Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighteen patients with dilated cardiomyopathy and a history of excessive ethanol intake were monitored for 3-98 months (mean 23 months). Six patients died (mean age 43.7 +/- 9.2 years) and 12 patients survived (mean age 48.8 +/- 9.5 years). Of the echocardiographic findings taken during heart failure, only the relative wall thickness to the internal dimension of the left ventricle (t/r ratio) differed significantly (survivors 0.33 +/- 0.77 vs. nonsurvivors 0.25 +/- 0.04, P less than 0.05). Of the hemodynamic data obtained after treatment of heart failure, left ventricular end-diastolic pressure differed significantly (survivors 6 +/- 2 vs. nonsurvivors 12 +/- 4 mmHg, P less than 0.001). The two groups could not be differentiated by ejection fraction, cardiac output, end-diastolic or end-systolic volumes, or semi-quantitative analysis of histologic findings obtained by right ventricular endomyocardial biopsy (light microscopy). Only two of six nonsurvivors (33%) succeeded in abstaining from alcohol, while eight of twelve survivors (67%) became teetotalers (P less than 0.05). Total abstinence from alcohol seems to be essential but was not necessarily followed by recovery in the most severe cases. Thus, the absence of adequate hypertrophy and high left ventricular filling pressure may predict the prognosis in alcoholic heart disease.
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PMID:Factors discriminating survivors and nonsurvivors in alcoholic heart disease. 384 91

The hypersplenism associated with portal hypertension usually resolves with a successful shunting procedure. Recurrent hypersplenism has been associated with shunt thrombosis. We describe a patient with pancytopenia, jaundice, and diffuse edema after a distal splenorenal shunt. His shunt was angiographically proved patent. Extensive evaluation revealed severe alcoholic cardiomyopathy with passive splenic congestion. He died of cardiac failure. Alcohol is a systemic toxin that affects other organs, as well as the liver.
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PMID:Recurrent hypersplenism caused by alcoholic cardiomyopathy after distal splenorenal shunt. 395 75

Computer assisted analysis is useful for measurements in left ventricular echocardiograms. After manual input in the computer with the aid of an electronic pen, dimensions and contractility are determined by our selfmade programs. The left-ventricular function analysis (on the basis of the circumferential fibre shortening rate) demonstrated for tricyclic antidepressant drugs a dose-dependant loss of myocardial contractility. This effect was pronounced by ethanol, propranolol, reserpine and was compensated by orciprenaline. Chronic ethanol consumption caused heart failure detected by this noninvasive investigation. In healthy volunteers the most striking result of our measurements was that amitriptyline-treated subjects showed a loss of myocardial contractility. After both mianserin and amitriptyline an increase of the mean arterial blood pressure and the heart rate was observed. The simultaneous investigation with the invasive and non invasive parameters of contractility in dogs demonstrated that echocardiography in combination with our semiautomatic computer-system is able to measure myocardial contractility with this noninvasive method.
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PMID:[Computer assisted echocardiography functional diagnosis. The question of inotropic effect of antidepressive drugs and ethanol]. 636 Aug 33

The effect on the heart of a combination of high blood pressure and chronic alcohol ingestion was studied in spontaneously hypertensive rats (SHR) fed ethanol in their drinking water in concentrations of 0%, 5% and 20% for sixteen weeks. Normotensive Wistar rats were used as controls (NCR). In addition some SHR were given alcohol for a shorter period of eight weeks at the end of which time there were no significant differences in mean arterial blood pressure between the groups. After sixteen weeks of ethanol the mean arterial pressure had fallen in those SHR receiving 20% ethanol to 136 +/- 24 mmHg compared to control (180 +/- 27 mmHg; P less than 0.001). This was associated with a lower left ventricular (LV)dp/dt (control 4800 +/- 872 mmHg sec-1; 20% ethanol group = 3450 +/- 1588 mmHg sec-1; P less than 0.025) and a reduced LV weight (corrected for body weight) due to an apparent lack of development of LV hypertrophy between eight and sixteen weeks. Similarly LV volume (corrected for LV weight), did not change from eight weeks to sixteen weeks in those SHR receiving 20% ethanol in contrast to the 0% ethanol SHR group in whom LV volume fell as LV hypertrophy developed. 5% Ethanol had no significant effect on mean arterial pressure, LV peak dp/dt, LV weight or LV volume. In the NCR ethanol had little effect on mean arterial pressure but those receiving 20% ethanol had significantly smaller LV volumes without any increase in LV weight probably reflecting blood volume depletion. Ethanol did not produce any blood pressure elevation in the NCR. No rats (SHR or NCR) developed overt heart failure or a typical cardiomyopathy. However, this study has shown that a high intake of ethanol reduces the blood pressure of a hypertensive rat most likely by its direct toxic action on the myocardium. Thus with chronic alcohol ingestion hypertension can be masked but may still contribute significantly to the development of myocardial disease.
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PMID:Effect of chronic alcohol ingestion on the heart and blood pressure of spontaneously hypertensive rats. 668 5

