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The impact of carvedilol on the defibrillation threshold
Brian F McBride1, C Michael White, James S Kalus
1Division of Clinical Pharmacology and John A. Oates Institute for Experimental Therapeutics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Background:
Defibrillation threshold (DFT) is the minimum energy required to successfully terminate ventricular fibrillation. Epinephrine has been shown to increase the DFT in the beta-blocker naïve, but using cardioselective beta-blockers leads to a reduction in the DFT on infusion of epinephrine and norepinephrine. We sought to determine the impact of carvedilol therapy on the DFT after infusion of epinephrine and norepinephrine.
Methods:
DFT was determined in patients receiving carvedilol by the step-down method (baseline DFT), and then patients (n = 27, 67.3 years, 70.0% were male, average left ventricular ejection fraction = 19%) were randomized to a 7-minute infusion of norepinephrine, epinephrine, or placebo in a double-blind manner. After the study drug infusion, DFT testing was repeated (experimental DFT) and results were compared between groups.
Results:
No differences in intragroup DFTs were observed among carvedilol-treated patients receiving norepinephrine (9.4 +/- 4.6 J vs 11.1 +/- 7.8 J; P = .589), epinephrine (10.6 +/- 5.3 J vs 9.8 +/- 6.3 J; P = .779), or placebo (11.1 +/- 7.0 vs 8.5 +/- 4.2; P = .349).
Conclusions:
Carvedilol prevents alterations in DFT produced by stress levels of catecholamines.
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