Prompt recognition of drug-induced QT prolongation and TdP, along with discontinuation of the offending agent and magnesium infusion, is central to avoiding poor outcomes.
Drug discontinuation plus magnesium remain essential for drug-induced TdP; leaves open need for prospective prevention trials in polypharmacy.
QT interval prolongation can be caused by several drugs. Torsade de pointes (TdP) is a form of ventricular proarrhythmia associated with QT interval prolongation, and in some cases, the development of U waves. The mechanism of TdP is believed to be related to an abnormality of repolarization in the ventricular myocardium and the development of early afterdepolarizations. QT prolongation leading to TdP can be caused by antiarrhythmic drugs (primarily class IA and III drugs), as well as a variety of other drugs. These other classes of drugs include phenothiazines, tricyclic antidepressants, antihistamines, antibiotics, antifungal agents, and antianginals. The recognition of a patient profile at increased risk for the development of TdP can help the patient avoid this drug-related complication. Treatment of TdP depends on the correct identification of the problem and discontinuation of the agent causing TdP, as well as correction of metabolic abnormalities, increase in the resting heart rate, and infusion of magnesium. Prompt diagnosis and treatment of this condition are central to avoid poor outcome.
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Fu et al. (1998) studied this question.
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