1979
DOI: 10.1177/000456327901600135
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Detection of Alcoholic Cardiomyopathy by Serum Enzyme and Isoenzyme Determination

Abstract: SUMMARY Serum creatine kinase and lactate dehydrogenase isoenzymes were studied in 73 patients with alcoholism, including two patients with clinical alcoholic cardiomyopathy and 28 patients with haemodynamic evidence (systolic time interval abnormality) of disordered myocardial function. No isoenzyme abnormalities suggestive of myocardial injury were observed. We conclude that isoenzyme examination is unsuitable for the early detection of myocardial damage from alcohol.Two patients showed clinical alcoholic ca… Show more

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Cited by 15 publications
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“…These results demonstrate the presence in human myocardium of a novel metabolite of ethanol that potentially may serve as a marker for exposure to alcohol and that could be relevant to the pathophysiology of excessive alcohol consumption leading to cardiac abnormalities. (Circ Res 52: 479-482, 1983) ALCOHOL-INDUCED heart muscle disease afflicts more than 200,000 patients (Bridgen and Robinson, 1964;Fink et al, 1979) and accounts for 3% of all cardiac admissions to city hospitals in the United States (Kramer et al, 1968). Manifestations include accumulation of myocardial triglycerides (Lochner et al, 1969;Regan et al, 1966;Ferrans et al, 1965;Kikuchi and Kako, 1970), decreased /J-oxidation of fatty acids (Kramer et al, 1968;Lochner et al, 1969;Regan et al, 1966;Segal at al., 1979), high grade atrial and ventricular arrhythmias, and congestive heart failure (Schwartz et al, 1975;Weishaar et al, 1977;Bing, 1978;Demakis et al, 1974).…”
mentioning
confidence: 99%
“…These results demonstrate the presence in human myocardium of a novel metabolite of ethanol that potentially may serve as a marker for exposure to alcohol and that could be relevant to the pathophysiology of excessive alcohol consumption leading to cardiac abnormalities. (Circ Res 52: 479-482, 1983) ALCOHOL-INDUCED heart muscle disease afflicts more than 200,000 patients (Bridgen and Robinson, 1964;Fink et al, 1979) and accounts for 3% of all cardiac admissions to city hospitals in the United States (Kramer et al, 1968). Manifestations include accumulation of myocardial triglycerides (Lochner et al, 1969;Regan et al, 1966;Ferrans et al, 1965;Kikuchi and Kako, 1970), decreased /J-oxidation of fatty acids (Kramer et al, 1968;Lochner et al, 1969;Regan et al, 1966;Segal at al., 1979), high grade atrial and ventricular arrhythmias, and congestive heart failure (Schwartz et al, 1975;Weishaar et al, 1977;Bing, 1978;Demakis et al, 1974).…”
mentioning
confidence: 99%