General mechanisms of coagulation and targets of anticoagulants (Section I)
نویسندگان
چکیده
Raffaele De Caterina1*; Steen Husted2*; Lars Wallentin3*; Felicita Andreotti4**; Harald Arnesen5**; Fedor Bachmann6**; Colin Baigent7**; Kurt Huber8**; Jørgen Jespersen9**; Steen Dalby Kristensen10**; Gregory Y. H. Lip11**; João Morais12**; Lars Hvilsted Rasmussen13**; Agneta Siegbahn14**; Freek W. A. Verheugt15**; Jeffrey I. Weitz16** 1Cardiovascular Division, Ospedale SS. Annunziata, G. d’Annunzio University, Chieti, Italy; 2Medical-Cardiological Department, Aarhus Sygehus, Aarhus, Denmark; 3Cardiology, Uppsala Clinical Research Centre and Department of Medical Sciences, Uppsala University, Uppsala, Sweden; 4Institute of Cardiology, Catholic University, Rome, Italy; 5Medical Department, Oslo University Hospital, Ulleval, Norway; 6Department of Medicine, University of Lausanne, Lausanne, Switzerland; 7Cardiovascular Science, Oxford University, Oxford, UK; 83rd Department of Medicine, Wilhelminenspital, Vienna, Austria; 9Unit for Thrombosis Research, University of Southern Denmark, Esbjerg, Denmark; 10Department of Cardiology, Aarhus University Hospital, Skejby, Aarhus, Denmark; 11Haemostasis Thrombosis & Vascular Biology Unit, Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK; 12Cardiology, Leiria Hospital, Leiria, Portugal; 13Department of Cardiology, Thrombosis Center Aalborg, Aarhus University Hospital, Aalborg, Denmark; 14Coagulation and Inflammation Science, Department of Medical Sciences, Uppsala University, Uppsala, Sweden; 15Cardiology, Medical Centre, Radboud University Nijmegen, Nijmegen, Netherlands; 16Thrombosis & Atherosclerosis Research Institute, Hamilton General Hospital, Hamilton, Ontario, Canada
منابع مشابه
General mechanisms of coagulation and targets of anticoagulants (Section I). Position Paper of the ESC Working Group on Thrombosis--Task Force on Anticoagulants in Heart Disease.
Contrary to previous models based on plasma, coagulation processes are currently believed to be mostly cell surface-based, including three overlapping phases: initiation, when tissue factor-expressing cells and microparticles are exposed to plasma; amplification, whereby small amounts of thrombin induce platelet activation and aggregation, and promote activation of factors (F)V, FVIII and FXI o...
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