What is a direct toxic effect of alcohol on cardiac tissue contributing to cardiomyopathy?

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Chronic alcohol exposure directly injures heart muscle cells, causing their death and loss of functional cardiomyocytes. This cell loss reduces the heart’s ability to contract, leading to dilated ventricles and systolic dysfunction characteristic of alcoholic cardiomyopathy. The toxic effects involve oxidative stress, mitochondrial damage, and impaired protein synthesis that push myocytes toward apoptosis or necrosis, so the net result is weakened contraction and remodeling of the heart.

Other options don’t fit this mechanism. Increasing capillary density isn’t a typical consequence of alcohol’s direct effect on the myocardium, valvular hyperplasia isn’t a feature of alcoholic cardiomyopathy, and while arrhythmias can occur, a decreased heart rate isn’t the primary direct toxic effect driving the cardiomyopathy.