SUMMARY Detailed drinking histories were taken in 38 patients in whom dilated cardiomyopathy was diagnosed by cardiac catheterisation and left ventricular biopsy. On the basis of the drinking history twenty patients were classified as being in an abstinent or light drinking group and eighteen patients as being in a heavy drinking group (daily alcohol intake in excess of 80 g or cumulative lifetime intake exceeding 250 kg). Activities of myocardial creatine kinase, lactate dehydrogenase, a hydroxybutyric dehydrogenase, malic dehydrogenase, and aspartate aminotransferase were all higher in the heavy drinkers and myocardial enzyme activity correlated with cumulative lifetime alcohol intake, maximum daily intake, and recent daily intake. Activities of creatine kinase, a hydroxybutyric dehydrogenase, and malic dehydrogenase correlated with ejection fraction, irrespective of the alcohol intake of the patient. These findings were not altered by exclusion of patients with hypertension.The results indicate that among patients with dilated cardiomyopathy there is a group characterised by a high alcohol intake and raised myocardial tissue enzymes which supports the concept of alcoholic heart muscle disease as a distinct entity.Although the association between excessive alcohol consumption and congestive (dilated) cardio-i myopathy has long been known,1 2 a causal relation remains controversial.3 There are no studies that relate quantitative alcohol intake to myocardial damage, as there are for alcoholic liver disease.4" Indeed the clinical diagnosis of alcoholic heart muscle disease merely reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease has been found.Requests for reprints to Dr P J Richardson, Cardiac Department,