Genetics of acquired long QT syndrome.
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.
Roden
Dan M
DM
Department of Medicine, Oates Institute for Experimental Therapeutics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. dan.roden@vanderbilt.edu
Viswanathan
Prakash C
PC
D000818:Animals; D000072237:ERG1 Potassium Channel; D051638:Ether-A-Go-Go Potassium Channels; D020022:Genetic Predisposition to Disease; D006801:Humans; D008133:Long QT Syndrome / Q000209:etiology* / Q000235:genetics* / Q000378:metabolism; D024642:Potassium Channels, Voltage-Gated / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors; D012737:Sex Factors; D016171:Torsades de Pointes / Q000209:etiology* / Q000235:genetics* / Q000378:metabolism
D000072237:ERG1 Potassium Channel; D051638:Ether-A-Go-Go Potassium Channels; D024642:Potassium Channels, Voltage-Gated