Discussion
Alcoholic cardiomyopathy is a common cause of dilated cardiomyopathy and the most common secondary cardiomyopathy1. An extensive review article by Silwa et al found alcohol to be a contributory factor in 45% of patients with DCM in Africa2,3.
The mechanism for the cardiac damage produced by alcohol remains unclear. Several theories have arisen over many years. Original theories regarding the mechanism focused on nutritional deficiencies (eg thiamine deficiency), secondary exposures (eg tobacco, cobalt, arsenic) and other comorbidities (eg hypertension). Although these mechanisms continue to play a role in selected patients, most evidence in the literature indicates that the effects of alcohol on the myocardium are independent of these factors and that the effect is a direct toxic result of ethanol or its metabolites4. Experimental studies show that alcohol and its metabolite acetaldehyde can disrupt cardiac calcium cycling, mitochondrial respiration, myocardial synthesis of proteins and lipid signal transduction, and myocardial redox state5-7. There is also evidence to support a direct toxic effect of alcohol on both cardiac and skeletal myocytes which may in turn increase the rate of cellular apoptosis8. Genetic factors play a role as evidenced by studies showing that individuals with the angiotensin – converting enzyme DD genotype have an increased risk of developing alcoholic cardiomyopathy9
DiscussionAlcoholic cardiomyopathy is a common cause of dilated cardiomyopathy and the most common secondary cardiomyopathy1. An extensive review article by Silwa et al found alcohol to be a contributory factor in 45% of patients with DCM in Africa2,3.The mechanism for the cardiac damage produced by alcohol remains unclear. Several theories have arisen over many years. Original theories regarding the mechanism focused on nutritional deficiencies (eg thiamine deficiency), secondary exposures (eg tobacco, cobalt, arsenic) and other comorbidities (eg hypertension). Although these mechanisms continue to play a role in selected patients, most evidence in the literature indicates that the effects of alcohol on the myocardium are independent of these factors and that the effect is a direct toxic result of ethanol or its metabolites4. Experimental studies show that alcohol and its metabolite acetaldehyde can disrupt cardiac calcium cycling, mitochondrial respiration, myocardial synthesis of proteins and lipid signal transduction, and myocardial redox state5-7. There is also evidence to support a direct toxic effect of alcohol on both cardiac and skeletal myocytes which may in turn increase the rate of cellular apoptosis8. Genetic factors play a role as evidenced by studies showing that individuals with the angiotensin – converting enzyme DD genotype have an increased risk of developing alcoholic cardiomyopathy9
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