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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overt coronary heart disease does occur at times in a setting of alcoholism. In an attempt to test the hypothesis that habitual excessive drinking may have an aggravating effect upon coexisting ischemic heart disease and may help precipitate new coronary events, we compared myocardial infarct prevalence among heavy drinkers and non-heavy drinkers with angiographically documented coronary artery disease. Infarct prevalence was found to be higher for heavy drinkers than for non-heavy drinkers under age 60 years, after controlling for differences in smoking habits and underlying atherosclerosis severity. A reversal in trend which may be due to the operation of selective factors causing premature coronary death among alcoholics was observed for individuals above age 60 years. These results, although open to differing interpretations, are consistent with the notion that heavy drinking has a destabilizing effect upon preexisting ischemic heart disease and may increase acute coronary event risk.
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PMID:Evaluation of habitual excessive alcohol consumption on myocardial infarction risk in coronary disease patients. 648 12

Compared to heavy drinking and abstinence, a moderate consumption of alcohol is associated with lower mortality rates due to coronary heart disease. About half of the protective effect of alcohol on cardiovascular risk can be explained by its ability to raise HDL-cholesterol. Alcohol can influence HDL metabolism at more than one site. Since light-to-moderate alcohol intake is associated with enhanced insulin sensitivity and improvement of insulin sensitivity results in higher HDL-cholesterol levels, it is suggested that this is one of the routes taken by alcohol to act upon HDL metabolism. Whether interrelated or not, both the HDL-cholesterol increase and enhanced insulin sensitivity are considered to have a beneficial effect on the process of atherosclerosis. Because of the well-known adverse consequences of excess alcohol use, these facts have not changed public health policy. On the other hand, they may have an impact on advice to selected patients, diabetics or non-diabetics.
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PMID:Alcohol and insulin sensitivity. 959 64

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

Alcohol taken in moderation may prevent atherosclerosis, whereas heavy drinking has the opposite effect, in part by promoting oxidation of low density lipoproteins (LDL), a pathogenetic factor in atherogenesis. We assess here: 1 ) whether similar alterations can be reproduced in baboons fed 50% of energy as ethanol (the average intake of alcoholics) for 7- 8 years, and 2 ) whether such alterations are affected by supplementation with polyenylphosphatidylcholine (PPC), a mixture of polyunsaturated phosphatidylcholines, shown to prevent alcoholic fatty liver, fibrosis, and cirrhosis. Ten animals were given the ethanol-containing diet and ten were pair-fed isocaloric control diets. In half of the pairs, the diets were supplemented with 2.8 g of polyenylphosphatidylcholine/1000 kcal. Alcohol feeding increased LDL-lipoperoxides and made LDL-proteins more negatively charged, changes that were attenuated or prevented by PPC. The oxidizability of LDL was determined in vitro by the formation of conjugated dienes after oxidation with copper. Alcohol shortened the lag time (which measures LDL antioxidant capacity); this effect was normalized by PPC supplementation. By contrast, PPC produced no changes in the controls. Thus polyenylphosphatidylcholine, by markedly attenuating the ethanol-induced increase in LDL oxidation, opposes one of the effects whereby alcohol promotes atherosclerosis.
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PMID:Oxidation of LDL in baboons is increased by alcohol and attenuated by polyenylphosphatidylcholine. 1035 29

The relationship between alcohol consumption and stroke is uncertain. Heavy alcohol consumption has been associated with an increased risk of stroke, while light drinking appears to be protective. However, the evidence is not uniform. We sought to examine the relationship between alcohol consumption and stroke, according to stroke type. We performed a population-based case-control study from September 1990 to December 1991. The study comprised 467 incident cases of stroke and 477 controls aged between 40 and 85. Case was defined following WHO criteria and control was randomly selected from the study base population. Alcohol exposure was obtained by medical interview. We found that consumption of less than 30 g/day of alcohol was protective against all stroke types combined, the multivariated adjusted odds ratio (OR) was 0.58 (95% confidence interval [CI], 0.41-0.83). Moderate alcohol drinking is also protective against all cerebral infarction combined (OR = 0.53; 95% CI, 0.35-0.80) and cortical infarction (OR = 0.40; 95% CI, 0.18-0.86). Drinking up to 30 g/day of alcohol has a borderline protective effect on deep cerebral infarction (OR = 0.40; 95% CI, 0.16-1.02) and has no effect on intracerebral hemorrhage (OR = 0.88; 95% CI, 0.44-1.74). Heavy alcohol drinking, over 140 g/day, is a risk factor for all stroke types combined (OR = 3.2; 95% CI, 1.1-9.7), all cerebral infarction combined (OR = 5.0; 95% CI, 1.5-16.3), small deep cerebral infarction (OR = 9.7; 95% CI, 2.6-36.7), intracerebral hemorrhage (OR = 6.2; 95% CI, 1.3-24.0), and is marginally associated with superficial cerebral infarction (OR = 4.6; 95% CI, 1.0-20.6). The relationship between alcohol and stroke depends on the alcohol dose and the pathology of the disease. Atherosclerosis of the large and medium cerebral arteries is found mainly in superficial cerebral infarction, and this type of stroke shows a J-shaped relationship with alcohol similar to that found in coronary heart disease, suggesting that they are similar diseases. On the other hand, arteriosclerosis of the penetrating arteries has been found in deep cerebral infarction and intracerebral hemorrhage, while atherosclerosis is not prominent. This may explain why alcohol does not have a protective effect on cerebral hemorrhage whereas heavy drinking is a strong risk factor in these two types of stroke.
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PMID:Alcohol and stroke: a community case-control study in Asturias, Spain. 1039 61

