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)

Embolization of thrombi from ulcerated plaques is an important cause of morbidity from atherosclerotic carotid artery disease. Factors controlling thrombus formation on these lesions are not well understood. Macrophages were isolated from atherosclerotic plaques to assess their potential to promote local fibrin deposition. Plaques were collected from 11 patients undergoing carotid endarterectomy and 9 patients undergoing reconstructive procedures for atherosclerotic disease of their distal aorta or femoral arteries. Blood was also collected concurrently to isolate monocytes. Procoagulant activity (PCA) of carotid macrophages (8.6 +/- 4.1 mU/10(6) cells) was significantly higher than that of macrophages from non-carotid lesions (0.35 +/- 0.20 mU/10(6) cells; P less than 0.05) or blood monocytes from either group of patients. The PCA of carotid plaque macrophages from patients with recent emboli was 16.1 +/- 8.4 mU/10(6) cells (n = 5) compared to 2.4 +/- 0.8 mU/10(6) cells (n = 6) for plaque macrophages from assymptomatic carotid endarterectomy patients. Carotid macrophage PCA was factor V and factor VII dependent. Its functional activity was inhibited by an anti-tissue factor antibody, and immunohistochemical studies on tissue sections from carotid plaques showed tissue factor in areas where macrophages were abundant. These studies demonstrate that macrophages within carotid artery plaques have augmented procoagulant activity compared with blood monocytes and macrophages from other atherosclerotic lesions and indicate that carotid plaque macrophages are activated. Augmented macrophage PCA may contribute to thrombus formation on ulcerated plaques.
Atherosclerosis 1989 Oct
PMID:Procoagulant activity expression by macrophages from atheromatous vascular plaques. 259 31

We have evaluated the potential relationships between plasma levels of certain coagulation factors, i.e. factor VII antigen (F VIIag) and factor VII coagulant activity (F VIIc), and parameters of lipid transport in a group of 90 normotriglyceridemic patients displaying hypercholesterolemia (Fredrickson's type IIa hyperlipoproteinemia). Levels of factor VIIc were significantly elevated (P less than 0.01) in this patient group as compared to a group of healthy normolipidemic subjects. By contrast, levels of factor VIIag were also increased, but such differences were not significant in relation to those of controls. Furthermore, concentrations of F VIIc and F VIIag in hypercholesterolemic males and females resembled each other. Similar observations were made when patients were divided into those either presenting or lacking symptoms of vascular disease. However, plasma levels of both F VIIc and F VIIag were positively correlated with circulating triglyceride concentrations in the hypercholesterolemic group, but not with other parameters of lipid transport such as serum cholesterol, HDL-cholesterol, and apolipoprotein B. When patients were treated with a lipid-lowering agent (cholestyramine), lower levels of both F VIIc and F VIIag were found concomitantly with a decrease of similar order in triglyceride concentrations. We conclude that serum triglyceride levels, even within the normal range, may be associated with elevation in the activity of factor VII in hypercholesterolemic patients, thereby increasing their risk of thrombosis.
Atherosclerosis 1989 Feb
PMID:Interrelationship of plasma triglyceride and coagulant factor VII levels in normotriglyceridemic hypercholesterolemia. 271 58

A community survey of factor VII coagulant activity (VIIc) and the lipoprotein profile in non-fasting plasma of middle-aged men in NW London was undertaken to search for the determinants of VIIc in the general community. The data demonstrates that associations between VIIc and the plasma concentrations of cholesterol and of triglycerides previously shown in the general population can be explained by the strong and positive associations between VIIc and the large lipoprotein particles, chylomicrons, VLDL and IDL. Consistent with the possibility that the concentration of large lipoproteins determines the in vivo reactivity of factor VII, the association between VIIc and the ratio of lipid in the d greater than 1.019 fraction to the total plasma lipid was also highly significant but negative. The observed correlations between VIIc and lipoproteins smaller than VLDL may be the product of the interrelations that exist between the lipoprotein fractions in plasma. However, the associations between VIIc and the chylomicron lipid concentrations are especially strong when allowance is made for the considerable bias towards zero in the observed correlation, due to large within-person variance in chylomicron concentration.
Atherosclerosis 1989 Apr
PMID:Factor VII coagulant activity is strongly associated with the plasma concentration of large lipoprotein particles in middle-aged men. 273 Jul 17

Diet was measured by 5-day weighed inventory to search for an association between fat intake in the general population and factor VII coagulant activity (VIIc), a strong predictor of coronary heart disease. Of 275 men aged 40-59 years registered with a medical practice, 203 (74%) participated and 170 (62%) provided a satisfactory record. After allowance for the increase in fat intake with body size, a statistically significant and positive association was found between dietary fat and VIIc (r = 0.18; P less than 0.05). The correlation coefficient was increased to 0.24 when adjusted for the effect of day-to-day variability in individual fat intake, thereby providing an improved estimate of the true strength of association. The mean difference in VIIc of 12% of standard between men in the highest and lowest quarters of the distribution of fat intake was similar to that reported between men experiencing coronary heart disease and those remaining free. The results support previous experimental fat-feeding studies and suggest that a high fat diet has adverse consequences for blood coagulability and coronary thrombosis.
Atherosclerosis 1989 Jul
PMID:Fat consumption and factor VII coagulant activity in middle-aged men. An association between a dietary and thrombogenic coronary risk factor. 275 83

