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Ibutilide, like dofetilide, slows cardiac depolarization by blockade of the rapid component (IKr) of the delayed rectifier potassium current. Activation of slow inward sodium current has also been suggested as an additional mechanism of action potential prolon-gation. After intravenous administration, ibutilide is rapidly cleared by hepatic metabolism. The metabolites are excreted by the kidney. The elimination half-life averages 6 hours.
Intravenous ibutilide is used for the acute conversion of atrial flutter and atrial fibrillation to normal sinus rhythm. The drug is more effective in atrial flutter than atrial fibrillation, with a mean time to termination of 20 minutes. The most important adverse effect is excessive QT-interval prolongation and torsades de pointes. Patients require continuous ECG monitoring for 4 hours after ibutilide infusion or until QTc returns to baseline.
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