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