Background: Alcohol-induced cardiac remodeling has been well documented. However, data regarding the dose-related ventricular electrical disturbances and the exact pathophysiologic mechanisms remained largely unknown. Methods: We examined in a community-dwelling cohort the cardiac electromechanical dysfunction among 260 participants (mean age: 64.9 years, 57.5% female) who had habitual alcohol consumption. In parallel, adult male C57BL/6 mice were fed a liquid diet containing 4% or 6% alcohol, or a normal diet (Ctrl) for 14 weeks followed by electrophysiological (whole heart optical mapping and single cardiomyocyte patch clamp technique) examination and analysis of sodium channel (INaV 1.5), gap junctions, and fibrosis. Results: When categorized by daily alcohol consumption (heavy group: >90 gm/day), the heavy alcohol consumption group demonstrated larger mass (trend p 30% decrement, both p<0.05). Expression of type 1 collagen markedly increased in the 6% alcohol groups. ![Figure][1] Figure 1 Conclusion: Chronic alcohol ingestion in humans manifested dose-related cardiac electrical disturbances and unfavorable LV geometry, which were highly mimicked by the mice model. The slower ventricular conduction in mice fed alcohol is attributed to the suppressed sodium channels and gap junctions, as well as an increase of fibrosis. [1]: pending:yes
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