Thrombosis research
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Thrombosis research · Jan 2008
Are patients with thrombophilia and previous venous thromboembolism at higher risk to arterial thrombosis?
Whether thrombophilic disorders, which are established risk factors for venous thromboembolism (VTE), also increase the risk of arterial thrombosis is still unknown. ⋯ The cumulative incidence of arterial thrombotic events in VTE patients is low, and the inherited thrombophilias do not seem to substantially increase the risk of arterial thrombosis.
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Thrombosis research · Jan 2008
Hypercoagulability in chronic kidney disease is associated with coagulation activation but not endothelial function.
Patients with chronic kidney disease exhibit features of a hypercoagulable state and have endothelial dysfunction, which may contribute to their increased cardiovascular risk. We examined the relationship between coagulation activation and vascular function in patients with chronic kidney disease. ⋯ Significant activation of the TF pathway of coagulation and depletion or reduction of some natural anticoagulants in chronic kidney disease was correlated with the degree of renal dysfunction, but not correlated with the abnormalities of vascular function. These data are consistent with a hypercoagulable state in chronic kidney disease that may be independent of endothelial based regulation but associated with an inflammatory state.
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Thrombosis research · Jan 2008
Visual evaluation of blood coagulation during mural thrombogenesis under high shear blood flow.
Mural thrombus generation at sites of damaged vessel walls is essential for both physiological haemostasis and pathological intravascular thrombosis. While thrombi are established by the concerted action of platelet aggregation and blood coagulation, most previous in vitro coagulation assays have evaluated fibrin clot formation in a closed stirring situation that lacks blood cells including platelets. We describe here a modified flow chamber system, established originally for platelet functional studies, that enables real-time observation of intra-thrombus fibrin accumulation during platelet thrombogenesis under flow conditions. ⋯ These observations were confirmed by perfusion of heparinized blood or blood from haemophilia patients with or without addition of activated factor VII. Thus, our experimental system provides visual evidence supporting the concept of "cell-based coagulation under whole blood flow", which might be the most physiologically relevant model of comprehensive thrombogenicity in vivo to date. This system promises to help formulate strategies for haemostatic management of congenital coagulation disorders as well as for antithrombotic therapy targeting fatal arterial thrombosis.
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Thrombosis research · Jan 2008
Influence of polymorphonuclear leukocytes on the plasma clot formation as evaluated by thromboelastometry (ROTEM).
It has been emphasized that polymorphonuclear leukocytes (PMN) participate in the regulation of coagulation. However, the mechanisms of action are not clear. Besides a procoagulant activity, anticoagulant or fibrinolytic properties are attributed to these cells. To explore their global effect, we have studied their involvement in the clot formation with thromboelastometry, which gives global view over the clotting process, in particular on the structure of the clot and on the kinetic of its formation. ⋯ The procoagulant activity of resting PMN was demonstrated as the initiation of fibrin formation with PMN-RP was significantly faster compared with both PRP and PPP. The kinetic of plasma clotting was remarkably improved with PMN-RP compared with PPP. However, the clot with PMN-RP had the same poor viscoelastical properties as PPP. Thromboelastometry gives a new point of view in the involvement of PMN in coagulation, in the absence of any PMN pre-activation. Their impact was centred on the kinetic and the facilitation of the clot formation.
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Thrombosis research · Jan 2008
Elevated D-dimer concentration identifies patients with incomplete recanalization of pulmonary artery thromboemboli despite 6 months anticoagulation after the first episode of acute pulmonary embolism.
Despite long-term anticoagulation in some patients after acute pulmonary embolism (APE) pulmonary thrombi are not completely resolved. We hypothesized that elevated D-dimer concentration reflecting increased endogenous fibrinolysis may indicate incomplete pulmonary thrombi resolution after the first episode of PE. ⋯ Elevated D-dimer after 6 months anticoagulation and right ventricular dysfunction at the diagnosis predict incomplete recanalization of pulmonary circulation after first episode of APE.