SPECTRUM OF ALCOHOL-INDUCED MYOCARDIAL DAMAGE DETECTED BY INDIUM-111-LABELED MONOCLONAL ANTIMYOSIN ANTIBODIES

Citation
M. Ballester et al., SPECTRUM OF ALCOHOL-INDUCED MYOCARDIAL DAMAGE DETECTED BY INDIUM-111-LABELED MONOCLONAL ANTIMYOSIN ANTIBODIES, Journal of the American College of Cardiology, 29(1), 1997, pp. 160-167
Citations number
59
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
29
Issue
1
Year of publication
1997
Pages
160 - 167
Database
ISI
SICI code
0735-1097(1997)29:1<160:SOAMDD>2.0.ZU;2-1
Abstract
Objectives. We sought to determine the prevalence, intensity and evolv ing changes of myocardial damage detected by myocardial uptake of anti myosin antibodies in patients with alcohol-induced dilated cardiomyopa thy, alcohol addicts attending a detoxification unit and healthy subje cts with short-term alcohol consumption. Background. Evidence of alcoh ol-induced myocardial damage may be provided by myocardial uptake of i ndium-111-labeled monoclonal antimyosin antibodies, The spectrum of su ch damage in patients who are heavy drinkers (>100 g for > 10 years), with or without cardiomyopathy, and the impact of short-term alcohol i ngestion on antimyosin antibody uptake have not been adequately explor ed. Methods. One hundred twenty antimyosin studies were performed in 5 6 patients with dilated cardiomyopathy (group I, 15 alcohol addicts at tending a detoxification unit (group II) and 6 volunteers far short-te rm alcohol ingestion (group III). Estimation of antibody uptake was ca lculated through a heart/lung ratio (HLR) (normal <1.55). Results. The 56 patients in group 1 (54 men, 2 women mean [+/-SD] age 46 +/- 11 ye ars) had consumed 123 +/- 60 g/day of alcohol for 21 +/- 9 years, for a cumulative intake of 914 +/- 478 kg. Mean duration of symptoms aas 4 6 +/- 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 ejec tion fraction were noted between 28 active and 28 past consumers, exce pt far 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, anti body 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 97 8 +/- 537 kg, an amount similar to that in patients in group I, but an timyosin antibody uptake aas detected in only 3 (20%) of 15 patients. None of six group III subjects developed antibody uptake after short-t erm ethanol ingestion. Despite the small sample size, the power to det ect clinically relevant differences in most variables that did not rea ch statistical significance nas amply sufficient. Conclusions. In alco hol-induced dilated cardiomyopathy, alcohol withdrawal is associated w ith the reduction or disappearance of myocardial damage and improvemen t of function. The difference in prevalence of antimyosin antibody upt ake in patients with and without cardiac disease who consume similar a mounts of alcohol suggests the presence of those with different myocar dial susceptibilities to alcohol. Short-term ethanol ingestion in heal thy subjects does not induce detectable uptake of antimyosin antibodie s. (C) 1997 by the American College of Cardiology