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

By promoting atherosclerosis and thrombosis, a blood-clotting diathesis could contribute to excess cardiovascular morbidity and mortality in patients with systemic hypertension and/or obstructive sleep apnoea. Since psychological states affect haemostatic activity, we wondered about the contribution of behavioural factors to a hypercoagulable state in subjects with increased risk of cardiovascular disease. To tease apart the potential additive nature of cardiovascular disease risk, we examined four patient groups - hypertensives and normotensives, with and without sleep apnoea. The procoagulant molecules thrombin-antithrombin III complex, fibrin D-dimer and von Willebrand factor antigen were measured in 88 subjects (mean age 47 years; range 32-64 years) who underwent full polysomnography. Subjects completed the Center for Epidemiological Studies - Depression (CES-D) Scale, the Cook-Medley (CM) Hostility Scale, and the Profile of Mood States (POMS). Sleep apnoea, hypertension status, age, body mass index and psychological variables (CES-D, CM Stress, and POMS Vigour-Activity) together explained 29% of the variance in D-dimer, a marker of fibrin turnover ( r (2)=0.29, P =0.001). CES-D, CM Stress and POMS Vigour-Activity explained 17% of this variance even after controlling for sleep apnoea, hypertension status, age and body mass index (Delta r (2)=0.17, P =0.001). Thrombin-antithrombin III complex and von Willebrand factor were not significantly related to psychological variables, but this may reflect limited statistical power. Thus psychological factors are independently associated with D-dimer and explain as much of its variance as do traditional correlates (hypertension, sleep apnoea, age and body mass index). These results may provide a rationale for linking behavioural aspects with cardiovascular events.
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PMID:Independent contribution of psychological factors to fibrin turnover in subjects with sleep apnoea and/or systemic hypertension. 1224 29

The damage of the vascular endothelial cells is considered as the primary factor of the development of atherosclerotic changes. The damaged vascular endothelial cells secrete lower amounts of tissue plasminogen activator, antithrombin III, thrombomodulin, endothelium devived relaxing factor (EDRF) prostacycline (PGI2) and glycosaminoglycans. An increase of plasma viscosity and blood procoagulation activity is observed in the peripheral arterial obliterative disease as a result of the interaction between platelets, leucocytes and erythrocytes from the walls of the damaged vessels together with the impairment of blood fibrinolytic activity. It is considered that one of the factors responsible for the development of the atherosclerotic changes is chronic inflammation process of the vascular endothelium. This causes a considerable participation of inflammation cells, i.e. lymphocytes and monocytes in atherosclerosis development. It is observed that an increased level of tissue factor (TF) and factor VII produced as a result of their releasing by the activated monocytes in the atheromatous lamina rupture exerts procoagulation effect. The tissue factor inhibitor inhibits VIIa/TF/Xa complex activity.
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PMID:[Participation of monocytes in the pathogenesis of peripheral arterial obliterating disease]. 1291 11

Systemic infection by various pathogens interacts with the endothelium and may result in altered coagulation, vasculitis and atherosclerosis. Endothelium plays a role in the initiation and regulation of both coagulation and fibrinolysis. Exposure of endothelial cells may lead to rapid activation of coagulation via tissue factor (TF) expression and the loss of anticoagulant properties by impairment of antithrombin III, TF pathway inhibitor (TFPI) and the protein C system. Endothelial-derived plasminogen activator inhibitor (PAI) is essential for the regulation of fibrinolysis and impaired endothelial function leads to imbalance in fibrinolysis, resulting in a procoagulant state. The interaction between inflammation and coagulation, soluble adhesion molecules and circulation endothelial cells is important in the pathogenesis of an unbalanced haemostatic system. Rather than being a unidirectional relationship, the interaction between inflammation and coagulation appears to be significant. In the crosstalk, the endothelium is playing a pivotal role.
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PMID:Infections and endothelial cells. 1452 5

