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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcoholic cardiomyopathy is a consequence of toxic effects of ethyl alcohol. Acute effects must be distinguished from chronic effects over many years. Chronic abuse of alcohol of 1.5-2 g ethyl alcohol per kg body weight (i.e. about 100-150 g/70 kg) per day for years can cause congestive cardiomyopathy in predisposed persons, usually between 30 and 50 years of age. The diagnosis is associated with some criteria for exclusion, i.e. coronary heart disease, hypertension, valvular heart disease, in addition all obstructive and restrictive cardiomyopathy must be excluded. On the other hand, a specific constellation of findings can be considered characteristic of alcoholic cardiomyopathy, namely the coincidence of a radiologically established cardiomegaly in the form of a congestive cardiomyopathy with a raised serum concentration of immunoglobulin A and a negative myocardial immunofluorescence test. Therapeutically, in addition to the classical principles of the treatment of heart failure, absolute abstention from alcohol and physical stress seemed to be effective.
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PMID:[Alcoholic Cardiomyopathy (author's transl)]. 13 Dec 48

The widespread use of ethyl alcohol suggests its potential importance in clinical medicine. There is no proven therapeutic effect in cardiac patients and its role as an etiologic factor in heart disease has been disputed over the years and attributed to coexistent malnutrition. The latter factor, however, has been dissociated from ethanol use in many patients with the cardiomyopathic form of heart failure. Major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period has been obtained in various species of animals, including the subhuman primate. Abnormalities include depression of ventricular function, and metabolic and morphologic changes that parallel the changes in humans with preclinical malfunction of the heart. While the mechanism of progression to heart failure or arrhythmias is not known, several factors may be associated. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, simultaneous exposure to trace metals in excess, and occasional specific nutritional deficiency or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the infrequency of heart disease in patients with cirrhosis or neuropathy supports the view that the cardiac abnormality is commonly not dependent on malnutrition. Clinical data indicate that the cessation of alcohol intake may reverse the disease or interrupt its progression in many patients. However, the pathogenic process may continue unabated in some patients who become abstinent.
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PMID:The role of ethanol in cardiac disease. 32 69

Marked T wave abnormality developed in a patient with alcoholic cardiomyopathy. The T negativity was of giant size and occurred in an alternating sequence in the presence of sinus rhythm. This change was rapidly transient, disappearing in 3 days. The complete electrocardiographic recovery was temporally related to successful treatment of severe heart failure, normalization of initially low serum magnesium level, and abolition of recurrent ventricular fibrillation.
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PMID:T-wave alternans associated with heart failure and hypomagnesemia in alcoholic cardiomyopathy. 118 70

Detection of alcohol abuse is of utmost importance in the diagnosis and management of alcoholic cardiomyopathy. The ability of laboratory tests and clinical signs to detect alcohol abuse was compared in 31 patients with severe heart failure due to underlying dilated cardiomyopathy. Alcoholic cardiomyopathy was diagnosed in 13 patients and a variety of nonalcoholic cardiomyopathies were diagnosed in the remaining 18 patients. At the time of hospital admission, all patients received a complete cardiovascular examination as well as routine hematologic and biochemical tests. Details concerning past and recent alcohol intake were obtained by an individual who was unaware of the diagnostic status of the patients. The two groups of patients did not differ with respect to clinical presentation, self-report of recent drinking patterns, or clinical signs and medical history items that have been found to be associated with chronic alcohol abuse. However, the group with alcoholic cardiomyopathy had significantly higher values for mean corpuscular volume and gamma-glutamyltranspeptidase. Our results suggest that a combination of routine laboratory tests may be effective in the detection of alcohol abuse in patients with dilated cardiomyopathy.
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PMID:Alcohol abuse in patients with dilated cardiomyopathy. Laboratory vs clinical detection. 197 Apr 74

Two cases of dilated, hypokinetic cardiomyopathy complicated by cardiac failure, are reported in a 29 year old woman and a 55 year old man, with no etiological factors other than chronic major alcoholism (consumption of over 100 ml of alcohol per day for over 5 years). This was completely reversed 10 and 14 months after cessation of alcohol consumption. The isotopic left ventricular ejection fraction increased from 22 to 70 p. 100 and from 12 to 73% respectively. These cases are are and are evidence in favour of an alcoholic cardiomyopathy rather than alcohol being an aggravating factor in patients with cardiomyopathy.
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PMID:[Dilated cardiomyopathy with deep, completely reversible dysfunction of the left heart in alcoholic patients. Report of 2 cases]. 214 69

