Figure 3.

Antithrombotic and vascular-protective effects of anticoagulants and platelet inhibitors. Atherosclerosis-mediated vascular injury causes atherothrombosis through activation of coagulation and platelets. Fibrin formation can be diminished by anticoagulants including heparins, vitamin K antagonists, and direct oral anticoagulants such as the thrombin inhibitor dabigatran and the factor Xa inhibitors rivaroxaban, edoxaban, and apixaban. Platelets can be inhibited by aspirin (ASA, effecting the thromboxane A2 receptor TxA2), P2Y12 receptor antagonists clopidogrel, prasugrel, or ticagrelor, or via inhibition of the thrombin receptor PAR2 by Vorapaxar. Inhibition of thrombin, factor Xa, and platelets will diminish cellular effects through attenuated activation of the protease-activated receptors PAR1 and PAR2 on endothelial cells, vascular smooth muscle cells, and macrophages.