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

Coagulation factor VIII, von Willebrand factor, antithrombin, fibrinogen, plasminogen activator capacity, and inhibitors of fibrinolysis, including a recently discovered fast inhibitor of tissue plasminogen activator, were measured three to six months after myocardial infarction in 116 male and 32 female patients aged less than 45 and in 136 age and sex matched random controls. Plasma concentrations of fibrinogen and the fast inhibitor of tissue plasminogen activator were raised in male patients (with or without correction for orosomucoid levels, blood group distribution, tobacco and alcohol consumption, and weight/height index) and plasminogen activator capacity was reduced. In female patients the concentrations of factor VIII, von Willebrand factor, the fast inhibitor of tissue plasminogen activator, alpha 2-antiplasmin, and C1 inhibitor were significantly increased. The increase in factor VIII concentrations depended strongly on a persisting inflammatory response. Multivariate analysis indicated that a combination of fibrinogen and tissue plasminogen activator inhibitor concentrations gave the best independent discrimination between male patients and controls. For female patients the best combination was von Willebrand factor and tissue plasminogen activator inhibitor. Male patients with multiple vessel atheromatosis at coronary angiography had higher fibrinogen concentrations than those with atheromatosis of a single vessel. Atheromatosis was defined as sharp-edged, plaque-like, or irregular indentations, often multiple, into the vessel lumen without features suggesting fibromuscular hyperplasia.
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PMID:Haemostatic function in myocardial infarction. 394 83

In order to investigate the relationship between the in vivo platelet activation in diabetes mellitus and the endothelial damage connected with the diabetic micro- and/or macroangiopathy, plasma levels of beta-thromboglobulin (B-TG) and of factor VIII-related antigen (VIII R:Ag) were studied (1) in juvenile-onset (Type I) diabetics without clinical signs of angiopathy (age under 12 years) and (2) in mostly maturity-onset (Type II) diabetics with and without overt angiopathy (age between 14 and 60 years). Normal controls and nondiabetics with atherosclerosis were also studied. Plasma levels of both proteins were found to be elevated in all the groups of diabetic and atherosclerotic patients in comparison with the controls. Highest levels were found in adult diabetics with angiopathy and in atherosclerotics even without diabetes, but values of the diabetic children were also elevated. The data suggest a causal relationship between the vascular damage and the enhanced platelet reactivity in which the former may play the primary role.
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PMID:Plasma levels of beta-thromboglobulin and factor VIII-related antigen in diabetic children and adults. 618 37

Primary cultures of confluent human endothelial cells (ECM) were grown in media containing the major lipoproteins (LP) and lipoprotein deficient serum (LDS). The release of 6-keto-PGF1 alpha, von Willebrand factor (VIII RAg) and apolipoproteins (apo) A-I and A-II were investigated by radioimmunoassay. The cell-associated VIII RAg, apo A-I and apo A-II were also confirmed by fluorescein antibodies, and the synthesis of the apolipoproteins was examined by incorporation of [3H]leucine. Apo A-I and apo A-II were located and synthesized in ECM, yet only apo A-I was released into the medium. Very low density (VLDL) and low density lipoproteins (LDL) in concentrations of 50-600 micrograms/ml stimulated release of apo A-I. Stimulation of ECM for 5 min with thrombin (T) or arachidonic acid (A) did not induce apo A-I release. VIII RAg was always released into the media from ECM. The release was not affected by the lipoproteins. VIII RAg was also localized on the cell surface (VIII RAgC) and approximately 80% was released by trypsin. LDL stimulated the occurrence of factor VIII RAg on the cell surface. 6-Keto PGF1 alpha was always released into the medium and the production was stimulated by T and AA. The main lipoproteins (50-600 micrograms/ml) and apo A-I and A-II did not affect the release of 6-keto-PGF1 alpha. This study shows that endothelial cells synthesize and release proteins important for thrombogenesis and atherosclerosis. The release of apolipoproteins A-I was stimulated by VLDL and LDL, and the concentration of cell-related factor VIII RAg was stimulated by LDL.
Atherosclerosis 1984 Mar
PMID:The effect of lipoproteins on the synthesis of prostacyclin, von Willebrand factor and apolipoproteins A-I and A-II in cultured human endothelial cells. 642 92

The prevalence of von Willebrand's disease (VWD) in Western European countries and Israel was assessed. Possible patients were identified initially by questionnaire and those with plasma levels of von Willebrand factor antigen ( WFAg ; factor VIII related antigen) less than 1 u/dl (less than 1%) were confirmed by immunoradiometric assay performed at four reference centres. The prevalences of severe VWD in Scandinavian countries were similar to each other and about 10 times greater than those in other Western European countries. The prevalence in Israel was intermediate. The Registry will form the basis for future non- invasive epidemiological studies of atherosclerosis in these individuals.
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PMID:Atherosclerosis and von Willebrand factor. I. Prevalence of severe von Willebrand's disease in western Europe and Israel. 660 12

Whole-blood viscosity (measured at 128, 23 and 0.2 s-(1) was significantly increased in 29 females with Raynaud's syndrome, 13 males with vibration-induced Raynaud's syndrome, and 18 males with calf claudication secondary to atherosclerosis, as compared with 50 healthy controls matched for sex, age and smoking habit. Viscosity was higher at low temperature (27 and 22 degrees C) in all three types of vascular disease and, despite symptoms of cold hypersensitivity, patients with Raynaud's syndrome did not show selective hypersensitivity at low temperature. Patients with vascular disease, irrespective of aetiology, also showed an increase in the acute-phase reactants haptoglobin, fibrinogen, and factor VIII antigen, together with reduced fibrinolytic activity and minor activation of platelets. These alterations in viscosity and haemostatic factors in vascular disease are probably related to the degree, rather than the aetiology, of endothelial damage and their cumulative effect may contribute to local stasis and thrombosis, particularly in cold extremities.
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PMID:Hyperviscosity and thrombotic changes in idiopathic and secondary Raynaud's syndrome. 677 75

