An association between chronic excessive alochol ingestion and heart disease was reported in the literature over a century ago. Wood, in 1855, mentioned alcohol as a causative factor in heart failure, and later Walshe described a 'form of localized cirrhosis in the myocardium in the absence of impaired coronary circulation' in a chronic alcoholic patient. Subsequently, other workers reported cardiac dilation, hypertrophy, and congestive heart failure in chronic users of alcohol, but these conditions were attributed to nutritional deficiencies rather than to the alcohol itself. More recently, heart disease and heart failure in alcoholics has been attributed specifically to thiamine defiency secondary to the alcoholism ('beri-beri heart disease') or to cobalt added to beer to enhance foaming ('beer drinker's cardiomyopathy'). In retrospect, these reports hampered recognition of the causative role of alcohol per se in heart disease. Only since the early 1960s has the entity 'alcoholic cardiomyopathy' been recognized and have attempts been made to characterize the disease. Some recent studies have specifically excluded individuals with evidence of malnutrition, lending support to the hypothesis that excessive alcohol consumption can itself cause cardiomyopathy. Studies with animal models of alcoholism have also supported this hypothesis. It now seems clear that alcohol itself has significant and deleterious physiologic and biochemical effects on the heart.
|Original language||English (US)|
|Number of pages||15|
|Journal||Medical Clinics of North America|
|State||Published - 1984|
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