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

Relationships between parental socioeconomic status and CHD risk factors were examined in the Finnish Multicentre Study on Atherosclerosis Precursors comprising a material of 3,596 study subjects aged 3-18 years in five university cities and 12 rural communes. The work is based on the hypothesis that socioeconomic status has associations with important lifestyle factors related to the evolution of CHD risk factors. Although there is some indication that parental status variables correlate with CHD risk factors, the majority of the data point to the conclusion that socioeconomic status indicators have little relevance for children's CHD risk factor levels. The main exceptions to the above stated were the lower P/S ratio of the diet in farmers' children compared to the other socioeconomic groups in all age cohorts, and the higher serum total and LDL-cholesterol levels in the farmers' children as compared to the others in some age cohorts. The explanation to these findings is the dietary practice in farmers' households, full milk and butter being favoured instead of other milk types and vegetable margarine, respectively. Our findings illustrate the importance of the families' dietary habits with regard to certain CHD risk factors.
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PMID:Atherosclerosis precursors in Finnish children and adolescents. IX. Socioeconomic status and risk factors of coronary heart disease. 391 27

Malonic dialdehyde (MDA) content was studied in 23 patients with CHD due to coronary atherosclerosis, and in 6 with neurocirculatory dystonia without clinical and angiographic signs of CHD. MDA content as an indirect equivalent of cyclic endoperoxides was higher in the platelets, LDL and VLDL in patients with CHD. It may be a cause of TxA2 and PGI2 unbalance in the blood circulation and leads to the activation of thrombus formation, the decrease in the synthesis of "antiatherogenic" biologically active substances, in particular PGI2, thus promoting the development of CHD due to coronary atherosclerosis.
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PMID:[Malondialdehyde content of plasma lipoproteins and thrombocytes in patients with ischemic heart disease]. 650 34

The blood serum of coronary and liver patients was shown to display a similar increase in the relative levels of cholesterololeate and a some what less marked elevation in the content of cholesterol esters with saturated fatty acids. The cholesterollinoleate concentration was enhanced in patients with viral hepatitis and decreased in coronary heart disease patients. The differences were especially distinct in changes of the relative content of cholesterolarachidonate and esters of cholesterol with eicosopentaen acid. Cholesterolarachidonate levels showed no changes in CHD whereas they lowered markedly in various diseases of the liver and biliary tracts. The role of changes in the relative content of cholesterol ester fractions in the genesis of atherosclerosis in patients with liver diseases is discussed.
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PMID:[Serum cholesterol ester level in patients with ischemic heart disease and liver disease]. 652 Nov 91

This study of cerebrovascular lesions at autopsy among Hawaiian Japanese men identifies similar risks factors for cerebral infarction and hemorrhage that have been identified in a previous incidence study. Demonstrated differences were essentially the same whether subjects with these tissue changes were compared to men showing no central nervous system disease at autopsy or when they were compared with men still alive. Cerebral infarcts accompanied myocardial infarction (CHD) in 58% of autopsy cases and were associated with CHD risk factors (high serum cholesterol, hypertension, severe atherosclerosis of the coronary arteries and aorta). These associations did not persist when CHD cases were removed from the analysis, indicating there were two subsets of men with cerebral infarction. Hypertension was strongly associated with hemorrhagic disease, as were cigarette use and alcohol consumption.
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PMID:Risk factors related to ischemic and hemorrhagic cerebrovascular disease at autopsy: the Honolulu Heart Study. 669 27

The effect of tobacco cigarette smoking on plasma and platelet fatty acid composition was studied in 219 male subjects. The effect of tobacco on plasma malondialdehyde-like material (MDA-LM) was also evaluated. In the total fatty acid percentage composition in plasma, an increase in the saturated fatty acids at the expense of polyunsaturated fatty acids was observed in those subjects who smoked more than 20 cigarettes/day. In the total fatty acid composition of platelets, an increase in myristic acid (14:0) and palmytoleic acid (16:1) was found. Additionally, when the fatty acid composition of the different platelet lipid fractions was evaluated, an increase in 14:0 and 16:0 + 16:1 was observed in phospholipids. Finally, the plasma MDA-LM level was significantly higher in those subjects who smoked more than 10 cigarettes/day. The biochemical variations found in this study may be compatible with the greater incidence of CHD observed in smokers.
Atherosclerosis 1984 Jan
PMID:Effect of smoking on plasma and platelet fatty acid composition in middle-aged men. 669 83

