Key result
Propranolol and captopril reduce VF duration and increase VF threshold versus controls.
Why the study?
Does propranolol or captopril reduce the duration of ventricular fibrillation in a rat model of sudden cardiac arrest?
RCT
Randomized
No
Does propranolol or captopril reduce the duration of ventricular fibrillation in a rat model of sudden cardiac arrest?
p-value: p=< 0.05
Propranolol and captopril shorten the duration of ventricular fibrillation and increase its threshold in a rat model, providing a potential mechanism for the reduced incidence of VF as a presenting rhythm in sudden cardiac arrest.
Hypothesis-generating in a rat VF model; leaves open translation to human sudden cardiac arrest.
OBJECTIVE: In the last two decades, the incidence of ventricular fibrillation has significantly decreased as the presenting rhythm in sudden cardiac arrest. We hypothesized that beta-adrenergic receptor blocker (beta-blocker) and angiotensin converting enzyme inhibitor, which were commonly used in the primary and secondary prevention strategies recommended by the American Heart Association during the same decades, decrease the duration of ventricular fibrillation after onset of cardiac arrest. DESIGN: Randomized prospective animal study. SETTING: University affiliated research laboratory. SUBJECTS: Male Sprague-Dawley rats. METHODS AND RESULTS: Male Sprague-Dawley rats, weighing 450-550 g were administered either beta-blocker, propranolol, angiotensin converting enzyme inhibitor, captopril, or placebo for 2 wks. In the phase 1 study, ventricular fibrillation was induced by ligation of the proximal left coronary artery. In the phase 2 study, the experiments were repeated with the measurements of duration of monophasic action potential and threshold of ventricular fibrillation. Both propranolol and captopril significantly decreased the duration of ventricular fibrillation in comparison with controls (p < 0.05). In the phase 2 study, both propranolol and captopril significantly increased the threshold of ventricular fibrillation (p < 0.05) and monophasic action potential (p < 0.05). CONCLUSIONS: Ventricular fibrillation remains as the leading causal rhythm of sudden cardiac arrest. However, the drugs widely used in primary and secondary coronary artery disease prevention strategies shortened the duration of ventricular fibrillation. This may result in the reduced incidence of ventricular fibrillation as the presenting rhythm in sudden cardiac arrest. Increased threshold of ventricular fibrillation and monophasic action potential after administration of those agents may be the potential mechanisms of reduced duration of ventricular fibrillation.
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Wang et al. (2008) conducted an RCT in Ventricular fibrillation in sudden cardiac arrest. Propranolol or captopril vs. Placebo was evaluated on Duration of ventricular fibrillation (p=< 0.05). Propranolol and captopril significantly decreased the duration of ventricular fibrillation and increased the threshold of ventricular fibrillation compared with controls (p < 0.05).
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