The impact of carvedilol on the defibrillation threshold.

Author(s): McBride BF, White CM, Kalus JS, Guertin DC, Clyne CA, Baker WL, Kluger J

Affiliation(s): Division of Clinical Pharmacology and John A. Oates Institute for Experimental Therapeutics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.

Publication date & source: 2008-01, Heart Lung., 37(1):67-71.

Publication type: Clinical Trial; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

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 naive, 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.