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)

We investigated heparin cofactor II (HC II) levels and their relationship to other haemostatic factors in the elderly in comparison with antithrombin III (AT III). We measured plasma HC II activity levels in 166 subjects aged from 61 to 99 years using a chromogenic method. HC II levels (94.4 +/- 18.5%) in the healthy elderly subjects were significantly (p less than 0.001) lower than in 40 healthy adult controls under 60 years of age (mean age: 51.5 years; 111.6 +/- 21.2%). HC II levels in the elderly subjects decreased further with age (r = 0.308, p less than 0.001) and the extent of the decrease was more marked than that for AT III (r = 0.179, p less than 0.05). There was no significant sex difference in HC II levels in the elderly. HC II levels correlated significantly with AT III levels and with acute phase reactants including sialic acid, fibrinogen, and PAI-1. HC II levels also correlated with factor VII, plasminogen, alpha 2-plasmin inhibitor, serum lipid, pseudocholinesterase, and albumin levels. These correlations were also found for AT III except active PAI-1 and tPA-PAI-1 complexes, but the correlations with acute phase reactants were stronger for HC II than AT III. We divided 154 elderly subjects into 4 groups by their pseudocholinesterase and albumin levels to estimate the effect of nutritional status on antithrombin activity in the elderly. HC II levels were normal in the elderly subjects with a good nutritional state (103 +/- 18%), but were significantly decreased in those with malnutrition (85 +/- 15%, p less than 0.001). AT III levels also showed the same tendency. These results indicate a decrease in the reserve capacity to inhibit thrombin generation at sites of atherosclerosis in response to trigger events. The deficiency of two major antithrombin factors in the elderly may indicate a tendency to thrombosis, especially in individuals with malnutrition. When considering the clinical significance of HC II, several other parameters, including age, nutritional status, hepatic synthetic ability, and the presence or absence of acute phase reaction should also be assessed.
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PMID:Heparin cofactor II deficiency in the elderly: comparison with antithrombin III. 138 49

Based on the results of previous investigations that pollen Typhae, a Traditional Chinese Medicine, Had antiatherogenic effects, several components were isolated successively from the drug and their effects on porcine aortic endothelial cell (EC) and smooth muscle cell (SMC) cultures as well as on platelet aggregation were examined. 12 components isolated from Pollen Typhae have been identified on their chemical structures and biological effects. 4 of them showed different evident antiatherogenic effects. 1) Isorhamnetin-3-O-rhamnosyl-glucoside could stimulate EC to produce tPA and PGI2; 2) Quercetin-3-O-neohesperidose could protect EC from injury by fibrin, as well as raise tPA activity; 3) beta-Sitosterol palmitate could inhibit SMC proliferation and 4) beta-Sitosterol glucoside showed an inhibitory effect on platelet aggregation. These results would provide some information for the search of new drugs in the treatment and prevention of atherosclerosis.
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PMID:The antiatherogenic effects of components isolated from pollen typhae. 211 85

Serum lipids, lipoprotein (a), plasminogen activator inhibitor and tissue plasminogen activator levels were measured in 260 subjects, constituting a cross-section sample of 30-60-year-old men and women. For Lp(a), there were positive correlations with age and cholesterol, but not with any of other measured parameters. Triglyceride, cholesterol, and HDL-cholesterol (inversely) levels were associated with waist-to-hip girth circumference ratio: this variable remained significant in a multiple regression model. PAI-1 activity and tPA antigen levels were positively associated with triglycerides and inversely associated with HDL-cholesterol. Moreover, tPA antigen was positively related to total cholesterol level. In multiple regression analysis, however, only triglycerides were found to contribute significantly to the variance of tPA antigen and PAI-1 activity levels, when BMI (in men) and abdominal skinfold thickness (in women) were entered into the model. Insulin or glucose postload responses to an OGTT were not independently related to any lipid or fibrinolytic variable. These data demonstrate the importance of anthropometric variables both for fibrinolytic variables and traditional lipid risk factors. Only Lp(a) was found to be largely unrelated to the endocrine-metabolic and anthropometric variables.
Atherosclerosis 1989 Nov
PMID:Interrelationships between plasma levels of plasminogen activator inhibitor, tissue plasminogen activator, lipoprotein (a), and established cardiovascular risk factors in a north Swedish population. 253 10

