Relative Contributions of von Willebrand Factor and Platelet
Myocardial infarction (MI) and ischemic stroke result from rapid, occlusive thrombus formation at the site of atherosclerotic plaque rupture [1]. Thrombus formation at atherosclerotic lesions occurs at high shear rates [2,3] and follows distinct pathways [4,5]. Briefly, collagen exposed by plaque cap rupture acts as a thrombogenic surface. At high shear rates, plasma von Willebrand factor (VWF) is adsorbed onto the surface. Platelets then bind to VWF at the A1 domain via platelet receptor GPIb. Bound platelets are activated by shear and/or soluble agonists and irreversibly bind via integrin ?IIb?3....