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

Adding less than 0.5% w/w of culture material of strain MRC 826 of the fungus Fusarium moniliforme to a carbohydrate diet low in fat resulted in an atherogenic plasma lipid profile in a non-human primate. Simultaneously increased plasma fibrinogen and activity of blood coagulation factor VII could enhance atherogenesis. This unique potential for promotion of atherosclerosis was probably secondary to chronic hepatotoxicity as indicated by liver fibrosis and elevated cholesterol, albumin and the enzymes AST, ALT, LD, GGT and ALP in serum. The cholesterol and enzymes responded in proportion to the calculated doses of fumonisin mycotoxins in the F. moniliforme MRC 826 cultures. Fumonisins are water soluble and heat stable. Thrombotic, hepatotoxic, carcinogenic and cerebral effects of MRC 826 culture material and fumonisins are well known in non-primates. The estimated fumonisin concentrations tested fall within a range due to natural contamination of human foods. The results suggest that all maize grain products should be analysed for fumonisins.
Atherosclerosis 1992 May
PMID:Atherogenic effects in a non-human primate of Fusarium moniliforme cultures added to a carbohydrate diet. 163 55

Dietary fat intake is often regarded as a major determinant of coronary heart disease (CHD) rate and it has been deemed unnecessary to invoke racial or other factors to explain the differences in CHD rates among different ethnic groups. Despite a high prevalence of CHD risk factors such as hypertension, obesity, and smoking, CHD remains a rarity in westernized black Africans. Cord blood total cholesterol (TC), low density lipoprotein cholesterol (LDLC) and apolipoprotein B (apo B) levels were measured and found to be respectively 12.1%, 18.3% and 22.4% lower in black neonates when compared to white neonates. These differences were again studied in a group of young black African males and a comparable group of age-matched whites who had been exposed to the same environment and western diet for at least 2 years. Although the body mass indices and serum albumin concentrations in the adult males were not significantly different, serum levels of TC, LDLC and apo B were 10.7%, 18.7% and 39.7% lower in the blacks, respectively. Furthermore, high density lipoprotein cholesterol (HDLC) and Apolipoprotein AI were 20.2% and 9.5% higher, homocysteine 45.6% lower and coagulation factor VII 26.6% lower in the adult black Africans. It is concluded that blacks are biochemically less responsive to an atherogenic diet than whites and these differences are already present at birth.
Atherosclerosis 1991 Aug
PMID:Ethnic immunity to coronary heart disease? 179 43

To investigate the age-related increase in coagulation factor VII (FVII) and its significance in the elderly, we measured FVII coagulation activity (FVIIc), FVII antigen (FVIIag), and D-dimer levels in 150 normal subjects ranging in age from 60 to 98 years. We also measured blood lipid fractions and serum cholinesterase activity (ChE), as an indicator of hepatic protein synthesis. FVIIc (141 +/- 36%), FVIIag (136 +/- 28%), and D-dimer (0.150 +/- 0.372 microgram/ml) levels were significantly higher in the elderly than in younger controls (p less than 0.01). Both FVIIc and FVIIag levels were significantly higher in elderly women than in elderly men (p less than 0.01). FVIIc levels significantly correlated with FVIIag levels, but not with D-dimer levels. FVIIag was more closely correlated with ChE levels in both sexes (men: r = 0.425, women: r = 0.365, p less than 0.001) than with the lipid fractions. When the elderly subjects were divided into atherosclerotic and non-atherosclerotic groups, both FVIIc (p less than 0.01) and FVIIag (p less than 0.05) levels were higher in the former group. Moreover, the FVIIc/FVIIag ratio and ChE levels were higher in both the elderly men and women with atherosclerosis. These results suggest that in elderly subjects, especially with atherosclerosis, hepatic FVII synthesis and the activation of FVII zymogen are both accelerated.
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PMID:Factor VII hyperactivity in the elderly. 202 36

