As a thrombus grows in a stenosis, the lumen narrows producing very high shear rates as blood velocities increase. Binding platelets are subjected to drag forces exceeding 10,000 pN. These forces could be balanced by 100 simultaneous 100 pN GPIbα-vWF-A1 bonds. The density of GPIbα ligands on platelets is sufficiently high; however, platelet capture under high shear would require the vWF-A1 density on the thrombus surface to be increased to over 416 μm−2. A computational model is used to determine platelet capture as a function of shear rate, surface receptor density, surface contact and kinetic binding rate. vWF-A1 density could be increased by: (i) plasma vWF attaching to the thrombus surface and elongating under shear; (ii) elongated vWF strands creating nets with 3-D pockets; and (iii) vWF releasing from activated platelets. With all three events, A1 densities increase with high shear to provide sufficient multivalency (>850 bonds) for capture even at 500,000 s−1. If the on-rate is greater than 108 M−1 s−1, then a platelet could be captured within 3 μs, the time limit to form bonds before the platelet is swept away. This mechanism of vWF nets can capture circulating platelets at a sufficiently high rate to cause arterial thrombotic occlusion.