Taipei Medical University

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Yang, V. W-C
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------>paper_name=Peptide inhibitor of fibrinogen blood clotting, US6413931
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------>fullAbstract=AIMS: Our study sought to evaluate mechanisms of the current strategies for optimal anticoagulation during percutaneous coronary intervention (PCI). METHODS AND RESULTS: Thirty-two high risk acute coronary syndrome patients were randomised to bivalirudin and provisional GPIIb/IIIa inhibition (GPIIb/IIIa) or unfractionated heparin (UFH) and mandatory GPIIb/IIIa. Flow cytometric measurements immediately after anticoagulation showed that, unlike UFH, bivalirudin did not activate platelets as indicated by P-selectin expression and fibrinogen binding while decreasing platelet-monocyte aggregates and monocyte expression of tissue factor. UFH released tissue factor pathway inhibitor (TFPI) during and immediately after PCI while bivalirudin (irrespective of GP IIb/IIIa) did not. Lower levels of TFPI with bivalirudin were seen during and immediately after PCI (P<0.01). Thrombin generation as indicated by prothrombin fragment F 1+2 levels was reduced during PCI in the UFH group (P<0.01) but not with bivalirudin. Soluble CD40 ligand is associated with thrombosis and levels were higher in the bivalirudin group irrespective of GPIIb/IIIa at the same stages (P<0.05). CONCLUSIONS: Bivalirudin has some early advantages on platelet activation when compared to UFH. However, there are significant limitations in its mechanism of action, particularly a lack of release of tissue factor pathway inhibitor.
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------>authors2=Hook, M
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------>authors=Yang, V. W-C
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------>updateTitle=A comparison of anticoagulation with bivalirudin and provisional GPIIb/IIIa inhibition with unfractionated heparin and mandatory GPIIb/IIIa inhibition during percutaneous coronary intervention in relation to platelet activation and the inhibition of coagulation.
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------>patent_SDate=2002-07-02 00:00:00
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------>publish_year=2002
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A B C D E F G H I J K L M N O P Q R S T U V W X Y Z