Hemostatic factors play a crucial role in generating the occlusive thrombotic plug at sites of vascular damage (atherothrombosis). It remains uncertain, however, whether hemostatic factors contribute directly or indirectly to the pathogenesis of atherosclerosis. For example, 'hypercoagulable states' (eg, antithrombin deficiency, Factor VLeiden) generally predispose to venous thrombotic events, but not atherosclerosis. Further, 'hemophilic states' (eg, factor VIII deficiency, von Willebrand's disease) do not protect against atherosclerosis. Nevertheless, research has been stimulated by several clinical studies showing that an elevated fibrinogen level is a strong and independent risk factor for cardiovascular (arterial) thrombotic events. Moreover, basic investigations have demonstrated fibrin(ogen) antigens in evolving atherosclerotic plaques, and have suggested a smooth muscle mitogenic effect of fibrin. Other factors that may contribute to atherogenesis include platelets and platelet-derived microparticles, coagulation factor VII and lipoprotein (a) [Lp(a)]. Lp(a) is of particular interest since elevated levels of this lipoprotein particle are strongly linked to cardiovascular disease. Lp(a) appears to inhibit natural fibrinolysis, suggesting that this factor could represent an important link between thrombotic and lipid atherogenic mechanisms. Further work defining a role for the hemostatic system in atherogenesis is important because of the potential benefit of pharmacological manipulation of hemostatic risk factors, such as agents that lower fibrinogen levels.
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PMID:Hemostasis and atherosclerosis. 775 46

Strong evidence from large observational epidemiological studies links haemostatic variables to the future risk of myocardial infarction and stroke. Recent data provide further evidence for an early involvement of haemostatic parameters in atherosclerosis. So far, a variety of markers of a procoagulatory tendency e.g. elevated fibrinogen, coagulation factor VII, factor VIII and von Willebrand factor, platelet hyperaggregation, increased plasma levels of D-dimer, and decreased fibrinolytic capacity, e.g. characterized by increased levels of PAI-1 activity and decreased t-PA concentrations have been identified prospectively. Thus, a complex disturbed haemostatic system plays an important role in the development of atherothrombotic events in several vascular beds. This review discusses the epidemiologic evidence of the association between the haemostatic system and cardiovascular disease.
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PMID:Haemostatic risk factors for cardiovascular diseases. 959 24

Tissue factor is the primary cellular initiator of blood coagulation via interaction with coagulation factor VII. Aberrant expression of tissue factor is responsible for thrombosis during septic shock, atherosclerosis and cancer. However, recent evidence has accumulated that tissue factor may have functions beyond controlling fibrin-dependent hemostasis. It is expressed as an immediate early gene by growth factors and cytokines, it transduces intracellular signals via its cytosolic domain, triggers production of growth factors and has been implicated in immune function, smooth muscle migration and metastasis, the latter via mechanisms requiring intracellular signaling as well as the proteolytic activity of the tissue factor-factor VIIa complex. Further evidence for a possible alternative role of tissue factor has been provided from tissue factor gene inactivation studies, indicating that tissue factor controls vascular integrity by affecting the maturation of the muscular wall around endothelial cell lined channels. Surprisingly, however, deficiency of factor VII does not affect vascular integrity and tissue factor may act independently of fibrin formation during embryogenesis. Elucidation of the mechanism of its action may provide insights for selective interference with the hemostatic versus morphogenic properties of tissue factor.
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PMID:Tissue factor. 969 23

The dextran-sulfate cellulose (DSC) column used for low-density lipoprotein (LDL) apheresis adsorbs plasma constituents other than LDL that have the following characteristics: proteins containing apolipoprotein B, proteins involved in the initial contact phase of the intrinsic coagulation pathway (coagulation factor XII, high molecular weight kininogen and prekallikrein), factors with lipophilic characteristics (coagulation factor VII, VIII, and vitamin E), and proteins with adhesive or other characters (von Willebrand factor, fibronectin, and serum amyloid P components). Adsorption of these proteins seems to serve in the prevention or regression of atherosclerosis. Moreover, plasma treatment by the DSC column may be useful for treatment of such inexorable diseases as amyloidosis. On the other hand, the column generates bradykinin by activation of the initial contact phase of the intrinsic coagulation pathway. Bradykinin generation may explain hypotension during LDL apheresis observed in patients taking angiotensin converting enzyme (ACE) inhibitors.
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PMID:Plasma constituents other than low-density lipoprotein adsorbed by dextran-sulfate column. 1022 21

