Mechanical factors affecting hemostasis and thrombosis.

Both physical and chemical factors can influence the activity of platelets and coagulation factors responsible for the formation of thrombotic and hemostatic masses in the vicinity of an injured vessel wall. Studies performed in controlled shear devices (viscometers) have indicated that physical factors alone can induce platelet aggregation, even in the absence of exogenous chemical factors. The physical considerations which appear to be important for the local activation of hemostatic/thrombotic mechanisms appear to be related to the magnitude of the shear rate/stress, the duration of the applied physical force and the local geometry. Blood flow alone has multiple influences on platelet and coagulative mechanisms. It has been well established that at physiologically encountered shear conditions, increases in the local shear rate enhance the attachment of platelets to the vessel wall and the growth of platelet aggregates on adherent platelets. In contrast, increases in local shear conditions inhibit the production of fibrin formation on surfaces where tissue factor (TF) is exposed. At levels of shear rate/stress high as compared to normal physiological conditions, but comparable to those observed at the apex of severely stenosed vessels, platelet aggregate formation is dependent on the duration of the exposure time. Considerable advances in our understanding of flow-related mechanisms have evolved from the use of well-defined perfusion chambers employing parallel flow streamlines. However, processes leading to hemostasis and thrombosis generally occur in more complicated flow situations where flow streamlines are not parallel and in which abnormally high, as well as abnormally low, shear rates and shear stress levels may be encountered in close proximity to each other.