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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease. During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index. To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis. Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol. These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.
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PMID:Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy. 430 60

After heart disease and cancer, alcoholism is America's third largest health problem; it affects 10 million people, costs $ 60 billion, and is implicated in 200 000 deaths annually. Alcohol is involved in 50% of deaths by motor vehicle and fire, 67% of murders, and 33% of suicides. It contributes to morbidity in certain malignancies and to many diseases of the endocrine, cardiovascular, hematopoietic, gastrointestinal, and nervous systems. The fetal alcohol syndrome occurs in a third of the infants born to women who drink more than 150 g of ethanol daily during pregnancy; another third of the infants become mentally retarded. The prevalence of alcoholism is lower in elderly than in middle-aged persons, but detection is difficult and vulnerability to harm is great in the elderly, due to both pharmacokinetic factors and increased tissue sensitivity. Alcohol and aging are additive in their harmful effects. Although modern medical treatment is helpful, alcoholics are frequently misdiagnosed and mismanaged by health professionals. Total abstinence from alcohol should be a primary goal of treatment.
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PMID:Alcoholism. 636 12

In 98 deaths certified to be due to accidental alcohol poisoning, maximum antemortal blood ethanol concentrations were estimated as the sum of postmortal concentration and the product of blood ethanol elimination rate (0.258 g/liter/hr) and the time interval between the discontinuation of drinking and death. The estimated mean maximum concentration (g/liter) was 4.63 for uncomplicated cases, 4.26 for cases with heart disease, 3.98 for cases in which aspiration of stomach contents had contributed to death, 3.59 for ethanol-barbiturate poisonings, and 3.11 for combinations of ethanol and other psychotropic drugs. The mean for this last group was significantly lower than that for the first or the second group (p less than .001). The mean concentration for ethanol-barbiturate poisonings was signicantly lower than the mean for the uncomplicated cases (p = .01). In the two first groups combined, the higher the age, the lower the ethanol concentration (r = -.27; p = .02). Likewise, the postmortal blood ethanol concentration correlated negatively with age (r = -.26; p = .02), after controlling for the time interval. The lethal ethanol concentration for the aged seems to be lower than that for young people. A possible explanation for this phenomenon is the loss of ethanol tolerance.
Alcohol Clin Exp Res
PMID:Estimated lethal ethanol concentrations in relation to age, aspiration, and drugs. 637 35

The typical occupational cohort study includes all causes of mortality. However, emphasis is usually placed on the presence or absence of excess cancer mortality. A systematic review of completed occupational cohort studies to assess the findings and patterns of cardiovascular mortality would be useful. Although many of these studies will illustrate the "healthy worker effect" with deficits in mortality, particularly from cardiovascular causes, a thorough review should indicate certain exposures needing further research. A recently published study of heart disease mortality in the rubber industry illustrates the potential use of such a literature review with subsequent follow up. Production workers in the rubber industry have shown small excesses in CAHD mortality. A follow-up study at one plant confirmed the known association between carbon disulfide and atherosclerosis, as well as suggested two new causal associations between CAHD and the use of phenol and ethanol as solvents. What additional techniques can be used to generate hypotheses on heart disease and occupation? Some possibilities include: A recent article describes the use of the results of occupational disease surveillance systems for occupational cancer research. A review of such systems for heart disease would be equally useful. It would be useful to review the quality and quantity of occupational data that has been collected in prospective cohort studies, such as those in Framingham and Evans County. The importance of examining the association between occupational exposures and heart disease include: Assessing whether adequate protection is afforded by current limits on exposure to substances known to cause heart disease (carbon disulfide, nitrates, and carbon monoxide).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular disease and work place exposures. 638 Apr 27

