Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to investigate the degree of platelet activation and thrombin generation in 40 patients with stable angina pectoris and in 20 patients with acute myocardial infarction (AMI) by determining the plasma beta thromboglobulin (BTG) and fibrinopeptide A (FPA) concentrations. In patients with angina pectoris increased platelet activation correlated with extensive coronary pathology; the activation, however, was not influenced by a previous myocardial infarction, use of oral anticoagulants, beta-blocking agents, or hyperlipidemia. The plasma beta thromboglobulin concentration predicted more accurately the extent of the coronary artery disease than the functional angina pectoris classification. Thrombin generation was within the normal range. In patients with acute myocardial infarction increased platelet activation and enhanced thrombin generation were found, which were not related to the infarct localization, infarct size, or the presence of complications. Consequently, in these patients determination of plasma beta thromboglobulin and fibrinopeptide A concentrations is useless for the diagnosis of venous thromboembolism.
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PMID:Fibrinopeptide A and beta thromboglobulin in patients with angina pectoris and acute myocardial infarction. 619 72

Thrombin is a crucial enzyme in blood coagulation cascade having both pro- and antithrombotic properties. Disorders of hemostatic balance increase possibility of clot formation and play significant role in the development of atherosclerosis. Statins applied in prevention of cardiovascular diseases, have not only hypolipemic activity but also many pleiotropic effects. The aim of this study was to evaluate the level of thrombin generation and clot bound thrombin in patients with hyperlipidemia type II (hlpII) before and after statins treatment. 81 patients were involved in this study: 59 patients with hlp II and 22 healthy. Patients with hlp II were treated with pravastatin (20 mg/day; n=10), simvastatin (20 mg/day; n=22), atorvastatin (10 mg/day; n=27). The treatment in each of groups lasted 8 weeks. Thrombin generation and clot bound thrombin level were estimated before and after therapy by means of spectrophotometric method with usage of chromogenic substrate S-2238. Our results demonstrate that therapy with atorva- simva- and pravastatin improves lipid levels in plasma and investigated hemostasis parameters. All three statins statistically significantly decrease total generated thrombin. Atorva- and simvastatin also significantly decrease activity both free generated thrombin and clot bound thrombin. No correlation between lipidogram and hemostatic parameters after treatment with statins suggests that observed changes are pleiotropic effect of statins treatment.
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PMID:[Evaluation of thrombin generation and clot bound thrombin in plasma of hyperlipidemic patients treated with statins]. 1652 18

Thrombin is clearly a key trigger of thrombosis, the proximal cause of most morbidity and mortality in atherosclerotic cardiovascular disease. Might thrombin also contribute to longer-term, structural changes in the arterial wall that promote narrowing and clotting? A study in this issue of the JCI argues that it can. Aihara et al. report that haploinsufficiency of heparin cofactor II, a glycosaminoglycan-dependent thrombin inhibitor, exacerbates injury- or hyperlipidemia-induced arterial lesion formation in mice, possibly by excessive thrombin signaling through protease-activated receptors (see the related article beginning on page 1514).
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PMID:Unchecked thrombin is bad news for troubled arteries. 1754 54

Arterial thrombosis occurs in atherosclerotic, but rarely in non-atherosclerotic arteries. The present study investigates how hyperlipidemic condition affects thrombus formation on macrophage-rich neointima or normal intima in rabbits. Rabbits were fed with a 0.5% cholesterol diet, and then the femoral artery on one side of each rabbit was injured with a balloon catheter. Three weeks later, bilateral femoral arteries were similarly injured with a balloon catheter to produce thrombi on neointima and normal intima. We compared the expression and activity of intimal tissue factor (TF) as well as thrombus size and composition between these femoral arteries. 0.5% cholesterol diet combined with a balloon injury induced macrophage-rich neointima in injured arteries. The whole blood coagulation activity or plasma thrombin generation activity did not differ after consuming the 0.5% cholesterol diet for 4 weeks, and an anti-TF antibody did not affect the measured parameters. TF activities were increased in the neointima/media compared with normal intima/media. Balloon injury induced large platelet-fibrin thrombi on macrophage-rich neointima, whereas small platelet thrombi were produced in normal arteries even under hyperlipidemic conditions. Recombinant human tissue factor pathway inhibitor (25microg/(kgmin)) and argatroban (100microg/(kgmin)), a specific thrombin inhibitor, significantly reduced thrombus formation on induced neointima, but not on normal intima. Thrombin generation mediated by TF in intima contributes to thrombus formation on macrophage-rich neointima, but not on normal intima. The TF content in disrupted atherosclerotic plaques might play a more important role than hyperlipidemia in the development of atherothrombosis.
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PMID:Thrombin generation by intimal tissue factor contributes to thrombus formation on macrophage-rich neointima but not normal intima of hyperlipidemic rabbits. 1937 74