Patients with peripheral arterial disease have a high risk of death from cardiovascular events. As defective fibrinolysis associated with leg atherosclerosis has been suggested as a predisposing factor, we sought a relation among decreased fibrinolysis, the presence of leg atherosclerosis and the incidence of thrombotic events in a case-control study nested in the PLAT. Fifty-eight patients with coronary and/or cerebral atherothrombotic disease, free of leg atherosclerosis at Doppler examination, were compared with 50 atherosclerotic patients with leg involvement. High D-dimer (153.0 vs 81.3 ng/ml, p < 0.001) and tPA antigen before venous stasis (14.4 vs 11.8 ng/ml, p < 0.03), and low tPA antigen (6.7 vs 15.6 ng/ml, p < 0.01) and fibrinolytic activity released after venous stasis (fibrinolytic capacity: 113.2 vs 281.4 mm2, p < 0.001) were found in patients with leg atherosclerosis. D-dimer and fibrinolytic capacity, in addition to age, were selected by stepwise discriminant analysis as characterizing patients with leg atherosclerosis. Moreover, higher D-dimer and tPA inhibitor characterized patients with leg atherosclerosis who subsequently experienced thrombotic events. These findings constitute evidence of high fibrin turnover and impaired fibrinolytic potential in patients with leg atherosclerosis. Thus impaired fibrinolysis may contribute to the prothrombotic state in these patients.
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PMID:Association of increased fibrin turnover and defective fibrinolytic capacity with leg atherosclerosis. The PLAT Group. 783 67

To clarify age-related and lipid-related hemostatic abnormalities in the elderly, we measured the plasma levels of active PAI-1 antigen (aPAI-1), tPA-PAI-1 complex (TPC), plasminogen, alpha 2-plasmin inhibitor (alpha 2-PI), plasmin-alpha 2-PI complex (PIC), and D-dimer, together with the plasma levels of fibrinogen, factor VII (F VII), and thrombin-antithrombin III complex (TAT) and the serum lipid levels in 68 hyperlipidemic and 82 normolipidemic elderly subjects. The aPAI-1 ratio was calculated as aPAI-1/(aPAI-1 + TPC). In the normolipidemic elderly subjects, plasma PIC and D-dimer levels were much higher when compared with healthy young controls, and there was also a decrease in plasma plasminogen and alpha 2-PI levels, an increase in plasma TPC levels, and high plasma F VII and fibrinogen levels. In elderly subjects with type IIb hyperlipidemia, both the plasma aPAI-1 level and the aPAI-1 ratio were significantly increased, while the plasma PIC and D-dimer levels were reduced despite higher plasma F VII, fibrinogen and TAT levels. Both serum total cholesterol and triglyceride levels were correlated positively with plasma F VII and TAT levels and with the TAT/PIC ratio, while only serum triglyceride levels showed a positive correlation with plasma TPC and aPAI-1 levels and with the aPAI-1 ratio. Thus, an increase of fibrinolytic activity appears to occur as part of normal aging to balance the increase of procoagulant activity. However, an imbalance between thrombin activity (increased procoagulant activity) and plasmin activity (hypofibrinolysis) appears to occur in elderly individuals with hyperlipidemia, perhaps resulting in a predisposition to thromboembolic disease.
Atherosclerosis 1993 Nov
PMID:Lipid-related hemostatic abnormalities in the elderly: imbalance between coagulation and fibrinolysis. 829 90

Associations between increased plasma concentrations of the three haemostatic factors--fibrinogen, Factor VII and plasminogen activator inhibitor 1 (PAI-1)--and cardiovascular disease (CVD) have recently been demonstrated in epidemiological studies. The relative risk of CVD is increased by 2-3 times in subjects whose levels of fibrinogen fall within the upper third of the general distribution in comparison to those subjects who fall into the lower third; a positive correlation exists between increased Factor VII activity and cardiovascular mortality. Many studies have demonstrated that elevated levels of PAI-1 and tPA antigen are associated with CVD. Several studies have also shown that there are important associations between conventional risk factors for atherothrombosis and haemostatic factors. Fibrinogen levels are strongly linked with smoking, and Factor VII levels are linked with cholesterol, triglycerides and fat intake. PAI-1 and tPA antigen levels, on the other hand, are closely associated with insulin resistance. This paper discusses the principal genetic and environmental determinants of the plasma levels of each of these three haemostatic factors and relates them to the risk of developing CVD.
Atherosclerosis 1996 Jul
PMID:Haemostatic parameters and vascular risk. 883 16