Alcohol has acute and chronic cardiovascular effects. Acutely, alcohol depresses cardiac function and alters regional blood flow. Even when withdrawn from alcohol for several days, alcoholics may still manifest evidence of left ventricular dysfunction. In some alcoholics a severe muscle disorder may ensue with the clinical features of a dilated cardiomyopathy. The concomitant presence of a thiamine deficiency or cirrhosis may produce hemodynamic changes that can obscure the clinical features of alcohol-induced heart muscle disease. Alcoholics may also develop acute myocardial infarction with patent coronary arteries; some may have cardiac arrhythmias even without other evidence of heart disease. Although epidemiological studies suggest that moderate users of alcohol have fewer coronary events than teetotalers, such studies also demonstrate a relation between alcohol abuse and hypertension and an increased occurrence of coronary disease. Thus, the injurious cardiovascular effects of alcohol must be considered when establishing recommendations for its use.
Alcohol
PMID:Cardiovascular effects of alcohol with particular reference to the heart. 639 13

Although the "holiday heart syndrome," highlighted by rhythm disturbances after acute alcohol ingestion, is well known, the potential arrhythmogenic effects of alcohol have not been studied. Fourteen patients (two with congestive cardiomyopathy) with a history of rhythm disturbances and alcohol consumption were studied electrophysiologically. One patient had nonsustained ventricular tachycardia, one had nonsustained atrial fibrillation, one had paired ventricular responses, and the remainder had no response to the extrastimulus technique. After 90 mL of 80-proof whiskey, 10 of the 14 patients developed sustained or nonsustained atrial or ventricular tachyarrhythmias. Significant prolongation of His-ventricular conduction was seen after alcohol intake; this was noteworthy as one of the patients had previously shown Mobitz II atrioventricular block after acute alcohol consumption. Alcohol in modest doses has the potential to produce rhythm disturbances in patients with a history of chronic alcohol consumption and heart disease.
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PMID:The "holiday heart": electrophysiologic studies of alcohol effects in alcoholics. 682 46

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

To characterize metabolic factors potentially associated with alcohol-induced heart disease, myocardial ethanol intermediary metabolism was studied in isolated, perfused rabbit hearts and whole heart homogenates. Results showed that intact rabbit hearts and homogenates of rabbit left ventricle incorporate carbon-14-labeled ethanol at 20 and 59 nmol/g/h, respectively, into a neutral lipid species that co-migrates with triacylglycerides in standard chromatographic solvent systems. After isolation and purification by thin layer chromatography in an apolar solvent system, the labeled species were identified by gas chromatographic-mass spectral analysis to be a family of fatty acid ethyl esters. Heat inactivation of incorporation and the kinetics of formation of products suggest that the process is enzymatic. Gas chromatography identified the fatty acid components as predominantly unsaturated moieties, especially oleic, linoleic, and arachidonic acids. These results provide insight into potential biochemical mechanisms contributing to the triacylglyceride accumulation, decreased beta oxidation of fatty acids, and other lipid abnormalities typical of effects of ethanol on the heart.
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PMID:Identification of fatty acid ethyl esters as products of rabbit myocardial ethanol metabolism. 703 Oct 53

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

One hundred and forty-five alcoholics without known causes of heart disease, who were serially admitted to the alcohol detoxification centre, were studied to see the incidence of cardiac abnormalities and dose related effects of ethanol. All patients were divided into heavy (consumed more than the equivalent amount of 125 ml of pure ethanol daily for 10 years or more) and moderate drinkers (consumed 75 to 125 ml of ethanol daily). All of them were ambulatory and free from cardiac symptoms. There was no difference among heavy and moderate drinkers in the incidence of abnormalities detected by the electrocardiograms and chest x-ray films. In the alcoholics, the most frequent finding was a prolonged QTc interval of more than 0.44 s on the electrocardiogram (62 patients, 42.8%), unrelated to serum electrolytes imbalance. Cardiomegaly on chest x-ray film was observed in 25 patients (17.2%). M-mode echocardiogram was recorded in randomly selected patients and compared with age and sex matched controls. The interventricular septum and posterior wall were thicker in alcoholics, while left ventricular volume showed no difference. Left ventricular muscle mass was significantly increased only in heavy drinkers. Left ventricular function at rest was not depressed in these patients at an average of 31 days after the last drink of ethanol. Severe heart failure was not found even among the group of heavy drinkers, of whom more than 90% had liver dysfunction. Cardiac hypertrophy seems to occur in heavy drinkers, but is clinically well compensated in the majority of alcoholics.
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PMID:Cardiovascular status in asymptomatic alcoholics, with reference to the level of ethanol consumption. 731 20


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