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)

Four male patients aged 32 to 42 years were followed up. The clinical picture of the disease was typical of dilated (congestive) cardiomyopathy with a subacute onset, development of pronounced heart failure; all the patients were found to have exudate pericarditis. All the men were of the same occupation; they worked at the hard alloy works at a bay of wet grinding in ethanol of metallic Co and hard alloy carbides. The content of Co in the air of the working premises exceeded the MAC and amounted to 7.8-10 mg/m3. Besides, 47 workers of the same occupation (90% of the number of persons engaged in making up powdered compositions of hard alloys) were examined in addition. 16 persons showed the signs of alcoholization, including 9 (out of 11) working at a bay of wet grinding. During the recent 20 years, no cases of respiratory occupational diseases were recorded at the bay. The cardiotoxic properties of Co manifest themselves after the preceding toxic exposures, among which the leading part is played by alcohol. Of the 4 patients, 3 developed the disease in the presence of alcoholism, in 1 patient, it was coupled with tuberculous intoxication. Marked tendency towards polycythemia and increase of the content of hemoglobin was a frequently occurring manifestation of Co action on the workers (rather than a sign of intoxication).
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PMID:[Cobalt-induced cardiomyopathy in workers engaged in the manufacture of hard alloys]. 206 57

Ethanol has long been recognized as a toxic agent that has acute and chronic effects on cerebral and hepatic function. Over the past two decades important influences on the cardiovascular system have been either rediscovered or observed for the first time. The combined use of tobacco cigarettes and alcohol appears to increase the risk of many of these clinical abnormalities. While many individuals addicted to ethanol have subclinical abnormalities of the heart, somewhat less than a majority develop symptomatic cardiac problems. These include heart failure and arrhythmias. In addition to supraventricular arrhythmias that often normalize spontaneously, there is an increased incidence of sudden death that peaks at about 50 years of age in the alcoholic population. A significant degree of blood pressure elevation occurs in individuals who abuse alcohol. This appears to be transient and is normalized in most individuals during abstinence. The increased incidence of hemorrhagic and nonhemorrhagic stroke in middle age also appears to decline when alcohol abuse is interrupted. A preventive effect of mild to moderate drinking on coronary artery disease is, at present, equivocal, largely due to the question of appropriate controls.
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PMID:Alcohol and the cardiovascular system. 219 48

A complex approach to the whole range of diseases of the heart in alcoholics is presented. The authors are concerned with different variants of cardiac diseases induced by chronic alcoholism, understood and referred to in the light of the WHO concept as "alcoholic diseases of the heart". These conditions fall within the category of specific diseases of the myocardium, which in the stage of evident manifestations of cardiac insufficiency and dilation of the cavities are termed alcoholic cardiomyopathies. Although the etiology is not yet fully understood, the direct toxic effects of ethanol and acetaldehyde upon the structure and function of the myocardium due to the decreased functional activity of alcohol dehydrogenase and catalase are known to be involved in the development of alcoholic diseases of the heart. In chronic alcoholism the changes in the myocardium become increasingly irreversible. Moleculo-biological, biochemical, clinical, and morphological changes on cardiomocytes arising after the extensive effect of alcohol on different systems of the body are described in detail. The specific characteristics of clinical manifestations of different alcoholic diseases of the heart are analyzed and the currently used therapeutic procedures are discussed in relation to the clinical form and stage of the disease in the light of close cooperation with micrological departments.
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PMID:[Heart diseases in alcoholics]. 233 55

A 79-year-old white male was admitted to the hospital for treatment of a right-lower-lobe pneumonia. His past medical history included: mild congestive heart failure, asymptomatic ventricular tachycardia, and ethanol abuse. He was initially treated with furosemide for his heart failure, lidocaine for his arrhythmias, and Bactrim for his pneumonia. On day 13 of hospitalization he experienced a tonic-clonic seizure during the time he was being converted from lidocaine to tocainide. At the time of the seizure both tocainide and lidocaine were well within their respective therapeutic ranges. Since the seizure, the patient has tolerated treatment with each drug separately, and at serum concentrations similar to those preceding the seizure, without neurological complications, indicating the possibility of a tocainide-lidocaine induced seizure.
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PMID:A seizure induced by concurrent lidocaine-tocainide therapy--is it just a case of additive toxicity? 308 Feb 99

