Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytochemical, biochemical and morphological changes in peroxisomes have been described in human metabolic disorders, in experimental models of disease and in response to drugs and toxins. These include the cerebrohepatorenal syndromes, in which peroxisomes can not be detected and mitochondrial respiration is inhibited, atherosclerosis, alcoholic cardiomyopathy, and tolerance to oxygen toxicity. Although information on the role of peroxisomes in disease is limited, increased awareness of their widespread distribution and the availability of an improved cytochemical procedure for staining peroxisomes in human specimens should provide new insights into their function.
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PMID:Peroxisomes in disease. 39 36

Cirrhosis is associated with several circulatory abnormalities. A hyperkinetic circulation characterized by increased cardiac output and decreased arterial pressure and peripheral resistance is typical. Despite this hyperkinetic circulation, some patients with alcoholic cirrhosis have subclinical cardiomyopathy with evidence of abnormal ventricular function unmasked by physiologic or pharmacologic stress. Florid congestive alcoholic cardiomyopathy develops in a small percentage, but the concurrent presence of cirrhosis seems to retard the occurrence of overt heart failure. Even nonalcoholic cirrhosis may be associated with latent cardiomyopathy, although overt heart failure is not observed. Tense ascites is associated with some cardiac compromise, and removing or mobilizing ascitic fluid by paracentesis or peritoneovenous shunting results in short-term increases in cardiac output. Cirrhosis also appears to be associated with a decreased risk of major coronary atherosclerosis and an increased risk of bacterial endocarditis. Small hemodynamically insignificant pericardial effusions may be seen in ascitic patients. The release of atrial natriuretic peptide appears to be unimpaired in cirrhosis, although the kidney may be hyporesponsive to its natriuretic effects.
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PMID:Cardiac abnormalities in liver cirrhosis. 269 Apr 63

Because of the high frequency of cardiovascular diseases and a steadily increasing consumption of alcohol the potentially causal relationship between alcohol and cardiovascular diseases gains great interest for public health policy. Alcohol and its metabolites induce a toxic damage of myocardial metabolism with an injury of electromechanic coupling. As a consequence of acute alcoholic intake cardiac arrhythmias and a reduced contractility of the myocardium are found not only for chronic alcoholics but also in healthy non-drinkers. Chronic abuse of alcoholic beverages for many years can be the cause of alcoholic cardiomyopathy in a small percentage of patients, who have a bad prognosis. Atria and ventricles are dilated, light and electron microscopic changes of the myocardium are unspecific. The pathogenesis of alcoholic cardiomyopathy is unknown, modulations of cardiomyocytic membranes are discussed in the course of a toxic damage. In the genesis of atherosclerosis alcohol can approach from different sites: Changings on thrombocytes and an increase of HDL-cholesterin can be protective, however an increase in blood pressure support the process of atherosclerosis. In numerous investigations a smaller degree of atherosclerosis was found for little or moderate alcohol intake, while in chronic heavy abuse of alcohol a higher extent of atherosclerosis was observed. As the amount of alcohol, assumed to be protective against the development of atherosclerosis, is consumed already by the majority of the population, there is no reason to propagate a regulate consume of moderate amount of alcoholic beverages.
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PMID:[Alcohol and the cardiovascular system]. 306 47

Evident disparities in relationships make it desirable to consider several disorders separately. (1) Alcoholic cardiomyopathy was perceived 150 years ago, but understanding was clouded by recognition of beriberi and of synergistic toxicity from alcohol with arsenic or cobalt. (2) A report of a link between heavy drinking and hypertension in WWI French soldiers was apparently ignored for > 50 years. Epidemiological and intervention studies have now firmly established this association, but a mechanism remains elusive. (3) The 'holiday heart syndrome', an increased risk of supraventricular tachyarrhythmias in alcoholics, has been widely known to clinicians for 25 years; data remain sparse about the total role of heavier drinking in cardiac rhythm disturbances. (4) Failure of earlier studies to distinguish types of stroke impeded understanding; it now seems probable that alcohol drinking increases risk of haemorrhagic stroke but lowers risk of ischaemic stroke. (5) Heberden reported angina relief by alcohol in 1786, and an inverse alcohol-atherosclerosis association was observed by pathologists early in this century. Recent population studies and plausible mechanisms support a protective effect of alcohol against coronary disease. International comparisons dating back to 1819 suggest beverage choice as a factor, but this issue (the 'French Paradox') remains unresolved.
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PMID:Alcohol and cardiovascular diseases: a historical overview. 994 84

Sudden cardiac death (SCD) is an integral term for several heart diseases among which SCD caused by ischemic heart disease (IHD) designated as sudden coronary death (SCD) ranks first. SCD associated with alcoholic cardiomyopathy ranks second. Risk factors and pathologic manifestations of SCD correspond to those of IHD, atherosclerosis, myocardial infarction. Cardiac arrest takes place because of fibrillation of ventricular myocardium. Factor inducing fibrillation is an advanced irreversable myocardial ischemia complicated with reperfusion. The latter promotes elimination of arrythmogenic substances from the ishemic zone leading to electric unstability of the myocardium and fatal arrythmia. Possibility of idiopathic ventricular fibrillation and its mechanisms is discussed.
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PMID:[Sudden cardiac death: state of the art]. 1607 3