Alcohol-induced cardiomyopathy (ACM) is a well-established form of heart disease that is characterized by susceptibility to electrical abnormalities, dilation, and reduced cardiac contractility. Despite this, the molecular signature of ACM and the direct impact of alcohol on myocardial function remains poorly characterized, with ACM diagnosis being prescribed to cardiomyopathies occurring in regular alcohol users with the notable absence of coronary artery disease. Further, even less is known about ACM and binge drinking—now the most common form of immoderate alcohol consumption. Thus, we set out to determine whether binge drinking impacted the myocardial function of mice provided alcohol for 14 weeks. We used left-ventricular slices to assess myocardial twitch force, passive mechanics, extracellular matrix stiffness, myofilament calcium sensitivity and assessed cardiomyocyte shortening in isolated ventricular myocytes. Notably, binge drinking had minimal effect on cardiac hypertrophy but both twitch force and myocyte contractility were suppressed. Binge drinking tended to reduce the passive stiffness of the left-ventricle and reduced left-ventricular calcium sensitivity; however, passive stiffness derived from the extracellular matrix was increased. Taken together these results indicate that the effect of binge drinking on the myocardium is consistent with the development of a dilated cardiomyopathy (namely, reduced contractility and increased fibrotic stiffness) even in the stages preceding the clinical development of ACM. Work is ongoing to better understand the molecular changes that drive this remodeling.
Wetzel et al. (Sun,) studied this question.