Free radicals are involved in the formation of both atherosclerosis and thrombosis. Therefore, considerable interest has recently been aroused by their role in the development of ischemic cerebral injury. Experimental observations suggest that antioxidants could reduce cerebral arterial vasospasm, reduce infarct size and prevent the development of both atherosclerosis and thrombosis. However, clinical evidence for these beneficial effects is still lacking. Alcohol can act as an antioxidant and an oxidant, and its intake seems to exert both beneficial and untoward effects on stroke, depending on drinking habits. Light-to-moderate regular alcohol intake has been suggested to protect against internal carotid artery atherosclerosis, a major cause of ischemic stroke. Ethanol metabolism in human blood vessel walls could antagonize the oxidation of LDL and thereby prevent the development of atherosclerosis. In addition, ethanol and the phenolic compounds of wine could decrease platelet aggregation and thromboxane formation and also prevent thrombus formation. Whether the effects are clinically significant remains to be proved. On the other hand, recent heavy drinking has been observed to worsen vasospastic ischemia caused by subarachnoid bleeding. Whether a lack of antioxidants is responsible for this effect also remains to be proved. Future stroke research should focus on solving these problems.
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PMID:Oxidants, antioxidants, alcohol and stroke. 1047 72

Stroke is a leading cause of death and morbidity, but incidence rates vary dramatically from one population to another. The reasons for this heterogeneity are being explored in several large-scale epidemiologic studies around the world. Much of the heterogeneity in stroke can be related to the prevalence of risk factors, but some populations have a higher stroke incidence than would be predicted from risk factor levels. Hypertension, including borderline hypertension, is probably the most important stroke risk factor based on degree of risk and prevalence. However, cardiac morbidity, cigarette smoking, diabetes, physical inactivity, and high levels of alcohol consumption are also strongly related to stroke risk. High levels of blood cholesterol and homocysteine may also increase stroke risk. Mortality after stroke is highest within the first 30 days but remains elevated to a degree that depends on the presenting stroke syndrome, stroke subtype, and other co-morbidities. Lacunar strokes have the best short- and long-term prognoses. Strokes due to large-vessel atherosclerosis frequently worsen; these and cardioembolic strokes have the poorest long-term prognosis. The risk for recurrence is also highest within 30 days after a first stroke, depending on the type of infarct, history of hypertension, and blood glucose levels on admission. Predictors of late recurrence include cardiac disease, hypertension, and heavy alcohol use. Only about half of stroke survivors are independent 6 months after a stroke, and quality of life is decreased. Understanding factors that predispose to stroke and determine its outcome will help in the design of acute stroke trials and in prevention programs.
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PMID:Risk factors and their management for stroke prevention: outlook for 1999 and beyond. 1053 44

