Uncertainty about the mechanism of alcohol-mediated arrhythmogenesis and the effect of alcohol use on arrhythmic risk among older adults is an increasing concern in light of population aging and recent reports that moderate alcohol consumption may protect older adults against coronary artery disease. In this review, a theoretical model of the role of brain stem nuclei in alcohol-mediated arrhythmogenesis in older adults is developed. The model is based on the hypothesis that the effects of alcohol on central autonomic pathways of cardiac control may alter the threshold for alcohol-mediated arrhythmogenesis among older adults. Findings from multiple lines of research including cellular, electrophysiological, epidemiological, experimental, and clinical studies in human, animal, and in vitro models were synthesized in developing the model. Suggestions for future research on the topic of alcohol-mediated arrhythmogenesis in older adults are offered.
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