Vulnerability to atrial fibrillation and flutter was examined in 11 alcohol abusers who did not have cardiomyopathy or manifest heart failure. Atrial extrastimulation was done with rapid pacing (drive cycle length 500 ms) to facilitate induction of atrial vulnerability, seen in four alcohol abusers. The remaining seven were retested 30 minutes after drinking 60 to 120 ml of 86 proof whiskey (ethanol blood levels were 49 to 101 mg/100 ml but pulmonary capillary wedge pressure remained normal in all) and atrial fibrillation or flutter was induced in three of the drinkers. Three nondrinkers, symptomatic with sinus bradycardia but not in heart failure, were found not to be vulnerable to atrial fibrillation or flutter, but flutter was induced in two of the three after drinking whiskey. Whiskey did not alter atrial functional refractory periods (mean +/- standard error of the mean 297 +/- 14 to 290 +/- 12 ms) or widen the dispersion among three disparate right atrial sites (57 +/- 13 to 47 +/- 12 ms). Thus, whiskey enhanced vulnerability to atrial fibrillation and flutter in patients without heart failure or cardiomyopathy, substantiating the "holiday heart" syndrome.
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PMID:Effect of whiskey on atrial vulnerability and "holiday heart". 682 72

The myocardium of both heart ventricles in acute (AAP) and chronic (CAP) alcoholic poisoning was studied in 90 randombred rats. Functional-morphological changes typical of alcoholic cardiomyodystrophy were shown to develop in the heart in AAP and CAP. In AAP, alcoholic cardiomyodystrophy may lead to acute cardiac insufficiency and in CAP to progressive reduction of the contractile function of the heart and disturbances of conductivity in it. In AAP, however, the leading factor is the disturbance of bioenergetics as a result of toxic effect of ethanol and its metabolites on mitochondrial membranes under conditions of markedly disordered microcirculation. In CAP, along disordered microcirculation. In CAP, along with compensatory-adaptative processes in cardiomyocytes there increase the defects of the contractile apparatus, and diffuse fine-focal cardiosclerosis. This is the result of a long-term effect of ethanol and progressive hypoxia due to the affected vessels and disorders in lipid metabolism. Disorders in the function of sarcoplasmic reticulum may contribute to reduced contractile capacity of the heart.
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PMID:[Myocardium in acute and chronic experimental alcoholic intoxication]. 689 Jul 96

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

Alcohol, adriamycin, viruses and excess deposition of iron in the heart are known to induce cardiomyopathy. Altered immune response in the form of defective T cell function, overactive anti-body-producing B lymphocytes and circulating anti-heart antibodies; increased fibrous tissue in the heart, with a tendency to develop mural thrombi, arrhythmias and cardiac failure are some of the important features observed in these cases. Prostaglandins can modify immune response, regulate fibrous tissue and collagen biosynthesis, are believed to be involved in the pathogenesis of cardiac arrhythmias and failure. Ethanol, adriamycin, viruses and iron are known to alter prostaglandin(PG) synthesis. The altered PG function may play a major role in cardiomyopathy.
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PMID:Possible role of prostaglandins in the pathogenesis of cardiomyopathies. 719 84

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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