Paraoxonase 1 (PON) may contribute to the cardioprotective action of high-density lipoprotein (HDL) because it inhibits low-density lipoprotein (LDL) oxidation, a prerequisite for the onset of atherosclerosis. Because light drinking and heavy drinking have diametrically opposite effects on cardioprotection, we have determined the effects of ethanol dosage on rat serum PON activity and its hepatic expression. Furthermore, we have investigated PON activity and polymorphism in human light and heavy drinkers. Our results confirm that HDL-PON inhibited LDL oxidation, destroyed oxidized LDL, and inhibited its uptake by macrophages. Light ethanol feeding caused a 20% to 25% (P <.05) increase in PON activity in both serum and liver and a 59% (P <.001) increase in the level of liver PON mRNA compared with pair-fed control rats. In contrast, heavy ethanol feeding caused a 25% (P <.05) decrease in serum and liver PON activities with a 51% (P <.01) decrease in liver PON mRNA level. Light drinkers had a 395% (P <.001) higher, whereas heavy drinkers had a 45% (P <.001) lower serum PON activity compared with nondrinkers. Significantly, the number of homozygotes versus heterozygotes with respect to high or low activity PON phenotype was similar in all the groups. Therefore, we conclude that light drinking upregulates, whereas heavy drinking downregulates PON activity and its expression, irrespective of its genetic polymorphism.
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PMID:Light, but not heavy alcohol drinking, stimulates paraoxonase by upregulating liver mRNA in rats and humans. 1456 80

Although moderate alcohol intake is associated with reduced risk of atherosclerotic disease in both the general population and in diabetic patients, a recent report suggests that heavy alcohol intake facilitates the development of atherosclerosis exclusively in diabetic individuals. We studied cross-sectionally the effects of the interaction between ethanol consumption category and the prevalence of diabetes on plasma total homocysteine (tHcy), a risk factor for atherosclerotic disease, in middle-aged men. Heavy drinking was associated with elevated tHcy levels only in diabetic subjects but not in non-diabetic subjects. Plasma tHcy of heavy drinkers (average ethanol consumption > 30 ml/day) was higher than that of abstainers in the diabetic subgroup (10.25 +/- 3.39 vs. 8.88 +/- 1.94 micromol/l, P < 0.05), whereas tHcy levels in heavy drinkers were comparable with that of abstainers in the non-diabetic subgroup (9.36 +/- 2.52 vs. 9.12 +/- 2.10 micromol/l, NS). In a two-factor anova, significant interaction was observed on the effects of ethanol consumption category and diabetes prevalence on tHcy levels (P < 0.01). Confounding factors including folate, vitamin B(12), creatinine, age or cigarette smoking did not contribute to the interaction. These findings may partly explain the reported association between heavy drinking and atherosclerosis in diabetic subjects.
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PMID:Heavy alcohol intake, homocysteine and Type 2 diabetes. 1617 97

While the effects of chronic ethanol consumption on liver have been well studied and documented, its effect on the cardiovascular system is bimodal. Thus, moderate drinking in many population studies is related to lower prevalence of coronary artery disease (CAD). In contrast, heavy drinking correlates with higher prevalence of CAD. In several other studies of cardiovascular mortalities, abstainers and heavy drinkers are at higher risk than light or moderate drinkers. The composite of this disparate relation in several population studies of cardiovascular mortality has been a "U-" or "J-"shaped curve. Apart from its ability to eliminate cholesterol from the intima of the arteries by reverse cholesterol transport, another major mechanism by which HDL may have this cardioprotective property is by virtue of the ability of its component enzyme paraoxonase1 (PON1) to inhibit LDL oxidation and/or inactivate OxLDL. Therefore, PON1 plays a central role in the disposal of OxLDL and thus is antiatherogenic. Furthermore, PON1 is a multifunctional antioxidant enzyme that can also detoxify the homocysteine metabolite, homocysteine thiolactone (HTL), which can pathologically cause protein damage by homocysteinylation of the lysine residues, thereby leading to atherosclerosis. We demonstrated that moderate alcohol up regulates liver PON1 gene expression and serum activity, whereas heavy alcohol consumption had the opposite effects in both animal models and in humans. The increase in PON1 activity in light drinkers was not due to preferential distribution of high PON1 genotype in this group. It is well known that wine consumption in several countries shows a remarkable inverse correlation to local rates of CAD mortality. Significantly, apart from its alcohol content, red wine also has polyphenols such as quercetin and resveratrol that are also known to have cardioprotective effects. We have shown that quercetin also up regulates PON1 gene in rats and in human liver cells. The action of quercetin seems to be mediated via the active form of the nuclear lipogenic transcription factor, sterol-regulatory element-binding protein 2 (SREBP2) that is translocated from endoplasmic reticulum to the nucleus. However, the mechanism of action of ethanol-mediated up-regulation of PON1 gene remains to be elucidated. We conclude that both moderate ethanol and quercetin, the two major components of red wine, exhibit cardioprotective properties via the up-regulation of the antiatherogenic gene PON1.
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PMID:Is alcohol beneficial or harmful for cardioprotection? 2001


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