Direct Oral Anticoagulants (DOACs) Versus “New” Oral Anticoagulants (NOACs)?  Lars M. Asmis, MD  Seminars in Hematology  Volume 51, Issue 2, Pages 87-88 (April 2014) DOI: 10.1053/j.seminhematol.2014.03.003 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 DOACs—sites of action. Based on the cellular model of hemostasis, this figure depicts DOACs’ sites’ of action. Tissue factor–bearing cells (TF+ cells) are key to initiating coagulation according the model originally described by Hoffman and Monroe.5 The complex of TF and activated factor VII (FVIIa) leads to the generation of activated factor X (FXa). In the subsequent amplification phase, the first traces of activated factor II (FIIa = thrombin) are generated, which in turn leads to activation of multiple targets. In the propagation phase, the surface of activated platelets then serves as a platform for the FXa-based generation of the thrombin burst necessary for the last phase, resulting in fibrin stabilization (insoluble fibrin: fibrini). Sites of action of direct inhibtors of FXa (anti-FXa) and thrombin (anti-FIIa) are depicted in red and in blue. Seminars in Hematology 2014 51, 87-88DOI: (10.1053/j.seminhematol.2014.03.003) Copyright © 2014 Elsevier Inc. Terms and Conditions