Platelets, blood flow, and the vessel wall.

Vessel wall injury and lipid deposition in the walls of arteries can contribute to the development of atherosclerotic lesions. The mitogen (platelet-derived growth factor) for smooth muscle cells that is released from platelets that adhere to the sites of injury contributes to vessel wall thickening, as does the organization of mural thrombi. Although many arterial thrombi result from fissure or rupture of the fibrous cap of lipid-rich atherosclerotic plaques, thrombi that result from shear-induced platelet aggregation and disturbed blood flow at stenotic lesions also contribute to the thromboembolic clinical complications of atherosclerosis. Prevention of thrombus initiation requires a better understanding of platelet interaction with injured vessel walls and of the ways in which this process may be inhibited. A crucial factor in the management of thrombus formation in severely injured vessels is restoration of a normal pattern of blood flow. Theoretically, it may be possible to use angioplasty (to remove atherosclerotic lesions and to dilate stenosed vessels) and to use new therapeutic interventions (to prevent the accumulation of an initial layer of platelets on the acutely injured surface) to reduce the probability of restenosis and thrombosis at these sites.