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)

This study shows that 33.3% of English patients with primary hyperlipidemia (52/156) had the S2 allele of the apo AI/CIII/AIV complex compared to 6.1% of normolipidemic individuals (3/49). The increased frequency of the allele was statistically significant in each of the hyperlipidemic groups (type IIA, excluding patients with FH, type IIB and IV) examined and was not specifically related to hypertriglyceridemia. This finding may account for the result of several studies which showed groups of patients with CHD had a significantly higher prevalence of the S2 allele than control groups. Our data do not support the notion that the increased frequency of this allele in CHD patients is independent of variations in plasma lipid levels, since we find the frequency of the S2 allele in an apparently healthy hyperlipidemic group of patients is very similar to a hyperlipidemic group with symptomatic premature atherosclerotic disease. This study also shows the BMI of the type IIB and IV hyperlipidemic patients is significantly higher than the type IIA (no xanthomas) group. This may modulate the expression of the defect associated with the S2 allele. When the type IIB and IV hyperlipidemic groups were divided into 2 groups according to their apo AI/CIII/AIV genotype (i.e., S1S1, S1S2 (including S2S2] there was no significant difference in the mean plasma level of total cholesterol, HDL-cholesterol and triglycerides between the 2 groups. In contrast the S1S2 type IIA individuals had higher plasma cholesterol levels.
Atherosclerosis 1989 Dec
PMID:Variation in the apo AI/CIII/AIV gene complex: its association with hyperlipidemia. 251 96

The associations of CHD, as defined by coronary arteriography, with hypertension history and causal blood pressure in 103 CHD cases and 103 non-CHD controls matching on sex, race, age(within 3 years)was studied. The odds ratio (i.e.OR) of CHD for patients with hypertension history is 4.64. For patients with higher causal blood pressure, it is 3.53 with both 99% confidence intervals not include 1. There are significant dose-response relationships between level of systolic hypertension and duration of hypertension with regards to odds ratio of CHD or the degree of coronary atherosclerosis. The relative risk of CHD may reduce 70-80% for hypertension patients by taking drugs to lower blood pressure. There are significant correlation between hypertension and myocardial infarction in clinical types of CHD. The CHD average incubation period caused by hypertension is 10 years. It is concluded that the relationship between hypertension and CHD is seemingly causality with part of patients suffering from other consequences.
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PMID:[Hypertension and angiographically defined coronary heart disease]. 261 69

The family at risk has at least one member who has (1) hyperlipidemia; (2) low HDL2-cholesterol; (3) essential hypertension; (4) a family history of premature CHD; or (5) actively smokes. The predictive value of CHD risk factors in adults is well documented and quantified. Familial aggregation, genetic studies, and tracking of blood pressure provide evidence that children born to families with a high prevalence of hypertension or who as adolescents track in the upper part of the blood pressure distribution are themselves at risk for hypertension. Similarly, familial aggregation, tracking, and autopsy studies provide evidence for the relationship of serum lipids to the subsequent development of coronary atherosclerosis. Smoking by parents adversely affects the hearts and lungs of children. In addition, the child with a parent who smokes is more likely to become an active smoker. Preventive strategies are now available to the pediatrician to reduce the risk of premature CHD.
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PMID:The management of the family at high risk for coronary heart disease. 265 86

Hyperlipidaemia and in particular hypercholesterolaemia is the best established cause of atherosclerosis. As awareness of this association grows amongst a more informed populace, there will be an increasing demand for plasma lipid screening. The traditional measurements of total plasma cholesterol and triglycerides for the assessment of hyperlipidaemia and its attendant CHD risk are now augmented by the availability of routine methods for separating and quantitating the different plasma lipoproteins, thus vastly improving diagnostic sensitivity. Because it is the major carrier of cholesterol in plasma and because the mechanistic evidence relating it to atherogenesis is strongest, elevated levels of the low density lipoproteins (LDL) are undesirable: high levels of high density lipoproteins (HDL), on the other hand, decrease the risk. Currently, plasma LDL and HDL concentrations are most frequently assessed by measuring their cholesterol content. However, the measurement of apolipoproteins, the protein components of the lipoproteins, may yet prove to be superior in predictive value, though they can hardly be expected to replace the older tests as first line screening tests by virtue of their relative costs and sophistication in terms of instrumentation and techniques. Additional diagnostic tests have been developed and newer ones will no doubt continue to evolve with further technical advancements and a better understanding of the pathogenesis of atheromas and vessel disease. The current lineup includes HDL subfractions, unique lipoproteins such as Lp(a) and beta-migrating VLDL and apolipoprotein E variants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma lipid profiles: the expanding repertoire of tests, their clinical significance and pitfalls. 267 44

