Thrombosis at high shear rates depends primarily on von Willebrand factor and platelets, with hemodynamics playing a critical role in each stage of rapid thrombus formation.
The final common pathway in myocardial infarction and ischemic stroke is occlusion of blood flow from a thrombus forming under high shear rates in arteries. A high-shear thrombus forms rapidly and is distinct from the slow formation of coagulation that occurs in stagnant blood. Thrombosis at high shear rates depends primarily on the long protein von Willebrand factor (vWF) and platelets, with hemodynamics playing an important role in each stage of thrombus formation, including vWF binding, platelet adhesion, platelet activation, and rapid thrombus growth. The prediction of high-shear thrombosis is a major area of biofluid mechanics in which point-of-care testing and computational modeling are promising future directions for clinically relevant research. Further research in this area will enable identification of patients at high risk for arterial thrombosis, improve prevention and treatment based on shear-dependent biological mechanisms, and improve blood-contacting device design to reduce thrombosis risk.
Casa et al. (2017) conducted a review in Arterial thrombosis. Thrombosis at high shear rates depends primarily on von Willebrand factor and platelets, with hemodynamics playing a critical role in each stage of rapid thrombus formation.