IBUTILIDE
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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