Spectrum of alcohol-induced myocardial damage detected by indium-111-labeled monoclonal antimyosin antibodies.

OBJECTIVES: We sought to determine the prevalence, intensity and evolving changes of myocardial damage detected by myocardial uptake of antimyosin antibodies in patients with alcohol-induced dilated cardiomyopathy, alcohol addicts attending a detoxification unit and healthy subjects with short-term alcohol consumption.
BACKGROUND: Evidence of alcohol-induced myocardial damage may be provided by myocardial uptake of indium-111-labeled monoclonal antimyosin antibodies. The spectrum of such damage in patients who are heavy drinkers (> 100 g for > 10 years), with or without cardiomyopathy, and the impact of short-term alcohol ingestion on antimyosin antibody uptake have not been adequately explored.
METHODS: One hundred twenty antimyosin studies were performed in 56 patients with dilated cardiomyopathy (group I), 15 alcohol addicts attending a detoxification unit (group II) and 6 volunteers for short-term alcohol ingestion (group III). Estimation of antibody uptake was calculated through a heart/lung ratio (HLR) (normal < 1.55).
RESULTS: The 56 patients in group I (54 men, 2 women; mean [+/-SD] age 46 +/- 11 years) had consumed 123 +/- 60 g/day of alcohol for 21 +/- 9 years, for a cumulative intake of 914 +/- 478 kg. Mean duration of symptoms was 46 +/- 49 months. Mean left ventricular end-diastolic diameter was 71 +/- 10 mm, and mean ejection fraction was 28 +/- 12%. No differences in New York Heart Association functional class, ventricular size or ejection fraction were noted between 28 active and 28 past consumers, except for the prevalence and intensity of antibody uptake (75% vs. 32%, p < 0.001) and HLR (1.75 +/- 0.26 vs. 1.49 +/- 0.17, p = 0.0001). In 19 patients in the active group restudied after alcohol withdrawal, antibody uptake decreased (from 1.76 +/- 0.17 to 1.55 +/- 0.19, p < 0.001), and ejection fraction improved (from 30 +/- 12% to 43 +/- 16%, (p < 0.001). No changes occurred in the 15 past consumers restudied. The 15 male patients in group II (mean age 36 +/- 4 years) had consumed 156 +/- 59 g/day for 17 +/- 5 years, for a cumulative alcohol intake of 978 +/- 537 kg, an amount similar to that in patients in group I, but antimyosin antibody uptake was detected in only 3 (20%) of 15 patients. None of six group III subjects developed antibody uptake after short-term ethanol ingestion. Despite the small sample size, the power to detect clinically relevant differences in most variables that did not reach statistical significance was amply sufficient.
CONCLUSIONS: In alcohol-induced dilated cardiomyopathy, alcohol withdrawal is associated with the reduction or disappearance of myocardial damage and improvement of function. The difference in prevalence of antimyosin antibody uptake in patients with and without cardiac disease who consume similar amounts of alcohol suggests the presence of those with different myocardial susceptibilities to alcohol. Short-term ethanol ingestion in healthy subjects does not induce detectable uptake of antimyosin antibodies.