Accelerated coronary atherosclerosis in cardiac allografts is a major factor limiting survival after heart transplantation, and activation of the coagulation system contributes to accelerated transplant atherosclerosis. Accordingly, increased tissue factor (TF) expression by monocyte/macrophages may play a pivotal role underlying deposition of fibrin in the affected vessels. To evaluate the potential effects of an important immunosuppressive agent, tacrolimus hydrate (FK-506), on monocyte/macrophages and their response to lipopolysaccharide (LPS), we exposed human monocyte/macrophage cell line (THP-1 cells), to LPS and characterized its procoagulant activity (PCA). FK-506 exerted a concentration-dependent inhibitory effect on LPS (10 micrograms/ml) induction of procoagulant activity, identified as TF activity as judged from immunostaining of TF antigen and by functional characterization with the use of coagulation factor VII-deficient plasma and an antibody against human TF. In addition, the reverse transcription polymerase chain reaction demonstrated reduced expression of TF mRNA in LPS-stimulated THP-1 cells exposed to FK-506. Thus, FK-506 acts favorably not only as a direct immunomodulating agent but also as an alleviator of local activation of the coagulation cascade contributing to transplant arteriopathy through modulation of monocyte expression of TF.
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PMID:Effects of tacrolimus hydrate (FK-506) on the expression of tissue factor in THP-1 human monocyte cell line. 1088 73

Studies in healthy subjects showed that blood coagulation factor VII (FVII) is activated postprandially after consumption of high-fat meals, but accompanying thrombin formation has not been demonstrated. In patients with coronary atherosclerosis, the arterial intima is supposed to present more tissue factor, the cofactor of FVII, to circulating blood; therefore, thrombin formation in response to FVII activation is more likely to occur in such patients. This hypothesis was tested in a randomized crossover study of 30 patients (aged 43 to 70 years) with stable angina pectoris and angiographically verified coronary atherosclerosis. They were served a low-fat (5% of energy from fat) breakfast and lunch and a high-fat (40% of energy from fat) breakfast and lunch on 2 different days. Venous blood samples were collected at 8:15 AM (fasting), 12:30 PM, 2:00 PM, 3:30 PM, and 4:45 PM and analyzed for triglycerides, activated FVII (FVIIa), FVII protein concentration (FVII:Ag), prothrombin fragment 1+2 (F1+2), and soluble fibrin. Triglyceride levels increased from fasting levels on both diets, but they increased most markedly on the high-fat diet. FVIIa and FVIIa/FVII:Ag increased with the high-fat diet and decreased with the low-fat diet. For both diets, FVII:Ag and F1+2 decreased slightly. No postprandial changes were observed for soluble fibrin. Postprandial mean values of triglycerides, FVIIa, FVII:Ag, and FVIIa/FVII:Ag were significantly higher for the high-fat diet than for the low-fat diet. Our findings confirm that high-fat meals cause immediate activation of FVII. The clinical implication is debatable because FVII activation was not accompanied by an increase in plasma F1+2 concentrations in patients with severe atherosclerosis. However, a local thrombin generation on the plaque surface cannot be excluded.
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PMID:Dietary factor VII activation does not increase plasma concentrations of prothrombin fragment 1+2 in patients with stable angina pectoris and coronary atherosclerosis. 1107 58

Several different techniques of low-density lipoprotein (LDL) apheresis are available for management of severe hypercholesterolemia. Among them, the adsorption system with a dextran-sulfate cellulose (DSC) column is most widely used. In addition to adsorption of LDL, DSC adsorbs plasma constituents that have the following characteristics: proteins containing apolipoprotein B (Lp[a]); proteins involved in the initial contact phase of the intrinsic coagulation pathway (coagulation factor XII, high-molecular-weight kininogen and prekallikrein); factors with lipophilic characteristics (coagulation factor VII, coagulation factor VIII, and vitamin E); and proteins with adhesive or other characteristics (von Willebrand factor, fibronectin, serum amyloid P component, hepatocyte growth factor). The adsorption of these proteins seems to ameliorate prevention or regression of atherosclerosis. Moreover, plasma treatment by the DSC column may be useful for treatment of inexorable diseases, such as amyloidosis. On the other hand, the DSC column generates bradykinin by activation of the initial contact phase of the intrinsic coagulation pathway. Bradykinin generation may explain the functional improvement in the circulatory system, as well as hypotension during LDL apheresis, which is observed in patients taking ACE inhibitors.
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PMID:Low-density lipoprotein apheresis and changes in plasma components. 1172 6


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