• Raffaele De Caterina, Steen Husted, Lars Wallentin, Felicita Andreotti, Harald Arnesen, Fedor Bachmann, Colin Baigent, Kurt Huber, Jørgen Jespersen, Steen Dalby Kristensen, Gregory Y H Lip, João Morais, Lars Hvilsted Rasmussen, Agneta Siegbahn, Freek W A Verheugt, Jeffrey I Weitz, and European Society of Cardiology Working Group on Thrombosis Task Force on Anticoagulants in Heart Disease.
• Institute of Cardiology, G. d'Annunzio University-- Chieti, Ospedale SS. Annunziata, Via dei Vestini, 66013 Chieti, Italy. rdecater@unich.it
• Thromb. Haemost. 2013 Apr 1; 109 (4): 569-79.

AbstractContrary 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 on platelet surfaces; and propagation, in which the Xase (tenase) and prothrombinase complexes are formed, producing a burst of thrombin and the cleavage of fibrinogen to fibrin. Thrombin exerts a number of additional biological actions, including platelet activation, amplification and self-inhibition of coagulation, clot stabilisation and anti-fibrinolysis, in processes occurring in the proximity of vessel injury, tightly regulated by a series of inhibitory mechanisms. "Classical" anticoagulants, including heparin and vitamin K antagonists, typically target multiple coagulation steps. A number of new anticoagulants, already developed or under development, target specific steps in the process, inhibiting a single coagulation factor or mimicking natural coagulation inhibitors.

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