A sample of in all 119 young adults below the age of 55, with ischemic cerebrovascular disease (TIA and minor stroke), was investigated later than three months after acute disease. Factor VIII biological activity and antithrombin antigen were significantly (p less than 0.001) increased as compared to 80 healthy controls. In combination, these two variables correctly classified 85 percent of patients and controls at a stepwise discriminant analysis. Factor VIII related antigen was increased (p less than 0.02) in patients with atherosclerotic signs at cerebral angiography and in postmenopausal female patients (p less than 0.001). It is suggested that high levels of factor VIII might predispose for thrombosis/atherosclerosis. Antithrombin biological activity was normal in spite of high antithrombin antigen levels, possibly indicating a relative insufficiency in the antithrombin defense line. It is concluded that young stroke patients provide good opportunities to look for early operating factors and predictors in human atherosclerosis and arterial thromboembolism.
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PMID:A study of hemostasis in ischemic cerebrovascular disease. I. Abnormalities in factor VIII and antithrombin. 681 Apr 96

In order to investigate the factor VIII complex trend in atherosclerosis, 96 patients suffering from atherosclerosis, divided in 6 groups (angina pectoris, previous myocardial infarction, transient ischemic attacks, previous cerebral thrombosis, diabetes without symptoms of vascular injury and diabetes with vascular complications), were studied and compared to a control group of normal subjects. Plasma levels of Factor VII Coagulant (VIII C), Factor VIII-Related von Willebrand Factor (VIII-RWF) and Factor VIII-related Antigen (VIII ARg) were measured in all subjects. A significant rise of VIII RAg was noticed in all groups of patients as compared to the control group: this increase appears to be related to the severity of vascular injury. A significant rise of VIII RWF, parallel to the VIII RAg increase, was also noticed in all groups. Besides, all groups of patients showed a significant and uniform increase of VIII C. The average ratio of VIII RAg/VIII C was raised in all groups, except diabetics without complications; but the increase was statistically significant only in those patients with a heavier vascular injury which is related to the marked rise of VIII RAg in such clinical situations. The findings of this study are discussed in relation to the literature data. The significance of the determination of VIII RAg/VIII C ratio and of the VIII RAg assay as methods for monitoring the severity of the vascular injury in atherosclerosis are also discussed.
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PMID:[The factor VIII complex in atherosclerosis]. 681 35

Forty patients with atherosclerotic peripheral vascular disease, as compared to 29 healthy controls, showed a significant increase in platelet number and activity, a neutrophil leucocytosis, and a raised level of several acute-phase reactant proteins (fibrinogen, antithrombin III, factor VIII, and serum globulin). The hyperproteinaemia was associated with increases in plasma-, serum-, and blood-viscosity and is the likely cause of the hyperviscosity of vascular disease. These multiple haemostatic abnormalities closely resemble the non-specific, haematological stress-syndrome response to acute and chronic inflammatory disorders. In atherosclerosis also they may represent a non-specific, secondary response and neither be of aetiological significance nor reflect continuing low-grade intravascular coagulation.
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PMID:Haematological stress syndrome in atherosclerosis. 725 88

We investigated the relationship between fasting insulin level and various hemostatic factors, including fibrinolytic factors (active plasminogen activator inhibitor-1 (PAI-1), tissue type plasminogen activator (tPA)-PAI-1 complex, plasmin-alpha 2-plasmin inhibitor (PIC), and D-dimer), coagulation factors (activated factor VII, factor VII coagulant activity and antigen, factor VIII, factor X, and fibrinogen), coagulation inhibitors (antithrombin III, heparin cofactor II, and protein C), and an acute phase marker (sialic acid) in 102 healthy individuals aged > or = 75 years (46 men and 56 women). Active PAI-1 levels had a significant negative correlation with PIC levels (r = -0.342, P = 0.0006), indicating that PAI-1 influences in vivo fibrinolytic activity in the very elderly. Gender differences were found in the relationship between insulin and hemostatic abnormalities, with the insulin level being positively correlated with coagulation factors in men (factor VIII activity: r = 0.422, P < 0.01; factor VII activity: r = 0.386, P < 0.01) and with hypofibrinolysis in women (active PAI-1: r = 0.549, P < 0.0001). Insulin levels were positively correlated with the levels of factor VII antigen and factor VII activity in men (P < 0.01), but there was no correlation with activated factor VII levels. The fasting insulin level was also correlated with the levels of heparin cofactor II and sialic acid in men (P < 0.05). However, other hemostatic factors were not related to the insulin level in either sex.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1995 Aug
PMID:Gender differences of disturbed hemostasis related to fasting insulin level in healthy very elderly Japanese aged > or = 75 years. 757 76

Two hundred ninety-nine human coronary artery paraffin-embedded tissue blocks were examined for intimal microvessel invasion by probing for factor VIII-associated antigen with indirect immunofluorescence and high resolution confocal microscopy. The results obtained confirm that intimal microvessels originate in the adventitia and show that the richness of intimal microvessels is strongly positively correlated with intimal thickness and negatively correlated with relative lumen size. A number of plasma constituents were examined in serial sections. Comparison of immunofluorescence distribution patterns of these components with intimal microvessel distribution patterns reveals that intimal microvessels leak plasma albumin into artery walls, exude fibrinogen, and are associated with the build-up of plasma cells within atherosclerotic lesions. Therefore, intimal microvessels are demonstrated to play important roles in the development of atherosclerosis.
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PMID:Immunohistochemical study of intimal microvessels in coronary atherosclerosis. 768 41


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