Atherothrombosis, characterized by rupture or erosion of an atherosclerotic plaque with superimposed thrombus formation, is the major cause of ischemic events in the heart and brain. Upon plaque rupture or erosion subendothelial plaque tissue becomes exposed to the blood stream which triggers a series of thrombogenic responses, potentially leading to occlusion of the atherosclerotic artery. 

Current studies, which are largely based on microfluidic studies and experimental mouse models, indicate that collagen- and ADP-receptor-dependent platelet activation in concert with thrombin/fibrin generation via the extrinsic and intrinsic coagulation pathways is essential in the atherothrombotic process [1]. Although the atherothrombus forming process appears to be regulated by similar mechanisms as the process of thrombus formation in damaged non-atherosclerotic vessels this does not imply that there are no differences herein which may be exploited for (more) selective targeting of atherothrombosis without causing bleeding.