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Prolongation of the QT interval is a serious electrocardiogram finding because of its association with torsades de pointes and sudden cardiac death.1 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.2
Acquired causes of QT prolongation include hypokalaemia, hypomagnesaemia, hypocalcaemia, human immunodeficiency virus infection, and myocardial ischaemia.2–4 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-go-related gene (HERG) encoded potassium channel; congenital mutations involving this gene lead to the LQT2 type of the inherited long QT syndromes.2,5
Cocaine use has been associated with many cardiac complications including ventricular arrhythmias and sudden death, …
Footnotes
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↵* QTc is the QT interval corrected for the patient’s heart rate. QTc = (QT)/(√ RR), where RR is the distance between consecutive R waves on the electrocardiogram.
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Conflicts of interest: none declared.