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American heart journal · Jun 2007
ReviewCurrent concepts in the mechanisms and management of drug-induced QT prolongation and torsade de pointes.
- Akshay Gupta, Andrew T Lawrence, Kousik Krishnan, Clifford J Kavinsky, and Richard G Trohman.
- Department of Internal Medicine, Section of Cardiology, Rush University Medical Center, Chicago, IL 60612, USA.
- Am. Heart J. 2007 Jun 1;153(6):891-9.
AbstractDrug-induced long QT syndrome is characterized by a prolonged corrected QT interval (QTc) and increased risk of a polymorphic ventricular tachycardia known as torsade de pointes (TdP). We review mechanisms, predispositions, culprit agents, and management of this potentially fatal phenomenon. Virtually all drugs that prolong QTc block the rapid component of the delayed rectifier current (I(kr)). Some drugs prolong QTc in a dose-dependent manner, others do so at any dose. Most patients that develop drug-induced TdP have underlying risk factors. Female sex is the most common. Implicated drugs include class 1A and III antiarrhythmics, macrolide antibiotics, pentamidine, antimalarials, antipsychotics, arsenic trioxide, and methadone. Treatment for TdP includes immediate defibrillation for hemodynamic instability and intravenous magnesium sulfate. Potassium levels should be maintained in the high normal range, and all QT prolonging agents must be promptly discontinued.
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