Sufficient evidence exists today pointing to the relationship between high levels of plasma cholesterol and coronary atherosclerosis. Up to now, however, the last criterion for validating the aetiopathogenetic relationship between dyslipidemia and CHD, i.e., the demonstration that reduction of plasma cholesterol reduced the formation or progression of the plaque and the incidence of its fatal or non-fatal cardiac and vascular complications, has been lacking. For more than two decades, numerous trials have had this aim in mind but until very recently results have not been substantiated owing to various deficiencies in the method. Before publication of the NHLBI Task Force of Atherosclerosis, eleven major randomised clinical studies based on hypolipidemia interventions were completed. The three studies involving dietetic interventions were considered non-conclusive overall because of the lack of a double-blind factor and of other important epidemiological criteria. Of three pharmacological trials only two involved studies of primary prevention carried out on a population of hypercholesterolaemics. These produced partial results on certain cardiac end-points but not on total deaths and at times not even on deaths from CHD. Multifactorial studies, finally, were even less demonstrative. Taken together, however, the trials based on hypolipidemia interventions point to interesting though not definitive evidence of a reduction in blood cholesterol levels to reduce the incidence and mortality from CHD. According to the NHLBI, many of these studies lacked important features that were codified and suggested for later studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The lipid hypothesis in the etiopathogenesis of ischemic heart disease: confirmations and doubts resulting from primary prevention trials]. 277 Oct 85

Human plasma contains a factor capable of stimulating vascular prostacyclin generation even in atherosclerotic vessels with minimal in-vitro capacity for PGI2-synthesis. The activity of this prostacyclin stimulating plasma factor (PSPF) has been reported to be elevated in renal failure and hepatic coma. We are not aware of any data as to whether this PSPF plays a role in maintaining hemostatic balance in patients with peripheral vascular lesions. Therefore, we examined 62 patients with peripheral vascular disease (PVD). This study group was subdivided into normo- and hyperlipemic subjects, patients with and without maturity onset diabetes, and plasma beta-thromboglobulin levels higher and lower than 50 ng/ml. 10 healthy sex and age matched persons served as controls. Vascular prostacyclin formation was studied in vitro after incubation of the patients' plasma and a buffer control with various tissue samples (human femoral artery, rat abdominal and thoracic aorta of healthy and of streptozotocin induced diabetic animals, swine endothelial layer and remaining tissue (media and adventitia) and cultured endothelial (EC) and smooth muscle cells (SMC) of minipig arota. In addition, 6-oxo-PFG1 alpha formation by cultured EC and SMC (minipig aorta source) after incubation with tris HCl-buffer or plasma were estimated by means of specific radioimmunoassays. In general, tissue samples and cells incubated in plasma exhibit a marked increase of in-vitro PGI2-formation as compared to buffer. No difference could be found between PSPF of CHD-patients and healthy controls. Similar findings were obtained using incubated vascular tissue and cultured cells by means of the bioassay and specific RIA, respectively. These findings indicate that the PSPF does not seem to be of any clinical relevance in hemostatic regulation in patients with advanced atherosclerosis.
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PMID:Prostacyclin synthesis stimulating plasma factor in patients with peripheral vascular disease. 295 84

Coronary heart disease should not be considered a male dominated disease. The incidence of clinical CHD lags by several years in women, but it remains a leading cause of death and disability in the adult female. Risk factors for the development of coronary atherosclerosis are essentially the same for both sexes. Management strategies are usually similar regardless of gender.
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PMID:Coronary heart disease in women: evaluation and management. 306 36

