Mechanical circulatory support devices perturb healthy blood flow, demonstrating supraphysiological shear rates (> 1-2,000 s-1) that induce platelet activation, amplify unfurling of the von Willebrand factor (vWF), and increase platelet adhesion. Elevated shear rates and shear rate gradients have been demonstrated to play a role in vWF-mediated platelet aggregation. The primary objective of this study is to observe the effect of variable shear rate and contributions of platelet receptors to platelet deposition in a stenotic, canonical model. Shear-induced platelet aggregation was observed at supraphysiological shear rates. Inhibition of vWF-binding receptors completely blocked adhesion and aggregation at >1,000 s-1. Inhibition of collagen-binding GPVI modestly decreased platelet adhesion at 5-10,000 s-1 but made larger thrombi more susceptible to embolization. This study yields further insight into mechanisms regulating rapid growth of arterial thrombi at supraphysiological shear rates.