Coronary angioplasty enhances platelet reactivity through von Willebrand factor release.

Shear induced platelet activation is responsible for arterial thrombosis. The role of fibrinogen is established at low shear stress, but at high shear stress von Willebrand factor (vWF), not fibrinogen, is essential for platelet adhesion and aggregation. Patients with vWF deficiency exhibit resistance to thrombosis, and raised vWF is a risk factor for acute coronary syndromes. Interpretation of vWF concentrations is, however, complicated since vWF may be an acute phase reactant. The effect of vWF on thrombosis in the normal (non-vWF deficient) population remains unknown. The aim of this study was to determine the effect of coronary occlusion on plasma vWF level in vivo and the effect of raised vWF on thrombosis/haemostasis in vitro.