Preclinical alcoholic cardiomyopathy, myocardial damage in the absence of overt congestive heart failure in chronic alcoholics, is well characterized at necropsy, but attempts to identify such a clinical entity before death have produced conflicting results. dying subjects only at rest, the inclusion of older alcoholics and limitations of noninvasive techniques may explain some of the disagreement. To determine if preclinical alcoholic cardiomyopathy could be identified independent of the aforementioned limitations, 2S asymptomatic chronic alcoholics aged S days per week for >S years, underwent radionuclide ventriculography for measurements of systolic and diastolic function at rest, peak supine exercise and during recovery, and echocardiography for assessment of chamber size, wall thickness and left ventricular mass. Red blood cell levels of selenium and thiamine were measured to determine whether abnormalities were present in these 2 potential mediators of alcoholic cardiomyopathy. For comparison, an age-matched group of healthy control subjects was also studied. For alcoholics and control subjects at rest, mean ejection fraction (67 +/- 7% vs 71 +/- 6%) and diastolic peak filling rate (3.4 +/- 0.6 vs 3.3 +/- 0.6 end-diastolc volumes per second [EDV/s]) were similar. At peak exercise, the mean ejection fraction 83 +/- 6 vs 82 4- 10), change in ejection fraction (14 /- 10 vs 14 7) and peak fining rate (8.9 +/- 2.0 vs 9.S +/- 1.9 EDV/s) were also similar, but election fraction failed to increase appropriately in 3 alcoholics (120/o), suggesting possible stress-induced myocardial dysfunction. Left ventricular chamber size, fractional shortening, wall thickness and ventricular mass by echocardiography were similar in the alcoholic and control groups, as were red blood cell levels of selenium and thiamine. Repeat studies aftor 4 weeks of abstinence from alcohol showed persistence of the exemise-induced abnormal response in 2 of the 3 alcoholics. These data suggest that the occurrence of preclinical cardiomyopathy in young, asymptomatic chronic alcoholics is rare and may require exercise stress testing to be detected. (Am J Cardiol 1991;67:183-187), Chronic alcoholism can result in heart disease and the appearance of clinical symptoms of congestive heart failure (weakness, breathlessness, abdominal discomfort, and pooling of blood in the extremities). This has been attributed to both a direct toxic effect of alcohol on the heart and the detrimental effect that chronic alcohol abuse has on nutritional status. The effects of alcoholism on the heart have been well documented at autopsy, but attempts to characterize the effects of excessive alcohol consumption on the heart before death have yielded conflicting results. To determine the effects of alcoholism on cardiovascular function in younger, relatively healthy alcoholics, 25 men under the age of 40 (average age 34 years) who had consumed one pint of whiskey or one six-pack of beer daily for at least five years were assessed. An age-matched group of nonalcoholic subjects served as a control group. On virtually all cardiovascular parameters measured (resting and exercise mean ejection fraction, diastolic peak filling rate, end-diastolic volumes per second, left ventricular size, wall thickness and mass, and red blood cell selenium and thiamine levels), there were no differences between alcoholics and control subjects. In three alcoholic subjects, exercise failed to induce an appropriate increase in ejection fraction (the percentage of blood ejected from the ventricle during maximal contraction of the heart), suggesting a possible dysfunction in these subjects. After four weeks of abstinence from alcohol, this deficit was still present in two of the three subjects. Hence, the occurrence of alcohol-induced cardiomyopathy in young alcoholics is quite rare, and may require exercise testing to be detected. (Consumer Summary produced by Reliance Medical Information, Inc.)