Abstract
Elektrocardiographic abnormalities and cases of sudden death are associated with the use of antipsychotic drugs in patients with schizophrenia. Explanations for such deaths have traditionally focused on drug-induced prolongation of the QT interval leading to the development of life-threatening ventricular arrhythmias such as torsade de pointes.
This review discusses potential mechanisms urderlying QTc prolongation and arrhythmogenesis and examines the evidence for a relationship between antipsychonic druts and prolongation of the QTc interval. New elecrophysiological and epidemiological data are presented which suggest there may not be a clear-cut cause-effect relationship between QTc prolongation and the development of ventricular tachyarrhythmias for all atypical antipsychotics.
For at least one of these agents (sertindole), counterbalancing mechanisms may act to reduce the risk of proarrhythmic activity arising as a result of QTc prolongation.