The mechanisms responsible for the decline in the density of beta-adrenoceptors in the failing myocardium have not been adequately defined. It is a possibility that the nature of the process leading to heart failure may determine, in large part, the pathogenesis of this decline. Sera of some patients with dilated cardiomyopathy contain antibodies directed against the beta-adrenoceptor, as judged by ligand binding inhibition, immunoprecipitation and immunoblotting assays. Because deranged immune function is thought to play a role in dilated cardiomyopathy, immunogenetic markers of the propensity to develop anti-beta-receptor antibodies were sought. The prevalence of HLA-DR4 was significantly higher in dilated cardiomyopathy patients (40 vs 24% in 511 normal subjects, pc less than 0.001). In contrast, no association was found between HLA phenotypes and alcoholic cardiomyopathy. Furthermore, 72% (13 of 18) of the HLA-DR4 dilated cardiomyopathy patients had anti-beta-receptor antibodies compared to 22% (7 of 33) HLA-DR4-negative patients; in the latter, presence of antibody was linked to the HLA-DR1 phenotype. Conversely, 67% (15 of 23) of the antibody-positive patients were typed as HLA-DR4 compared to only 10% of the antibody-negative patients. Interestingly, none of the 23 antibody-positive patients were typed as HLA-DR3 while 37% of the antibody-negative did. Only 25% of alcoholic cardiomyopathy patients had anti-beta-receptor antibodies and no preponderant HLA association could be demonstrated. These results suggest that the presence of anti-beta-receptor antibodies in patients with idiopathic dilated cardiomyopathy may be under the control of the major histocompatibility locus.
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PMID:Anti-beta-receptor antibodies in human dilated cardiomyopathy and correlation with HLA-DR antigens. 215 17

Enzymes in the human myocardium following sudden death were examined for activity in a quantitative histoenzymological study, these were NAD-dependent dehadrogenases of succinate (SDG), lactate (LDG), beta-hydroxybutyrate (beta-HOBDG), alpha-glycerophosphate (alpha-GPDG), alcohol (ADG), glucoso-6-phosphate (G-6-PDG), and NAD-diaphorase (NADse), and catalase. Autopsies were performed within 3 h after death. beta-HOBDG and LDG were found to show an increase in activity in the cardiomyocytes of sudden death subjects with coronary heart disease without apparent changes. In the myocardium from death subjects with coronary heart disease and large postinfarct cardiosclerosis, the activity of the enzymes was directly related to the severity of myocardial hypertrophy and signs of chronic heart failure. As myocardial hypertrophy developed, the enzyme activity increased; when there appeared signs of chronic heart failure it decreased. The myocardium from sudden death subjects with alcoholic cardiomyopathy showed diminished redox enzyme activity and higher activity of the enzyme utilizing alcohol (ADG and catalase). The findings suggest that changes in the enzyme activity in the myocardium are of various type and depend on previous cardiac abnormalities.
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PMID:Quantitative histoenzymological characteristics of the myocardium in sudden cardiac death. 252 98

Cirrhosis is associated with several circulatory abnormalities. A hyperkinetic circulation characterized by increased cardiac output and decreased arterial pressure and peripheral resistance is typical. Despite this hyperkinetic circulation, some patients with alcoholic cirrhosis have subclinical cardiomyopathy with evidence of abnormal ventricular function unmasked by physiologic or pharmacologic stress. Florid congestive alcoholic cardiomyopathy develops in a small percentage, but the concurrent presence of cirrhosis seems to retard the occurrence of overt heart failure. Even nonalcoholic cirrhosis may be associated with latent cardiomyopathy, although overt heart failure is not observed. Tense ascites is associated with some cardiac compromise, and removing or mobilizing ascitic fluid by paracentesis or peritoneovenous shunting results in short-term increases in cardiac output. Cirrhosis also appears to be associated with a decreased risk of major coronary atherosclerosis and an increased risk of bacterial endocarditis. Small hemodynamically insignificant pericardial effusions may be seen in ascitic patients. The release of atrial natriuretic peptide appears to be unimpaired in cirrhosis, although the kidney may be hyporesponsive to its natriuretic effects.
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PMID:Cardiac abnormalities in liver cirrhosis. 269 Apr 63

Among a group of 28 elderly veterans with dilated cardiomyopathy regularly attending an outpatient heart failure clinic, half had a history of habitual heavy drinking. It was concluded that chronic heavy drinking was the only identifiable factor responsible for the heart failure in three of these patients. Eleven other patients also had chronic heavy drinking as a possible etiological factor of their heart failure in addition to Coronary Artery Disease and/or hypertension. Less than 50% of the heavy drinkers totally abstained from alcohol after seeking medical treatment although they reduced their drinking significantly. All three patients with clear alcoholic cardiomyopathy discontinued drinking and showed marked improvement in cardiac status. The discontinuation of drinking did not appear to be associated with improvement in the remaining heavy drinkers and those patients who reported a history of moderate drinking.
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PMID:Alcohol and dilated cardiomyopathy: incidence and correlation with clinical outcome. 343 85

Chronic and heavy alcohol consumption has deleterious effects upon the cardiovascular system and may cause congestive cardiomyopathy. Evidence of cardiac malfunction has been found in chronic alcoholics without overt heart failure by invasive and noninvasive methods. Ethanol is the incriminated factor having a direct cardiotoxic effect. Electron microscopy and cardiac muscle biopsies show that ethanol may cause changes on plasmalemmal, mitochondrial, and sarcoplasmic membranes. The clinical picture and general management of alcoholic cardiomyopathy do not differ substantially from those of congestive cardiomyopathies of any type. It has, however, been demonstrated that cessation of alcohol consumption may lead to an improved prognosis, even to restoration of normal cardiac function, in individuals with preclinical and mild manifestations of cardiac dysfunction. The literature on the possible association of coronary heart disease with alcohol seems to be ambiguous. It has, however, been postulated recently that moderate alcohol intake may have a protective role against coronary heart disease, in contrast to alcoholic intemperance, which may be a factor favoring coronary heart disease.
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PMID:Effects of alcohol on the heart: current views. 374 May 49


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