Disturbances in lipid metabolism and in blood fibrinolytic system may play a role in pathogenesis of vascular complications of diabetes mellitus. The aim of the study was to evaluate fibrinolytic parameters (antigen of tissue plasminogen activator-tPA, its inhibitor-PAI, tPA/PAI complexes measured by enzyme immunoassays, euglobulin clot lysis time-ECLT), cholesterol, triglycerides, lipoprotein (a) and apolipoproteins (AI, AII, B) in diabetic patients with and without diabetic nephropathy. The studies were performed in 25 patients with type II diabetes mellitus (age range 42-69), 31 patients with diabetic nephropathy (age range 46-76) and healthy volunteers (age range 31-66). There were no significant differences among the groups studies in tPA:Ag, tPA/PAI complexes, total PAI:Ag and free PAI. ECLT was slightly prolonged in patients with diabetic nephropathy when compared to controls. Cholesterol and triglycerides were significantly elevated in patient with diabetic nephropathy and without nephropathy when compared to healthy volunteers. Triglicerides levels were higher in patients with diabetic nephropathy when compared to subjects without it. Apolipoprotein AI and AII were significantly lower, whereas lipoprotein (a) and apolipoprotein B were significantly higher in patient with diabetic nephropathy when compared to healthy volunteers and diabetic subjects without nephropathy. Lipid metabolism disturbances and impairment in fibrinolysis might contribute to the progression of atherosclerosis and nephropathy in diabetic patients.
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PMID:[Lipid metabolism and fibrinolysis in diabetic nephropathy in the course of diabetes type II]. 883 26

To investigate whether there are differences in haematology and coagulation indices in arterial and venous plasma, and whether those changes related to damage to the endothelium in atherosclerosis, we obtained blood samples from 22 subjects undergoing diagnostic angiography. There were no differences in any of the 15 routine haematological indices measured. There were no differences in prothrombin time, activated partial thromboplastin time, fibrinogen, tissue plasminogen activator, D-dimer, leucocyte elastase, soluble P-selectin or von Willebrand factor. In venous samples, von Willebrand factor was lower in serum than in plasma (p < 0.0001). Levels of the tissue plasminogen activator/plasminogen activator inhibitor-1 (tPA/PAI-1) complex were markedly higher in arterial blood than in venous blood (p = 0.004) and plasma viscosity was higher in venous blood (p = 0.0014). Consequently, with the exception of viscosity and the tPA/PAI complex, we can find no differences in arterial blood compared to venous blood which can contribute to the debate regarding the mechanism of damage to arterial endothelial cells but the relative protection of venous endothelial cells from injury in atherosclerosis.
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PMID:Haematology and coagulation indices in paired samples of arterial and venous blood from patients with arterial disease. 911 85

Fibrinolysis is essential for maintaining the fluency of blood flow. Attenuated fibrinolytic activity has been frequently detected in coronary artery disease, peripheral vascular diseases, diabetes, hyperlipidaemia and obesity. The biologically active product of fibrinolytic system is plasmin. Generation of plasmin is regulated by plasminogen activators (PA) and their inhibitors (PAI). Vascular endothelial and smooth muscle cells synthesize tissue-type and urokinase-type PA (tPA and uPA) and their major physiological inhibitor, PAI-1. The production of fibrinolytic regulators is modulated by a number of biological factors related to thrombosis and atherosclerosis, including coagulation factors, hormones, growth factors, inflammatory mediators and lipoproteins. Several anticoagulants, including heparin, hirudin and hirulog-1, affect the production of fibrinolytic regulators in vascular cells. Studies in knockout mice demonstrated that mice deficient in PA or plasminogen are susceptible to thrombosis during inflammation or injury. Overexpression of uPA or deficiency of PAI-1 promotes neointima and aneurysm formation, which is probably due to active remodelling of extracellular matrix in vascular wall caused by excess plasmin. Long-term effect of treatment with thrombolytic agents or in atheroscleronic cardiovascular diseases remains to be defined. Future studies on determination of the role of PA and PAI in vascular remodelling may help understand the mechanism for neointima formation and orient the prevention of restenosis following vascular procedures.
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PMID:Vascular cell-derived fibrinolytic regulators and atherothrombotic vascular disorders (Review). 985 42

tPA has been the independent risk factor of the thrombosis associated with atherosclerosis. There are increased tPA levels in type 1 diabetic patients with vascular complications and tPA is endothelial injury marker in this case. In type 2 diabetes mellitus elevated tPA antigen levels in early disease stage are caused by increased production of complexes with inhibitor (PAI-1) and tPA or fibrinolytic activity has been decreased.
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PMID:[Tissue plasminogen activator and diabetes mellitus]. 1042 7


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