Platelets contribute vitally to the complex processes involved in haemostasis and thrombosis. Even more complex is their contribution to atherogenesis. Many studies have been devoted to analysing the processes involved in platelet activation since, clearly, prevention of activation may have clinical value. There are now at least two systems of platelet activation under intensive study: (a) agonist (e.g. ADP and thrombin) induced platelet activation when fibrinogen is the ligand; this process occurs at low shear forces and is aspirin sensitive; (b) secondly, in marked contrast, at high shear forces, shear itself activates the platelets and von Willebrand's factor (vWf) is the ligand, and this process is aspirin insensitive.1