Thirty male patients with ischemic heart disease and cardiomyopathy entered a controlled study of the acute effects of alcohol on cardiac function evaluated by right heart catheterization. Twenty patients, nine with angina pectoris and 11 with congestive heart failure, were studied during alcohol intoxication, and ten patients, five with angina pectoris and five with heart failure, served as a control group. The mean serum ethanol concentration in the alcohol group was 93 mg/100 ml (S.D. 17). The systemic arterial blood pressure was reduced by 6% in the alcohol group, P less than 0.05 compared with the control group. No significant changes occurred in the central venous pressure, the pulmonary artery pressure, the pulmonary capillary wedge pressure, or in cardiac output, stroke volume and total peripheral resistance. Alcohol intake in moderate doses has no measurable effect on pulmonary blood pressures or cardiac output in patients with ischemic heart disease and cardiomyopathy. Such an effect may, however, be masked by a reduction of afterload.
Alcohol Alcohol 1988
PMID:Cardiac function after alcohol ingestion in patients with ischemic heart disease and cardiomyopathy: a controlled study. 335 19

In animal experiments, a new inotropic agent, (-)-(R)-1-(p-hydroxyphenyl)-2-[(3,4-dimethoxyphenetyl)amino] ethanol, designated TA-064 was found to possess a more positive inotropic than chronotropic action. Its effectiveness and lack of significant toxicity make it beneficial for clinical use as a cardiotonic in human heart failure. The effects of TA-064 were investigated in patients with various types of heart disease (n = 29). Cardiac output increased, left ventricular end-systolic dimension decreased, and left ventricular fractional shortening increased for 15 minutes after a single intravenous dose (1 mg). The plasma level of TA-064 at the cessation of infusion was 61.1 +/- 49.6 ng/ml and thereafter declined biexponentially. After a single oral dose (10 mg), TA-064 appeared in the plasma at 30 minutes and reached its peak levels of 13.7 +/- 5.6 ng/ml at 60 minutes. Seven hours later, the plasma level was 5.9 +/- 3.1 ng/ml which was considered to be within the effective range according to the results after intravenous administration. In conclusion, minimal effective plasma levels of TA-064 are obtained by oral administration of 10 mg three times a day.
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PMID:Clinicopharmacological studies of a newly synthesized cardiotonic agent (TA-064) in patients with congestive heart failure. 338 72

Eleven month old cardiomyopathic hamsters, which have enlarged hearts and anasarca, were given access to either an ethanol vehicle or an ethanol-digoxin solution in addition to a second water bottle. In comparison to controls, treated hamsters survived and showed significant amelioration of the pathological syndrome of heart failure. Thus, in this model of advanced congestive failure, digoxin has a clear-cut beneficial effect.
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PMID:The effect of chronic digitalis therapy on the course of heart failure and on endocrine function in cardiomyopathic hamsters. 343 75

Alcohol has been considered a cardiotoxin for over a century, but the pathogenesis and natural history of alcohol-related heart disease remains obscure. The diagnosis still rests on the coincidence of alcoholism and a dilated hypocontractile heart in the absence of any other cause of dilated cardiomyopathy. Advances have been made in our understanding of the effects of acute and chronic alcohol administration both at a haemodynamic and cellular level, and recent studies have indicated that preclinical changes in LV dimensions and function are common in alcoholics. It is not known whether clinical cardiomyopathy, which develops in only 1-2% of heavy drinkers, occurs because of genetic predisposition, or the presence of synergistic cardiovascular risk factors. Abstinence remains the mainstay of treatment, but the prognosis is poor after development of frank heart failure.
Alcohol Alcohol 1986
PMID:Alcohol and dilated cardiomyopathy. 352 84

This study examined the effects of ethanol and hereditary cardiomyopathy on sodium and water excretion by golden Syrian hamsters of both sexes. Ethanol (4 g/kg) or the isotonic saline vehicle were injected IP into 60-70-day-old hamsters of normal and cardiomyopathic (BIO 14.6) strains. Urine and blood were collected after 90 or 350 min in different groups. Cardiomyopathic hamsters more quickly lost their righting responses, eliminated ethanol more slowly, and had lower urine volume and sodium excretion than normal hamsters after ethanol injections. Plasma creatine kinase levels were normal in all animals tested, indicating no active skeletal or cardiac lesioning in the cardiomyopathic hamsters at the time of the experiment. Some factors which could contribute to the increased CNS and renal sensitivity to ethanol in cardiomyopathic hamsters include impaired ethanol metabolism, enhanced myocardial depression, and reduced atrial content of natriuretic peptides. The results do not owe to decompensated heart failure. Thus, the genetic mutation which causes skeletal and cardiac myopathy in these hamsters may also affect the metabolism and sensitivity to ethanol.
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PMID:Ethanol in cardiomyopathic hamsters: Na and water excretion and righting response. 371 87

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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