Key result
Intravenous and oral amiodarone therapy induced torsade de pointes in a patient with dilated cardiomyopathy, suggesting different proarrhythmic mechanisms depending on the route of administration.
Case Report (n=1)
No
This case highlights that amiodarone can induce proarrhythmias like Torsade de Pointes when administered both intravenously and orally, potentially through different mechanisms.
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May warrant ECG monitoring with amiodarone in DCM regardless of route; single case leaves open route-specific proarrhythmic mechanisms.
A 70-year-old woman with dilated cardiomyopathy and ventricular tachyarrhythmia was initially treated in 1990 with intravenous amiodarone (240 mg). She developed a junctional escape rhythm (48 beats/min) with QT prolongation (QT: 0.68 s) and 8 h later developed torsade de pointes (TdP). Because other antiarrhythmic drugs did not suppress the arrhythmia, oral amiodarone (100 mg/day) was started in 1995, 7 weeks before she presented with congestive heart failure. The QT prolongation (QTc: 0.64) increased after administration of dopamine, and TdP again developed. This case suggests that amiodarone induces proarrhythmias by different mechanisms when administered intravenously or orally.
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Yamada et al. (2001) conducted a case report in Dilated cardiomyopathy and ventricular tachyarrhythmia (n=1). Amiodarone was evaluated on Development of Torsade de Pointes (TdP). Intravenous and oral amiodarone therapy induced torsade de pointes in a patient with dilated cardiomyopathy, suggesting different proarrhythmic mechanisms depending on the route of administration.
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