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)

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

Immunomorphological and biochemical study of the myoglobin in the myocardium of 118 males at the age of from 30 to 55 years who died suddenly from coronary insufficiency, chronic pulmonary-cardiac insufficiency and from alcoholic cardiomyopathy in Magadan and Moscow is described. A decrease of the myoglobin concentration is revealed in the myocardium of the practically healthy Magadan citizeus as compared to that of moscovites. When the death occurred suddenly reduction of the myoglobin content is noted in the left ventricle simultaneously with its hypertrophy. It is shown immunomorphologically that myoglobin in the cytoplasm of cardiomyocytes is observed in the form of dense foci, granules and streaks. The myoglobin concentration tend to the reduction when there was hypertrophy of the right ventricle in patients dying from chronic pulmonary-cardiac insufficiency. Almost two-fold decrease of the myoglobin concentration in the left ventricle without its visible hypertrophy was observed in alcoholic cardiomyopathy, this may serve as a complementary test in the diagnosis of this disease.
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PMID:[Myocardial myoglobin in some types of cardiac pathology in the far northeastern USSR]. 407 41

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

Prognosis of 36 patients with congestive cardiomyopathy was studied in relation to various clinical factors. Half life of the survival curve after overt heart failure was about 7 years. Although left ventricular function was a major determinant of clinical course in congestive cardiomyopathy in general, its relation to prognosis was variable according to the type of cardiac involvement. In peripartal cardiomyopathy and in a type of cardiomyopathy named subacute cardiomyopathy with pulmonary thrombosis in this paper, factor(s) other than left ventricular function, possibly including pulmonary thrombosis, may be operative as more important determinant of extremely poor prognosis in these subtypes. Alcoholic cardiomyopathy was also unique in its favorable prognosis in association with reversible cardiomegaly following abstention from alcohol.
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PMID:Variable prognosis in congestive cardiomyopathy. Role of left ventricular function, alcoholism, and pulmonary thrombosis. 742 Jul 29

The mitochondrial respiration rate and morphometric indices in endomyocardial biopsy samples were measured in 43 patients with dilated cardiomyopathy selected in accordance to WHO criteria by endomyocardial biopsy studies after excluding of various forms of myocarditis, alcoholic cardiomyopathy and other specific diseases of the heart. A group of 13 patients with unusually high mean myocyte diameter, 30 +/- 4 microns, and nuclear size, 57 +/- 5 microns, was selected. The remainder of patients (n = 30) had significantly lower mean myocyte diameter and nuclear size, 23 +/- 3 and 42 +/- 6 microns, respectively, (p < 0.01). Creatine-stimulated elevation in mitochondrial respiration rate as measured in saponin-skinned fibers was found in the former group to be much lower (36 +/- 4%) as compared with the remainder (90 +/- 12%). Also, the former group of patients had higher left ventricular enddiastolic pressure and volume index with concomitantly decreased ejection fraction. The results indicate that marked nuclear and cellular hypertrophy is associated with lower creatine-stimulated mitochondrial respiration rate and more severe cardiac failure. They suggest that disorders in energy supply to myofibrils may be related to disturbances in cellular genetic apparatus.
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PMID:Cellular hypertrophy in cardiomyopathic patients is associated with lower creatine-stimulated mitochondrial respiration. 777 53

A pretransplant diagnosis was compared with the diagnosis made after macroscopic and microscopic examination of the explanted hearts in 112 cardiac transplant recipients. A coronary angiogram was recorded in 87.5% and endomyocardial biopsy was performed in 12.5% of patients within 1 year of the transplant. Echocardiograms were obtained in all patients. Before transplantation, 57.1% of patients were classified as having ischemic cardiomyopathy and 33.9% were classified as having idiopathic dilated cardiomyopathy (IDC). At explantation, severe coronary artery disease was found in all patients with a pretransplant diagnosis of ischemic cardiomyopathy, in 9 patients with a pretransplant diagnosis of IDC (6 of them had a "normal" pretransplant angiograms), and in 3 of the 4 patients with presumptive alcoholic cardiomyopathy. Left ventricular hypertrophy, undetected on echocardiography, was found at autopsy in 11 patients with presumed IDC, and acute myocarditis was found in 3 patients with a pretransplant diagnosis of IDC. A correct pretransplant diagnosis can lead to different management (e.g., bypass surgery rather than transplant), and may also portend different pre- and post-transplant prognoses. The results of this study suggest that an "in-depth" search for a cause should be conducted in all patients with heart failure, regardless of their clinical presentation. Our study also emphasizes the limitations of coronary angiography and echocardiography in patients with IDC and the need for improving current diagnostic techniques in these patients.
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PMID:Discrepancy between pre- and post-transplant diagnosis of end-stage dilated cardiomyopathy. 797 22

