Von Willebrand factor activity and platelet adhesion under flow conditions in patients with CAD

What is it about?

We hypothesize that the functional disturbance of Von Willebrand factor (VWF) and the changes in the binding activity of this protein with platelets affects thrombus formation at the initial stage and thus contributes to the development of CAD. This paper examines VWF antigen levels in blood plasma, VWF activity using VWF-ristocetin cofactor activity, VWF collagen-binding activity, and platelet adhesion to collagen under flow conditions in patients with and without CAD.

Featured Image

Why is it important?

VWF is essential for platelet adhesion to the subendothelium of the damaged endothelial layer at the high shear rates characteristic of small-diameter arteries, especially at stenotic sites. At high shear rates, platelet adhesion is mediated by the glycoprotein (GP) Ib-IX-V receptor complex located on the platelet surface, as well as by vascular wall collagen and von Willebrand factor. Considering that VWF facilitates primary hemostasis and a local inflammatory response at high shear rates, its dysfunction may contribute to the development of coronary artery disease and its complications. This study elucidated changes in VWF–collagen-platelet interactions associated with CAD. We suggest that these changes can be associated with the development of CAD.

Perspectives