Hypothyroidism has been associated with atherosclerosis. The mechanisms of atherosclerosis in patients with thyroid failure remain controversial. Hypofibrinolysis might be a risk factor for thromboembolic disease in subclinical hypothyroidism (SH). We measured fibrinolytic activity in patients with SH before and after levothyroxine (LT(4)) treatment and compared it to those of controls. We prospectively included 35 patients with SH and 30 healthy controls. We treated patients with LT(4) until almost 6 months after the euthyroid state has been achieved. We measured fibrinogen, D-dimer, antithrombin III (ATIII), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA) activity, and factor VII. Clinical and anthropometric variables were recorded for both groups. We found increased levels of fibrinogen, PAI-1, and factor VII and decreased levels of ATIII activity in patients compared to control (p < 0.001 and p < 0.05). Decrease of tPA was not significant (p > 0.05). At the end of the LT(4) treatment, significant decreases were determined in PAI-1 and factor VII (p < 0.05). In conclusion, our data suggest an important role of hypofibrinolytic and hypercoagulable state on the development of atherosclerosis in patients with SH and beneficial effects of LT(4 )treatment for decreasing the risk of atherosclerosis.
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PMID:Hemostatic system as a risk factor for cardiovascular disease in women with subclinical hypothyroidism. 1558 88

We investigated the effect of highly purified eicosapentaenoic acid ethyl ester (EPA-E) on blood coagulation abnormalities and dysfunction of vascular endothelial cells in spontaneously diabetic Otsuka Long-Evans Tokushima Fatty rats. The animals were treated with either EPA-E or lard at a daily dose of 0.3 g/kg/day for 52 weeks by gavage, and their coagulation/fibrinolytic parameters, platelet aggregation, and functions of the vascular endothelial cells were examined. EPA-E significantly improved coagulation-related parameters including prothrombin time, activated partial thromboplastin time, fibrinogen level, and activities of factor II, V, VII, VIII, IX, X, XI, and XII, and antithrombin III, and fibrinolysis-related parameters including plasminogen, tissue-type plasminogen activator, alpha(2)-plasmin inhibitor, and plasminogen activator inhibitor. It also suppressed ADP- or collagen-induced platelet aggregation and the cholesterol/phospholipid molar ratio in platelet membranes at a dose of 0.3 g/kg. In addition, it significantly increased the migration activity of vascular endothelial cells, and decreased the binding of vascular endothelial cells to vascular endothelial growth factor. In contrast, lard had no effect on hypercoagulation, hypofibrinolysis, and platelet hyperaggregation but significantly aggravated the dysfunction of vascular endothelial cells. These data demonstrate that EPA-E beneficially altered certain factors known to promote thrombosis and atherosclerosis in this animal model.
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PMID:Long-term administration of highly purified eicosapentaenoic acid ethyl ester improves blood coagulation abnormalities and dysfunction of vascular endothelial cells in Otsuka Long-Evans Tokushima fatty rats. 1461 17

Hypercoagulability is a risk factor for atherosclerosis (As) and plays an important role in the development of As. Hypercoagulability results from mutation and unusual expression of clotting system-related genes, anticlotting system-related genes, fibrinolytic system-related genes and other related genes. Factor V gene, prothrombin gene and tissue factor gene in clotting system, thrombomodulin gene and antithrombin III in anticlotting system, plasminogen activator inhibitor-1 gene in fibrinolytic system, are related with hypercoagulability tightly.
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PMID:[Mutation and unusual expression of clotting system-related genes and hypercoagulability]. 1499 14

As a risk factor for cardiovascular and cerebrovascular disease, hypertension and hyperlipidemia are believed to provoke vascular damage leading to a hypercoagulative state. The aim of the present study was to investigate the coagulative and fibrinolytic activity and hepatic mRNA expression of the coagulative factors in spontaneously hypertensive and hyperlipidemic female rats (SHHR:>150 mmHg of systolic blood pressure, >150 mg/dl of plasma cholesterol). Plasma levels of fibrinogen, thrombin-antithrombin III (ATIII) complexes and ATIII in the SHHR at 9 months of age increased significantly compared with those of age-matched Sprague-Dawley rats (SD). In the SHHR, the hepatic mRNA expression of the alpha- and beta-chains, but not the gamma-chain of fibrinogen and prothrombin was significantly enhanced. Therefore, the hyperfibrinogenemia in the SHHR was demonstrated to be due to the increase in hepatic mRNA expression of alpha- and beta-chains of fibrinogen. The pathological findings of the aortic arch from the 9-month old SHHR were cytoplasmic vacuolization and intimal thickening in the endothelium. These results suggest that hypercoagulation concomitant with the increase in hepatic mRNA expression of fibrinogen components may contribute to the development of atherosclerosis in the SHHR.
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PMID:Enhancement of the coagulation system in spontaneously hypertensive and hyperlipidemic rats. 1614 22