In patients with alcoholic cardiomyopathy there is evidence that mild heart failure is reversible if patients abstain from alcohol, but there is no consensus whether the disease is progressive once structural myocardial dilation has evolved. The aim of the present study was to compare the long-term course of congestive heart failure due to alcoholic and idiopathic dilated cardiomyopathy. Of 75 patients with overt congestive heart failure, 23 had alcoholic cardiomyopathy and were compared to 52 patients with idiopathic cardiomyopathy. The mean age was 48 +/- 12 years. Despite medical therapy, heart failure class New York Heart Association III-IV was present in 52% of patients with alcoholic and 47% of patients with idiopathic cardiomyopathy (not significant). Their mean left ventricular ejection fraction was 30 +/- 12% vs 28 +/- 12% and left ventricular end-diastolic volumes were 264 +/- 125 ml and 254 +/- 100 ml respectively (not significant). Overall survival at 1, 5 and 10 years was 100%, 81% and 81% for the group with alcoholic dilated cardiomyopathy and 89%, 48% and 30% for the group with idiopathic cardiomyopathy, respectively (P = 0.041), and the difference was even greater for transplant-free survival P = 0.005). Clinical and invasive signs of left and right heart failure as well as left ventricular dimensions were predictive of a fatal outcome; however, symptom duration and left ventricular volumes were only predictive in patients with idiopathic cardiomyopathy, suggesting that in the two patient groups different mechanisms may lead to death. Mortality in patients with severe congestive heart failure and left ventricular dilatation due to alcoholic cardiomyopathy is significantly lower than that in patients with idiopathic cardiomyopathy and similar degrees of heart failure. Thus, despite structural changes inherent in marked left ventricular dilatation, disease progression in alcoholic dilated cardiomyopathy is different from that in idiopathic cardiomyopathy and thus may have implications for the choice of therapy.
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PMID:Differences of disease progression in congestive heart failure due to alcoholic as compared to idiopathic dilated cardiomyopathy. 873 67

Chronic alcohol consumption has been postulated as an important pathogenetic mechanism for the development of alcoholic cardiomyopathy. This form of chronic heart failure shares with other forms of cardiomyopathy the pronounced alterations of the adrenergic signal transduction systems. These alterations include a significant reduction of beta-adrenergic receptors and a reduced responsiveness of the adenylyl cyclase. Changes of other receptor systems such as alpha-adrenergic and muscarinic receptors have not been studied extensively so far. To address the question if changes of the adrenergic signal transduction systems may occur early in the development of alcoholic cardiomyopathy and if alpha 1-adrenergic receptors and muscarinic receptors may be subjected to an altered expression even before severe impairment of the left ventricular function becomes obvious, rats were chronically fed with an alcohol diet containing 35% of total calorie intake as ethanol. In cardiac plasma membranes beta-adrenergic receptors, alpha 1-adrenergic receptors, muscarinic receptors and adenylyl cyclase activities were determined after 4 and 8 weeks of chronic alcohol treatment. After these periods of chronic alcohol diet no signs of overt heart failure such as pleural effusion or increased lung wet weight as parameters for congestion were present. Body weight gain was comparable in the controls and under chronic alcohol treatment in these adolescent rats. Both after 4 and 8 weeks of chronic alcohol treatment the density of cardiac beta-adrenergic receptors remained unchanged and all adenylyl cyclase activities remained fully responsive. In contrast, after 8 weeks of alcohol treatment the developmental increase of cardiac muscarinic receptors in the adolescent rats was greatly impaired resulting in a significantly reduced expression of these receptors even before clinical signs of heart failure. In contrast the density of cardiac alpha 1-adrenergic receptors were significantly reduced already after 4 weeks of chronic alcohol treatment with an additional impairment of the developmental increase after 8 weeks of alcohol treatment. These data characterize for the first time early changes of cardiac receptor system in chronic alcohol treatment which precede the development of overt heart failure. These changes include alpha 1-adrenergic and muscarinic receptors, but in contrast to severe heart failure, leave the beta 1-adrenergic system and the responsiveness of the adenylyl cyclase intact. Additionally these data show the developmentally increased expression of cardiac alpha 1-adrenergic and muscarinic receptors in rat heart.
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PMID:Changes in cardiac signal transduction systems in chronic ethanol treatment preceding the development of alcoholic cardiomyopathy. 880 3

The direct toxic effect of alcohol and its metabolite acetaldehyde has been demonstrated both in laboratory animals and in humans. Alterations in the mitochondrial ultrastructure and the dilatation of the sarcoplasmatic reticulum have been shown after an acute infusion of alcohol in the heart. These changes correlate with decreased mitochondrial function, defects in protein synthesis and the occurrence of arrhythmias. The risk of developing alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking, but there is much individual susceptibility to the toxic effect of alcohol. Most patients, in whom alcoholic cardiomyopathy develops, have been drinking over 80 g/d for more than 5 years. The clinical diagnosis of alcoholic cardiomyopathy reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease was found. In studies focussing on alcoholic cardiomyopathy the surprising histologic findings in endomyocardial biopsy in about 30% of all cases was myocarditis with a lymphocytic infiltrate in association with myocyte degeneration or focal necrosis. In myocarditis, the network of microtubules and intermediate filaments is also disrupted by the inflammatory reaction which involves resident cells (myocytes, fibroblasts, endothel cells) and systemic cells (granulocytes, macrophages, monocytes, lymphocytes). Changes in the cardiac cytoskeleton and the extracellular matrix may affect contractile function, since the cytoskeleton organizes the intra- and intercellular architecture. After all, in patients with alcohol abuse and myocarditis the immune functioning appears to be compromised. Several studies suggest that heavy drinking alters both lymphocyte and granulocyte production and function. Alcohol consumption per se might harm the immune system. Furthermore, the myocardial damage due to alcohol consumption could initiate autoreactive mechanisms comparable to those in viral or idiopathic myocarditis. Patients with alcohol abuse and myocarditis have a poor prognosis: signs of biventricular failure including tachycardia, hepatomegaly, and peripheral and lung edema are observed. These symptoms are as nonspecific as are various echocardiographic and electrocardiographic changes such as atrial and ventricular arrhythmias which may be associated both with myocarditis, alcoholic cardiomyopathy and acute effects of drinking without hemodynamic alterations. For the management of patients with alcohol abuse the prevention of further alcohol intake is mandatory to reverse the myocardial damage and the unfavorable predisposition for infection. Specific treatment of myocarditis is the second important option, and treatment of heart failure by reducing the size of the dilated heart and alleviating the signs and symptoms of heart failure is a logical third step.
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PMID:[Alcohol and myocarditis]. 880 5


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