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
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