A progressively increasing number of cardiac and noncardiac drugs prolong the ventricular action potential duration(QT interval of the electrocardiogram)and cause a distinctive polymorphic ventricular tachycardia termed torsades de pointes(TdP)that can degenerate into ventricular fibrillation and sudden cardiac death.Drugs prolong the QT interval and cause TdP by blocking cardiac K⁺ channels in general and selectively blocking the rapidly activating delayed rectifier channel I_Kr.Coassembly of HERG(human−ether−ago−go−related gene)α−subunits and MiRP1(MinK−related peptide 1)β−subunits recapitulate the behavior of native human I_Kr and mutations of HERG and MiRP1 decrease the repolarizing current, delay ventricular repolarization and prolong the QT.Thus, drug−induced QT prolongation and TdP might represent an iatrogenic reproduction of the congenital LQTS.In patients with silent forms of the congenital LQTS associated with mutations in I_Kr, arrhythmic symptoms developed almost exclusively after exposure to QT−prolonging drugs.This review centers on the possible cellular mechanisms underlying drug−induced QT prolongation and TdP, the description of specific drugs and risk factors facilitating the development of TdP, and the recommendations for preventing and treating this potentially fatal arrhythmia.