The strong activation of the clotting cascade that occurs during total hip arthroplasty places patients at increased risk for venous thromboembolism. The risk is higher in those patients with the following predisposing factors, listed in approximate order of importance: hip fracture; malignancy, particularly if associated with chemotherapy; antiphospholipid syndrome; immobility; history of venous thromboemholism; administration of tamoxifen; raloxifene; oral contraceptives or estrogen; morbid obesity; stroke; atherosclerosis; and an American Society of Anesthesiologists physical status classification of 3 or greater. The following risk factors are weak or controversial: advanced age; diabetes mellitus; congestive heart disease; atrial fibrillation; varicose veins; and smoking. However, 50% of patients who develop thromboembolism after total hip arthroplasty have no clinical predisposing factors. In a matched, controlled study, we defined the major genetic predispositions that increase the risk of venous thromboembolism after total hip arthroplasty: deficiency of antithrombin III (< 75%) and protein C (< 70%), and prothrombin gene mutation. Preoperative genetic screening in conjunction with the recognized clinical risk factors can help categorize postoperative venous thromboembolism risk and differentiate patients who can be protected with milder and safer prophylaxis (eg, aspirin, intermittent pneumatic compression) compared with those at higher risk who need to be anticoagulated.
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PMID:Thromboembolic disease after total hip arthroplasty: who is at risk? 1700 73

According to current concepts, hypertension and hyperlipidemia cause vascular damage that leads to a hypercoagulative state. In this study, we investigated whether spontaneously hypertensive and hyperlipidemic rats (SHHR) can be a useful experimental model for complications in combined hypertension and hyperlipidemia, by comparing coagulative and fibrinolytic activities in SHHR with those in spontaneously hypertensive rats (SHR) and spontaneously hyperlipidemic rats (HLR). We measured coagulation and fibrinolysis markers in plasma and levels of fibrinogen and prothrombin mRNA in livers of eight-month-old male Wistar Kyoto rats (WKY), Sprague-Dawley rats (SD), SHR, HLR and SHHR. The plasma levels of fibrinogen in SHR, HLR and SHHR were significantly higher than those in WKY and SD, and were highest in SHHR. Higher plasma levels of antithrombin III and plasminogen were detected in increasing order in SHR, HLR and SHHR as compared to those in WKY and SD. Hepatic mRNA expressions of fibrinogen chains and prothrombin were enhanced in SHR, HLR and SHHR, resulting in increased plasma fibrinogen levels in SHHR. These results suggest that hypertension and hyperlipidemia can each cause hypercoagulation, with hyperlipidemia being a stronger factor than hypertension. Since a greater hypercoagulative state is a complication of combined hypertension and hyperlipidemia, the SHHR model is a good system for studying the early stage of atherosclerosis ensuing from hyperfibrinogenemia.
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PMID:Development of hyperfibrinogenemia in spontaneously hypertensive and hyperlipidemic rats: a potentially useful animal model as a complication of hypertension and hyperlipidemia. 1728 85

To assess the existence of endothelial dysfunction and the possibility of the early onset of atherosclerosis in the chronic stage of Kawasaki disease (KD), we examined endothelial function in adult patients late after the onset of KD. We evaluated two age-matched groups: 35 adult KD patients (KD group) (mean age, 27.0 years; mean interval time, 24.1 years), and 36 healthy adults (control group). To assess vascular endothelial function, flow-mediated dilatation (%FMD) of the brachial artery and urinary nitrites and nitrates (NOx) were examined. We also measured adhesion molecules and several coagulation-fibrinolysis markers. In addition, we measured high-sensitive C-reactive protein (hs-CRP) as a chronic inflammatory marker, and brachial-ankle pulse wave velocity (baPWV) as a marker for arterial stiffness. %FMD was significantly reduced in the KD group when compared with that of the control group (KD group, 10.4 +/- 2.6%; control group, 14.4 +/- 3.2%, p<0.05), particularly in patients with coronary artery lesions. Thrombin-antithrombin III complex values were higher in the KD group, although no significant differences were observed in the other markers for endothelial function. Hs-CRP was significantly elevated only in the patients with coronary aneurysms. Furthermore, in the male KD patients, the baPWV values were significantly higher than those in the control subjects. This study revealed that the adult patients with a history of KD had systemic vascular endothelial dysfunction, and also suggested that a history of KD was possibly one of the risk factors for early onset of atherosclerosis.
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PMID:Endothelial dysfunction in adult patients with a history of Kawasaki disease. 1734 94


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