Thrombosis research
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Thrombosis research · Jan 2008
Aspirin response evaluated by the VerifyNow Aspirin System and light transmission aggregometry.
Patients with inadequate platelet inhibition by aspirin, referred to as aspirin resistance, might have an increased risk of suffering cardiovascular events. Therefore, identification of these patients by measuring platelet function is of great interest. Our objectives were to evaluate performance parameters of VerifyNow and to determine the agreement between VerifyNow and light transmission aggregometry (LTA) ad modum Born. ⋯ VerifyNow was highly repeatable, but further studies are needed to investigate the relevance of the cut-off level at 550 ARU for detecting aspirin resistance.
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Thrombosis research · Jan 2008
Impaired flow mediated dilatation as evidence of endothelial dysfunction in chronic atrial fibrillation: relationship to plasma von Willebrand factor and soluble E-selectin levels.
Impaired endothelial-dependent flow-mediated dilatation (FMD) has been used to demonstrate endothelial dysfunction in a wide variety of cardiovascular disease, but previous studies have excluded patients with atrial fibrillation(AF). We therefore hypothesised that endothelial dysfunction exists in AF and that this could be demonstrated by impaired FMD, and related to plasma indices of endothelial damage/dysfunction [soluble E-selectin (sE-sel), von Willebrand factor (vWf), and soluble thrombomodulin (sTM)], as well as total body nitrate/nitrite product (NOx, a measure of endothelial nitric oxide production). ⋯ Endothelial dysfunction, as demonstrated by impairment of FMD and raised vWF and E-selectin, is present in AF. Such endothelial perturbation may contribute to the increased risk of stroke and thromboembolism in this common arrhythmia.
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Thrombosis research · Jan 2008
Platelet anaesthesia during extracorporeal circulation: differential effects of GP IIb/IIIa blockers on platelet activation marker P-selectin expression at hypothermia.
Blood contact with artificial surfaces of extracorporeal circulation (ECC) and hypothermia as applied in cardiac surgery cause platelet dysfunction possibly followed by bleeding complications. "Platelet anaesthesia" is a pharmacological strategy to protect platelets against ECC-induced damage using a GP IIb/IIIa blocker, which should be short acting to achieve maximal therapy control thereby avoiding post-ECC haemorrhage. However, GP IIb/IIIa blockers can paradoxically induce platelet activation, which may limit their efficiency as anti-platelet drugs. This in-vitro study investigated potentially platelet-activating effects of short-acting GP IIb/IIIa blockers during normothermic and hypothermic ECC. ⋯ Especially regarding its ultra-short half-life FK633 has the best properties for platelet protection during normothermic ECC. However, at hypothermia FK633 and eptifibatide induce platelet activation. In relation with "platelet anaesthesia" possible hypothermia-associated prothrombotic side effects of GP IIb/IIIa blockers should be considered.
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Thrombosis research · Jan 2008
Association between thrombosis and bloodstream infection in neonates with peripherally inserted catheters.
Peripherally inserted catheters are essential for infants in the neonatal intensive care nursery for administration of medications, parenteral nutrition and blood transfusions. We hypothesized that there is an association between catheter associated thrombosis and catheter associated blood stream infection. The primary objective of this study was to determine the association between catheter associated blood stream infection (CABSI) and catheter-related thrombosis in the Neonatal Intensive Care Unit. ⋯ Further study is warranted to determine the pathophysiology between the association between thrombosis and infection and to determine if interventions may decrease the risk of these potentially life-threatening complications.
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Thrombosis research · Jan 2008
Hyperfibrinolysis in alcoholic cirrhosis: relative plasminogen activator inhibitor type 1 deficiency.
Over activity of the fibrinolytic system (hyperfibrinolysis) occurs in cirrhosis and has been shown to correlate with the risk of variceal hemorrhage. We have developed a model for assessing acute tissue plasminogen activator (t-PA) release in vivo in man. The aims of the study were to assess the contribution of basal and stimulated t-PA release to hyperfibrinolysis in patients with alcoholic cirrhosis. ⋯ Patients with alcoholic cirrhosis have a higher basal plasma t-PA activity because of a failure to increase plasma concentrations of its inhibitor, PAI-1. Furthermore, despite releasing normal amounts of t-PA acutely, higher t-PA activity remained due to the relative deficiency of PAI-1. This suggests that the pathogenesis of hyperfibrinolysis in alcoholic cirrhosis is the result of a relative PAI-1 deficiency and enhanced basal t-PA release.