Cocaine induced prolongation of the QT interval.

P rolongation of the QT interval is a serious electrocardiogram finding because of its association with torsades de pointes and sudden cardiac death. Both congenital and acquired factors can lead to abnormal lengthening of the QT interval. Six types of congenital long QT syndrome (LQT1– LQT6) have been described, each involving mutations in genes encoding potassium or sodium transmembrane channel proteins. Acquired causes of QT prolongation include hypokalaemia, hypomagnesaemia, hypocalcaemia, human immunodeficiency virus infection, and myocardial ischaemia. Numerous drugs have also been found to cause prolongation of the QT interval. A listing of these drugs can be found on a web site (http://www.qtdrugs.org). The main membrane channel these drugs affect is the human ether-a-go-gorelated gene (HERG) encoded potassium channel; congenital mutations involving this gene lead to the LQT2 type of the inherited long QT syndromes. 5 Cocaine use has been associated with many cardiac complications including ventricular arrhythmias and sudden death, 7 and cocaine induced torsades de pointes in patients with idiopathic long QT syndrome has been described in two case reports. 9 A case report of cocaine induced QT prolongation (in the absence of congenital long QT syndrome) was published in 1997. In a study of 45 patients (with a history of chest pain, somnolence, or disorientation) admitted to the hospital after cocaine use, Gamouras et al showed that the QT interval was increased in patients with and without chest pain and that those with chest pain had greater QT prolongation. Cocaine and its metabolites, like many other substances shown to prolong the QT interval, have been shown to block HERG encoded potassium channels.