Key points are not available for this paper at this time.
Design
Review
May inform genetic risk stratification before QT-prolonging drugs; leaves open prospective validation for clinical adoption.
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.
No takes yet. Share an insight, caveat, or question.
D M Roden (2005) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: