Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
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The toxic effects of chronic ethanol abuse on cerebral and hepatic function have long been recognized. The role of ethanol abuse as an etiologic factor in heart disease is less clear and is often attributed to coexistent malnutrition. However, malnutrition has been dissociated from ethanol use in many patients with congestive cardiomyopathy. Studies in various animals provide major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period. Abnormalities that result from ethanol in test animals include depression of left ventricular performance and metabolic and morphologic changes that parallel the changes in human alcoholics with subclinical mechanical dysfunction of the heart, such as symptomatic cardiac arrhythmias, particularly during intensive alcohol ingestion. What causes the progression to heart failure or arrhythmias is not known, but several factors may be involved. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, excessive exposure to trace metals or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the apparent infrequency of heart failure in patients with cirrhosis or neuropathy supports the view that the cardiac abnormality is often 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 pathogenetic process may continued unabated in some who become abstinent.
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PMID:Ethanol abuse and heart disease. 702 Sep 81

Alcohol decreases myocardial contractility through direct, toxic effect. Ingestion of more than 150 g per day for more than 10 years carries a high risk of developing alcoholic cardiomyopathy. The discontinuance of alcohol intake--if put into effect early in the natural history of patients with alcoholic cardiomyopathy--commonly but not invariably results in remission of heart failure. In order to evaluate the left ventricular (LV) function and to find out a possible correlation between the degree of cardiac dysfunction and the severity of the morpho-functional aspects of alcoholic liver disease, 20 chronic alcoholic patients without clinical evidence of heart disease were examined. Echocardiography, systolic time intervals, mechanical polygraphic recordings and liver biopsy were obtained. According to the morphological alterations showed by the needle biopsy of the liver, we separated 12 patients with liver steatosis (Group I) from 8 subjects with alcoholic hepatitis and fibrosis. In Group I LVET, ICT, PEP/LVET indices and LV fractional shortening (delta %) were not statistically different from control subjects. Patients of Group II showed marked impairment of myocardial function, as revealed by significant ICT, PEP, PEP/LVET prolongation and by an equally significant reduction of fractional shortening of the LV. The noninvasive method has proved to be quite useful in detecting early LV dysfunction in asymptomatic chronic alcoholics and has revealed a correlation between the severity of the morphological involvement of the liver and the impairment of cardiac performance.
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PMID:[Non-invasive evaluation of left ventricular function in chronic alcoholics. Histo-morphological and echo-polygraphic correlations]. 718 10

The mean absolute heart weight and mean heart weight to body weight ratio of a group of 43 alcoholics, screened from 1,970 consecutive autopsy reports at the Detroit General Hospital by selecting alcoholics with only ethyl alcohol abuse as an etiology of heart disease, are compared to those of a group of similarity selected age-matched nonalcoholic controls. None of the alcoholics was clinically suspected of having had cardiomyopathy. The statistically significant increased mean absolute heart weight and heart weight to body weight ratio of the alcoholic group reflected the presence of subclinical alcoholic cardiomyopathy. In addition, several of the patients in the alcoholic group displayed gross and microscopic cardiac pathologic changes consistent with alcoholic cardiomyopathy occurring in the absence of cardiomegaly.
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PMID:Prevalence of clinically occult cardiomyopathy in chronic alcoholism. 721 76

Based on anecdotal impressions, there is a common clinical perception that alcoholics with liver disease do not develop cardiomyopathy and that those with alcohol-induced cardiac disease are spared cirrhosis. To determine the relationship between alcoholic cardiomyopathy and cirrhosis, we carried out a prospective cross-sectional study that included: (1) 30 alcoholic men with cardiomyopathy; (2) 30 alcoholic men without cardiomyopathy (left ventricular ejection fraction > 55%); (3) 20 actively drinking alcoholics with cirrhosis; (4) 15 abstaining alcoholics with cirrhosis; and (5) 15 nonalcoholics with cirrhosis of other etiologies. Cirrhosis was observed in 13 of 30 patients with alcoholic cardiomyopathy (43%), compared with 2 of 30 alcoholics without cardiomyopathy (6%) (P < .001). Ten of the 20 active alcoholics with cirrhosis (50%) showed evidence of dilated cardiomyopathy. Actively drinking alcoholics with cirrhosis had a significantly lower mean ejection fraction and shortening fraction, as well as a greater mean end-diastolic diameter and left ventricular mass than abstaining alcoholics with cirrhosis. Cardiac studies of patients with nonalcoholic cirrhosis were normal. We conclude that a positive correlation exists between alcoholic cardiomyopathy and cirrhosis. Alcoholics admitted solely for cardiomyopathy have a higher prevalence of cirrhosis than unselected alcoholics without heart disease. Actively drinking alcoholics admitted only for cirrhosis show impaired cardiac performance, whereas abstaining alcoholics with liver disease tend to manifest normal cardiac function.
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PMID:Relationship between cardiomyopathy and liver disease in chronic alcoholism. 763 21

1. Serum samples from patients with alcoholic heart muscle disease and from control subjects with and without heart disease who did not drink to excess were screened by Western immunoblotting for antibodies to acetaldehyde-modified cardiac cytosolic proteins. 2. Two of the 64 control samples (from subjects with and without heart disease who were not drinking and from subjects with alcoholic liver disease) had detectable (IgG) antibody to acetaldehyde-modified cardiac proteins. 3. By contrast, 7 of 21 (33%) patients with alcoholic heart muscle disease had antibodies against cyanoborohydride-stabilized, acetaldehyde-modified human cardiac cytosolic protein antigens (P < 0.001). 4. Antibodies were of IgG class in six patients and IgA class in five. The molecular sizes of the protein antigens observed ranged from 58 to 120 kDa. 5. These results suggest that a proportion of patients with alcoholic heart muscle disease develop immunogenic cardiac protein-acetaldehyde adducts. The presence of antibodies to these adducts may be a marker for the diagnosis of this heart disease, or possibly for its pathogenesis.
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PMID:Circulating antibodies to cardiac protein-acetaldehyde adducts in alcoholic heart muscle disease. 773 94

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.
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PMID:[Alcoholic cardiomyopathy and heart transplantation]. 974 63

Alcoholic heart disease is caused by a lifestyle in which alcoholics are continue to consume an excessive amount of alcohol over a long period of time. Total abstinence is a very effective way to treat them to prevent the development of the final stage of this disease. In contrast, repetitive drinking of massive amount of alcohol is very harmful and causes exacerbation of this disease. From our clinical studies, six candidates were nominated as symptoms of alcoholic heart disease, namely(1) tachyarrhythmias (incidence: 33%), (2) left ventricular hypokinesis(17%), (3) QT interval prolongation(17%), (4) hyperthickened LV wall(13%), (5) LV dilatation with pump failure: alcoholic cardiomyopathy(0.1%), and (6) sudden cardiac death (unknown %). In the beginning of alcoholic heart disease, the patient usually complains of no symptoms, and physical signs are quite poor. Ordinarily, either transient atrial fibrillation and/or left ventricular hypertrophy which is initially documented by electrocardiography or echocardiography is one of the first signals in the diagnosis. Without such early signals, an early diagnosis is impossible. To make a definite diagnosis of alcoholic heart disease, a clinical follow-up is by all means necessary. Improvement of cardiac function after total abstinence, it's worsening after drinking again, and again improvement after abstinence a second time is a diagnostic clue. In this follow-up study, electrocardiography and echocardiography were employed as important ways to gather date. In treatment, total abstinence is essential. To achieve this therapeutic goal, education of the patient is necessary, because approximately 70 per cent of patients with alcoholic heart disease fail to continue abstinence within two years even if they have good training.
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PMID:[Alcoholic heart disease]. 1088 4

Apoptosis of cardiac muscle cells may contribute to the development of cardiomyopathy and heart failure. Alcohol (ethanol) abuse is a major cause of cardiomyopathy, but its underlying mechanism remains unknown. To determine whether ethanol causes apoptosis in cardiac muscle and whether insulin-like growth factor I (IGF 1) improves cardiac muscle survival upon ethanol exposure, we have defined the effects of ethanol and IGF I in primary cardiomyocytes. Ethanol decreased cell viability in dose-response manner from 0.2% to 1%. In contrast, ethanol (0.2-1%) did not alter viability of cardiac fibroblasts. To assess the occurrence of apoptosis, DNA fragmentation was determined with quantitation of nucleosomes. Nucleosomes were increased in ethanol-treated cells, thus confirming the apoptotic effects of ethanol. The pro-apoptotic Bax protein and Caspase 3 are important proteins of apoptotic signaling. The content of Bax and the activities of Caspase 3 were increased upon ethanol exposure. IGF I partially suppressed Bax induction, Caspase 3 activation, DNA fragmentation, and increased cardiomyocyte survival. The effects of IGF I on ethanol-induced apoptosis can be inhibited with a chemical inhibitor of PI 3 Kinase (LY-294002), suggesting that anti-apoptotic actions of IGF I involves PI 3 Kinase. These results may have important implications on further understanding the pathogenesis of alcoholic heart disease and the development of new strategies to treat alcoholic cardiomyopathy.
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PMID:Insulin-like growth factor I retards apoptotic signaling induced by ethanol in cardiomyocytes. 1102 53

The incidence, presentation, clinical features, and evolution of several cardiomyopathies have clear gender-related differences. In general, women show a different response to noxious cardiac agents than men, and they differ in myocardial adaptation to a variety of cardiac insults. Specifically in alcohol-induced heart disease, women have shown different alcohol metabolism features and distinct pathophysiologic mechanisms leading to a higher sensitivity to alcohol-induced heart damage. In preclinical alcohol-induced ventricular dysfunction, women were more sensitive to the toxic effects of ethanol than men. In overt alcoholic cardiomyopathy, women showed about the same prevalence of cardiomyopathy as men, despite having consumed far less ethanol. This supports a greater female propensity to alcohol-induced cardiac damage.
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PMID:Gender differences in alcoholic cardiomyopathy. 1185 86

Alcohol abuse can cause cardiomyopathy indistinguishable from other types of dilated nonischemic cardiomyopathy. Most heavy drinkers remain asymptomatic in the earlier stages of disease progression, and many never develop the familiar clinical manifestations that typify heart failure. We review the current thinking on the pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy. The relationship of alcohol to heart disease is complicated by the fact that in moderation, alcohol has been shown to afford a certain degree of protection against cardiovascular disease.
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PMID:Alcoholic cardiomyopathy: a review. 2196 23


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