Abstract

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. Studying 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, 25 asymptomatic chronic alcoholics aged <40 years (mean 34), each of whom had consumed a minimum of 1 pint of whiskey or one 6-pack of beer ≥5 days per week for ≥5 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-diastolic volumes per second [EDV/s]) were similar. At peak exercise, the mean ejection fraction (83 ± 6 vs 82 ± 10), change in ejection fraction (14 ± 10 vs 14 ± 7) and peak filling rate (8.9 ± 2.0 vs 9.5 ± 1.9 EDV/s) were also similar, but ejection fraction failed to increase appropriately in 3 alcoholics (12%), 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 after 4 weeks of abstinence from alcohol showed persistence of the exercise-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.

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