 - Patients with unstable angina have elevated levels of P-selectin, an integral membrane protein involved in platelet adhesion. Pulsatile shear stress, as occurs in stenotic arteries, can cause platelet aggregation via an increased expression of P-selectin. Hydrodynamic shear stress, resulting from plaque rupture, can activate platelets and cause both platelet aggregation via glycoprotein IIbIIIa and von Willebrand factor and platelet-mediated neutrophil aggregation via upregulation of P-selectin. Although levels of P-selectin decrease during the first month after treatment, levels remain higher than normal even with therapy with glycoprotein IIbIIIa inhibitors, suggesting continued platelet activation. 