Low (LDL) and high density lipoproteins (HDL) stimulated prostacycline (PGI2) synthesis in rabbit and human aorta smooth muscle cells growing in culture. The lipoproteins were added to the cells in concentrations equal to that of cholesterol. It was shown that HDL exerted a stronger stimulating effect as compared to LDL. The maximal effect was observed with HDL3. HDL3 isolated from blood serum of healthy volunteers appeared to be more active in PGI2 synthesis promotion than those of CDH patients with documented coronary atherosclerosis. Purified Apo A-1 stimulated the transformation of [14C]arachidonic acid into the products of its metabolism with increased accumulation of 6-keto-PGF1 alpha among labeled metabolites. Estradiol (1.10(-7) M) showed a stimulating effect; norepinephrine (1.10(-6) M) and progesterone (1.10(-7) M) showed an inhibiting effect, whereas corticosterone (1.10(-6) M) and deoxycorticosterone (1.10(-6) M) did not influence the rate of LDL-dependent PGI2 synthesis.
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PMID:[Lipoprotein-dependent synthesis of prostacyclin in smooth muscle cells]. 312 34

A massive body of scientific evidence from clinical, experimental, pathological and epidemiological studies as well as from risk factor intervention trials and community studies has emerged until the 1980s; interpreted as a whole it leaves no more doubt about the major role of hyperlipidaemia, hypertension, cigarette smoking and some other modifiable factors in the aetiology of atherosclerosis and CHD, and about the great potential for primary prevention of CHD. In response to this challenge, the World Health Organization Expert Committee in its report in 1982 outlined the general principles and strategies for the primary prevention of CHD, and these principles and strategies have then been reinforced and further developed toward practical action plans by international and national experts groups. The perspectives for the primary prevention during the future decades may be envisaged to include: (1) further strengthening of preventive action in those countries with high or relatively high CHD rates in which favourable changes in life-styles and risk factor levels are already going on and CHD rates are declining; (2) development and implementation of effective plans for preventive action in those countries with high or relatively high CHD rates in which these rates are not yet declining or even increasing, and (3) development and implementation of effective plans for a real primordial prevention of CHD, i.e., preventing the appearance of unhealthy life-styles and elevated risk factor levels, in those developing countries in which CHD threatens to emerge in connection with socio-cultural changes toward urbanization and industrialization.
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PMID:Perspectives for the primary prevention of coronary heart disease. 330 37

The plasma lipoproteins are the primary means of transport of cholesterol among tissues. In particular, the apo B-containing lipoproteins (VLDL, IDL and LDL) are important for the delivery of cholesterol from the liver to peripheral tissues, while HDL appear to mediate the reverse process of movement of cholesterol from tissues back to the liver. Both of these transport processes are necessary for efficient whole body cholesterol homeostasis, because the liver is the major site of both the production and excretion of cholesterol. However, deviations from a proper balance of transport of cholesterol, either increases in LDL levels or decreases in HDL cholesterol flux, may result in accumulation of cholesterol in extrahepatic tissues. Increased risk of atherosclerosis and CHD may be associated with elevation in the number of LDL particles, increase or decrease in LDL particle size, or changes in the composition of plasma LDL. These modifications of plasma LDL may be brought about following perturbation of one of several aspects of LDL metabolism. These include decreased LDL receptor activity, increased VLDL production and cholesterol enrichment of the liver-derived VLDL. The events in the arterial wall that make some LDL particles apparently atherogenic are not well understood. In the case of nonhuman primates, large-size LDL are associated with an increased risk of CHD. One characteristic of these LDL is that their core lipids are rich in saturated cholesteryl esters and their transition temperatures are frequently above body temperature. The liquid crystalline cholesteryl ester cores of such LDL may modulate the conformation of apo B on the surface and thereby affect the interaction of these LDL with cellular receptors or connective tissue matrix proteoglycans. It is likely, though, that changes in LDL particle number, LDL particle size and LDL particle composition may each contribute to progression of atherosclerosis. The presumed metabolic events that make HDL protective against atherosclerosis have been termed reverse cholesterol transport, and suggest that small HDL that are deficient in free cholesterol acquire this lipid from cell membranes. The HDL cholesterol is esterified by LCAT in the circulation, forming large HDL that can then deliver the cholesteryl ester to the liver by both direct and indirect means. In most circumstances, it is assumed that an increase in plasma HDL cholesterol concentration reflects an increase in the rate at which HDL is removing cholesterol from tissues and, consequently, a decrease in atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lipoproteins and atherosclerosis. 333 Apr 21


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