In cultured human monocytes/macrophages, surface expression of procoagulatory activity (PCA) was induced by chemically modified LDL (acetyl-LDL and MDA-LDL) in a dose- and time-dependent manner. Maximum PCA (30-fold increase) was detected after 24 h of culture with modified LDL at doses of 25-750 micrograms protein/ml. Using factor VII deficient human plasma and phospholipase C this PCA was identified as tissue thromboplastin activity (factor III). These results suggest a further atherogenic potential for modified LDL through stimulation of the conversion of fibrinogen to fibrin in the atheromatous lesion.
Atherosclerosis 1989 Aug
PMID:Enhanced procoagulatory activity (PCA) of human monocytes/macrophages after in vitro stimulation with chemically modified LDL. 278 95

Blood samples were taken for haemostatic analysis from 225 patients with angina pectoris who were admitted to hospital for coronary angiography. beta thromboglobulin, platelet factor 3, platelet factor 4, factor VII:C, factor VIII:C, von Willebrand factor antigen, activated partial thromboplastin time, fibrinogen, antithrombin III, protein C:Ag, plasminogen, and antiplasmin were measured before angiography. Patients who had had a myocardial infarction in the two months before the investigation were excluded from the study. Multiple linear regression analysis showed that none of the haemostatic variables contributed independently to the prediction of an angiographic score that indicated the extent of coronary atherosclerosis. History of myocardial infarction, male sex, worsening of angina pectoris, serum triglycerides, and ejection fraction were independently associated with the angiographic score. There were some significant correlations between haemostatic variables and conventional risk factors for coronary heart disease. Thus data obtained from haemostatic analyses of peripheral venous blood do not permit the presence or the extent of atherosclerosis in coronary arteries to be predicted.
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PMID:Lack of association between haemostatic variables and the presence or the extent of coronary atherosclerosis. 325 21

A 66-year-old man with homozygous deficiency of factor VII (less activity than 4 percent of normal) had a minimal hemorrhagic tendency and severe coronary atherosclerosis, and underwent aortocoronary saphenous vein bypass surgery. Although plasma factor VII coagulant activity and cross-reacting material were markedly reduced, comparable amounts of factor VII antigen were detected in peripheral blood mononuclear cells of both the patient and of a normal subject by Western blotting techniques. Accelerated coagulation was observed following brief exposure of the patient's phytohemagglutinin-stimulated peripheral blood mononuclear cells to low concentrations of ambient factor VII in vitro. Evidence indicates that factor VII plays a role in vivo in both hemostasis and atherogenesis and it might be assumed that factor VII deficiency would both predispose to excessive bleeding and forestall atherosclerosis. However, these observations suggest that factor VII-mediated thrombin generation may proceed by partitioning of small amounts of factor VII on tissue factor-expressing cells and that factor VII contained within monocytes may facilitate tissue factor-induced coagulation by these cells. These features may provide efficient coagulation activation despite a deficiency of the plasma coagulant protein. The current results may explain, at least in part, the minimal bleeding tendency, and also the occurrence of thrombosis and atherosclerosis in certain persons with factor VII deficiency.
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PMID:Atherosclerosis and coronary bypass surgery in hereditary factor VII deficiency. 325 74

Associations of plasma testosterone and estradiol with some haemostatic factors (factor VII activity, fibrinogen, antithrombin III and alpha 2-antiplasmin) were cross-sectionally examined in 251 healthy, middle-aged men participating in the Paris Prospective Study II on risk factors for ischaemic heart disease. Testosterone levels were negatively correlated to factor VII activity and alpha 2-antiplasmin, the main inhibitor of fibrinolysis. No association was found either between testosterone levels and both fibrinogen and antithrombin III, or between estradiol levels and the set of haemostatic variables. The associations between testosterone and both factor VIIc and alpha 2-antiplasmin were independent of HDL-cholesterol, LDL-cholesterol, triglycerides, smoking, alcohol, body mass index and blood pressure. These results suggest that low circulating testosterone levels might be associated with a hypercoagulability state and therefore could contribute to an increased risk of IHD.
Atherosclerosis 1988 May
PMID:Relationship between sex hormones and haemostatic factors in healthy middle-aged men. 337 81

Repeated measurements were made in 8 adults of factor VII coagulant activity (VIIc) and fibrinogen concentration (two haemostatic variables associated with cardiovascular mortality), together with factor VII concentration, factor X, prothrombin, and serum cholesterol and triglyceride concentrations, while the usual diet was recorded by precise weighing over 12-14 days. In 6 subjects measurements were continued while low-fat and high-fat diets were taken for a further 2 and 3 weeks respectively. Plasma VIIc was related positively and independently to fat and protein intake, whereas factor VII concentration was associated only with protein consumption. In a second study, consumption of 50% extra energy for one day increased VIIc significantly when taken mainly as fat but not when taken mostly as carbohydrate. The character of the VIIc response to fat intake suggested an association with post-prandial lipaemia. A high fat intake may lead not only to coronary atheroma but also to fibrin deposition and thrombus formation through direct activation of the coagulation system.
Atherosclerosis 1986 Jun
PMID:Association between dietary fat intake and plasma factor VII coagulant activity--a predictor of cardiovascular mortality. 373 46

Intact arterial vessel wall is not thrombogenic. Disorders of the endothelium in connection with pathological coditions such such as atherosclerosis, hyperlipidaemia, hypertension and hyperuricemia induce interaction of surfaces of high thromboplastic activity with the blood stream. In such situations local formation of thrombin will take place immediately. Evidence is presented for the essential and unique activation of the extrinsic pathway of the plasmatic coagulation system. The local formation of thrombin at pathologically altered arterial wall seems to be an important trigger for arterial thrombosis and haemostasis. It could be that in vivo the initial step of thrombogenesis depends upon the formation of the activator complex between tissue-thromboplastin and factor VII.
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PMID:Thromboplastic activity of human arterial walls and its interaction with the plasmatic coagulation system. 744 Nov 81


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