Arterial thrombosis can lead to acute myocardial infarction or stroke. Thrombosis has been found to occur on atherosclerotic lesions and can fully occlude the blood vessel. Atheromas create a stenosis in the flow field. Thrombus forming in these regions is characteristically composed mostly of platelets with the addition of von Willebrand Factor (vWF) and polymerized fibrin. Previous studies of thrombosis under arterial-like stenotic flow conditions have shown that the thrombus growth rate increases under increasing shear rates up to 40000 s−1 [1]. The obstructive atheroma can lead to wall shear rates even greater than 40 times the average wall shear rate for an artery [2]. The shear rate dependency can be ascribed to mass transport [3]. Additionally, it can be ascribed to platelet binding mechanisms, such as vWF, that dominate at high shear, while other binding mechanisms, such as fibrinogen, bind at lower shear in the arteries [4].

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