The alcohol-induced cardiomyopathy: A cardiovascular magnetic resonance characterization.

BACKGROUND: Alcoholic cardiomyopathy(ACM) is part of the non-ischaemic dilated cardiomyopathy(NI-DCM) spectrum. Little is known about cardiovascular magnetic resonance(CMR) features in ACM patients. The aim of this study is to describe CMR findings and their prognostic impact in ACM patients. METHODS: Consecutive ACM patients evaluated in five referral CMR centres from January 2005 to December 2018 were enrolled. CMR findings and their prognostic value were compared to idiopathic NI-DCM(iNI-DCM) patients. The main outcome was a composite of death/heart transplantation/life-threatening arrhythmias. RESULTS: Overall 114 patients (52 with ACM and 62 with iNI-DCM) were included. ACM patients were more often males compared to iNI-DCM (90% vs 64%, respectively, p ≤ 0.001) and were characterized by a more pronounced biventricular adverse remodelling than iNI-DCM, i.e. lower LVEF (31 ± 12% vs 38 ± 11% respectively, p = 0.001) and larger left ventricular end-diastolic volume (116 ± 40 ml/m2 vs 67 ± 20 ml/m2 respectively, p < 0.001). Similarly to iNI-DCM, late gadolinium enhancement (LGE), mainly midwall, was present in more than 40% of ACM patients but, conversely, it was not associated with adverse outcome(p = 0.15). LGE localization was prevalently septal (87%) in ACM vs lateral in iNI-DCM(p < 0.05). Over a median follow-up of 42 months [Interquartile Range 24-68], adverse outcomes were similar in both groups(p = 0.67). CONCLUSIONS: ACM represents a specific phenotype of NI-DCM, with severe morpho-functional features at the onset, but similar long-term outcomes compared to iNI-DCM. Despite the presence and pattern of distribution of LGE was comparable, ACM and iNI-DCM showed a different LGE localization, mostly septal in ACM and lateral in iNI-DCM, with different prognostic impact.

[Alcoholic cardiomyopathy and heart transplantation]. / Cardiomyopathie éthylique et transplantation cardiaque.

The recognition of alcoholic cardiomyopathy in patients with dilated cardiomyopathy is essential as they may regress, at least partially in a relatively short period, with abstention. The clinical history is the key to diagnosis because no other specific feature can identify the cause. Between January 1984 and July 1995, 26 candidates for cardiac transplantation with dilated cardiomyopathy and chronic alcoholism improved after withdrawal of alcohol. None of these patients was placed on the surgical waiting list. Patients with ischaemic cardiomyopathy, valvular disease or previous surgery for valvular hypertensive or congenital heart disease, documented viral myocarditis or connective tissue diseases, were excluded. The diagnostic criterion of chronic alcoholism was a total alcohol consumption of 292 kg and a duration of alcohol abuse of over 10 years. In addition to the clinical features, biological, electrocardiographic, echocardiographic and haemodynamic parameters were analysed. The mean age of the patients was 48 +/- 8 years. There were 25 men and 1 woman. The total mean alcohol consumption was 1,492 kg. The average follow-up period was 63 +/- 41 months. The interval between the onset of symptoms and abstention was 25 months. Haemodynamic improvement was observed in 25 cases. The average interval between alcoholic abstention and recovery was 11.7 months. One patient died suddenly. Improvement of symptoms, decrease of the cardiothoracic ratio and improvement of echocardiographic parameters were statistically significant. The increase in angiographic or isotopic ejection fraction and cardiac index and the decrease in mean pulmonary artery pressures were also statistically significant. These results confirmed the diagnosis of alcoholic cardiomyopathy. Therefore, patients with chronic alcohol abuse and dilated cardiomyopathy must be identified and treated for this problem and not placed on the waiting list for cardiac transplantation unless no improvement is observed after about 3 months of abstention.

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.

Comparative study of dilated cardiomyopathy and specific heart muscle diseases from pathophysiological aspects--echocardiographic observation.

To investigate the causative factors of dilated cardiomyopathy (DCM), 29 DCM patients were echocardiographically and histopathologically compared with 17 patients with specific heart muscle diseases mimicking DCM. These consisted of 6 cases of myocarditis and 11 of alcoholic heart muscle disease. Myocarditis patients had less dilation of the left ventricle, more marked segmental wall motion abnormality on admission and more extensive myocardial fibrosis than patients with alcoholic heart muscle disease and DCM. Four myocarditis patients died of congestive heart failure before showing a marked dilatation of the left ventricle. The alcoholic heart muscle disease patients revealed diffuse wall motion abnormality on admission. Out of these 8 patients who had abstained showed amelioration. However, in 3 who had not abstained, both wall motion abnormality and dilatation of the left ventricle markedly progressed and 2 died of congestive heart failure. Although the DCM patients as a group showed deterioration throughout the follow-up period, individual patients revealed a variety of echocardiographic and pathological findings, which led to the regrouping of 29 patients with DCM into 2 subgroups. One group had characteristic features similar to these of patients with myocarditis, and the other had characteristics similar to these of patients with alcoholic heart muscle disease. These findings suggested that different causative factors might coexist in DCM.

111-indium human antimyosin monoclonal antibody-fragment study on alcoholic (and diabetic) cardiomyopathic patients (ACM-DCM) with Centocor Europe Myoscint (Msc).

The criteria of Msc-positivity were: typical accumulation of hot spots in 2 directions of planar scan in the 24-48-hr measurements, while in atypical cases the hot spots were present only in the 48 hr picture. Twenty-one male volunteers were assessed. 18 of them had ACM (2 patients were studied repeatedly). The negative and positive control cases exhibited the expected Msc pattern. Seven ACM patients were regarded typically positive, in 5 cases atypical positivity was stated, and 6 patients were classified as Msc negatives. The heart lung activity ratio was 1.75 +/- 0.45 and 1.68 +/- 0.44 for typical and atypical positive cases, respectively. The control and DCM H/L ratios were 1.15 and 1.3 +/- 0.2, respectively, in AMI the H/L was 1.91, in DCM of dilatative phase it was 1.55 +/- 0.06 with serum myosin in the normal range. Heart dilation in the DCM groups: 5 dilated out of 7 typically positive cases while in atypically positive, and negative cases the dilation occurred in 2 out of 5 and 1 out of 6 cases, respectively. Low LV-EF (less than 45%) were found in ratios of 4/7, 2/5, and 1/6 in typically positive, atypically positive and negative cases, respectively. Elevated PCP similar ratios. In the same groups pathological ECG was seen in ratios of 5/7, 1/5, and 1/6, respectively. The g-GT activity was enhanced in all cases, there was, however, no evident correlation between the actual enzyme activity and intensity of hot accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)