The ultrastructure of the terminal arteries and arterioles was studied on biopsy samples obtained during aortocoronary bypass surgery in ten patients with stenosing atherosclerosis of the major coronary arteries and a history of chronic CHD. A complex of morphofunctional shifts was identified affecting all layers of the vessel wall and leading to readjustment of every coat. The major cellular populations directly involved included endotheliocytes, smooth muscle cells and stromal cells. Fibroblastic elements, penetrating by their processes up to the subendothelial zone stimulated total fibrosis of the vessel wall. The changes detected are indicative of the impaired patency and alterations in the responsiveness of resistant vessels which can considerably affect the microcirculation and trophicity of tissue.
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PMID:[Ultrastructure of terminal myocardial arteries in chronic ischemic heart disease]. 672 20

Gel-filtered platelets (GFP) from normal human subjects bound both low density lipoproteins (LDL) and high density lipoproteins (HDL). This binding was saturable and 125I-labelled lipoprotein uptake was inhibited by plasma. Platelets are also able to degrade lipoproteins but only to a limited extent. LDL appeared to compete with 125I-labelled HDL for platelet uptake, whereas the ability of HDL to displace 125I-LDL was limited. Cyclohexanedione-treated LDL (CHD-LDL), unlike CHD-HDL, did not compete with [125I]LDL for platelet accumulation, suggesting that arginine residues are necessary for LDL but not HDL binding. Addition of HDL or LDL to GFP did not alter platelet aggregation. However, in the presence of thrombin (0.5 U/ml), 1 mg/ml LDL incubated for 1 h at 23 degrees C enhanced platelet aggregation (215% increase) whereas HDL under similar conditions decreased aggregation by 53%. LDL also shortened the time of maximal aggregation whereas HDL had the opposite effect.
Atherosclerosis 1983 Mar
PMID:Platelet interaction with high and low density lipoproteins. 684 42

Atherosclerosis is a multifactorial disease. There are many theories surrounding its pathogenesis, none of which is more popular than the "lipid" hypothesis. There is an extensive body of evidence from experimental, epidemiological and pathological studies linking diet to plasma cholesterol on the one hand and plasma cholesterol to heart disease on the other. These data suggest strongly that education of the public about diet modification as one means of reducing CHD risk is a safe, appropriate and feasible approach to the prevention of the disease at the present time. The recommendations to the public are to reduce the fat content of their diets, specifically saturated fats, and limit the daily intake of dietary cholesterol to 300 mgs/day.
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PMID:Diet and coronary heart disease. 694 40

We have attempted to review the majority, if not all, of the available literature concerned with the Type A behavior pattern. The data indicate that the concept of TABP has construct validity and that it does not reflect the distinguishing characteristics of personality traits or psychopathology that are measured by standard psychometric inventories. They support the belief that TABP is an interplay of certain personality attributes and the environmental milieu. This behavior pattern is found to have a causal association with the prevalence and incidence of coronary heart disease and the severity of coronary atherosclerosis in both sexes and predictive strength that is equivalent to the standard risk factors for CHD. The concept of TABP and its relevance for CHD are shown to have cross-cultural validity and to have specificity for CHD in a relationship that has a biological gradient of pathogenecity. TABP can be assessed with substantial replicability and probably can be quantified. The National Heart, Lung, and Blood Institute recently assembled a review panel of more than 50 eminent scientists representing a variety of biomedical and behavioral specialties in order to critically examine the evidence for the association between TABP and CHD. In the opening paragraph of the panel's final report, it was stated that "The Review Panel accepts the available body of scientific evidence as demonstrating that Type A behavior (as defined by the structured interview, JAS, and Framingham scale) is associated with an increased risk of clinically apparent CHD in employed, middle-aged U.S. citizens. This increased risk is over and above that imposed by age, systolic blood pressure, serum cholesterol, and smoking and appears to be of the same order of magnitude as the relative risk associated with any of these factors" (402).
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PMID:The relationship of type A behavior pattern to coronary heart disease. 699 93

The body of evidence incriminating genetic factors in the etiology of CHD includes familial clustering of cases, with or without major hyperlipidemia; genetic influence on serum lipids levels in the general population; effect of genes belonging to normal polymorphisms on serum lipid levels and their variability; atherogenic effect of the genetically determined Lp(a) lipoprotein; and genetic influence on HDL apoproteins. Recent findings concerning the inherited apoE variation and genetic control of LDL cell membrane receptor activity in the general population are potentially of considerable interest. An improved understanding of the interaction between the products of "susceptibility genes" and environmental/dietary factors is important for attempts to prevent or delay the manifestations of atherosclerosis.
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PMID:The genetics of the hyperlipidemias and coronary artery disease. 716 16


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