modified ...
Computed action potentials, using the Luo-Rudy simulation (94) modified to include a transient outward current. This simulation incorporates physiologically realistic numerical models of individual ion currents and other electrogenic events (e.g., exchangers) and thereby allows in silico prediction of the effects of lesions in individual components on the whole physiologic system. A and B each show (from top to bottom) epicardial action potential, IKr and IKs during the epicardial action potential, midmyocardial action potential, IKr and IKs during the midmyocardial action potential, and an ECG signal computed from a 1-dimensional fiber consisting of endocardial, midmyocardial, and epicardial cells connected through resistive gap junctions (95). (A) Control. The numbered phases of the action potential are shown on the epicardial signal. Note the increase in IKr at the beginning of phase 3; as discussed in the text, this serves to enhance repolarization. The dotted lines indicate the ends of repolarization in the epicardial and midmyocardial cells and correspond roughly to the peak and end of the T wave, respectively. (B) 75% IKr blockade. Note that action potentials at both sites are prolonged, and the difference between them is exaggerated. The T wave abnormality in the computed ECG also reflects formation of EADs in endocardial cells (not shown).
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