Abstract
Thrombin, a serine protease, is the keystone of the twin processes of hemostasis and thrombosis. Through procoagulant, anticoagulant, and antifibrinolytic mechanisms, thrombin helps maintain vascular integrity in the face of hemorrhage. These same mechanisms, however, allow for the pathologic formation of thrombi in response to endothelial damage, which accompanies the erosion or rupture of atherosclerotic plaques. Alone or incorporated into plaques, thrombi can cause vessel occlusion resulting in acute coronary syndromes (ACS). Inhibiting thrombin can improve clinical outcomes in ACS, as well as in procedures such as percutaneous coronary interventions, which are designed to open the occluded vessels that cause ACS. Such improvements in outcomes with thrombin inhibition reflect the central and multivariate role of thrombin in thrombus formation.
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