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Ibutilide: enhanced defibrillation via plateau sodium current activation
R C Wesley1, F Farkhani, D Morgan
1Division of Cardiology, Veterans Affairs Medical Center, Long Beach 90822.
The American Journal of Physiology
|April 11, 1993
Summary
Ibutilide, a type III antiarrhythmic, significantly reduced defibrillation energy and current needs in dogs. This agent also increased the ventricular effective refractory period and action potential duration, aiding defibrillation success.
Area of Science:
- Cardiology
- Pharmacology
- Electrophysiology
Background:
- Type III antiarrhythmic agents can reduce defibrillation energy requirements by blocking potassium channels.
- Ibutilide is a type III antiarrhythmic agent that prolongs action potential duration via sodium channel activation.
Purpose of the Study:
- To investigate the effect of ibutilide on defibrillation current and energy requirements.
- To assess ibutilide's impact on cardiac electrophysiological parameters.
Main Methods:
- Pentobarbital-anesthetized dogs underwent serial ventricular fibrillation episodes.
- Defibrillation requirements were determined using interactive and dose-response methods before and after ibutilide administration.
- Ventricular effective refractory period and action potential duration were measured.
Main Results:
- Ibutilide significantly reduced defibrillation current (10.9 vs. 14.1 A) and energy (16.0 vs. 27.7 J) compared to placebo.
- Ibutilide shifted the 50% successful defibrillation current dose from 14.8 A to 8.9 A.
- Spontaneous defibrillation occurred in 8 of 15 animals; refractory period and action potential duration increased significantly.
Conclusions:
- Ibutilide effectively lowers defibrillation energy and current requirements.
- The observed proarrhythmic effects of ibutilide may contribute to its defibrillation efficacy.
- Ibutilide's electrophysiological effects enhance its potential as an antiarrhythmic agent for defibrillation.