Platelet and vessel wall interaction and the genesis of atherosclerosis.

On the basis of in vitro studies, biochemistry and cell biology the interactions between platelets, other circulating blood cells and the vessel wall are complex and wide-ranging. In essence, the effects of platelets adhering to injured luminal surface might include: Aggregation and adherence of further platelets; Activation of coagulation and fibrin formation; Displacement of AT-III from endothelial surface; Recruitment and activation of potentially injurious polymorphonuclear leukocytes and monocytes; Recruitment and proliferation of smooth muscles cells from the vessel media to the intima; Vasoconstriction; Initiation of feedback mechanisms such as PGI2 release to limit the process. These effects are capable of contributing to the initial lesions and the progression of the atherosclerosis. As the lesions become more complex, and particularly as the normal endothelium is lost, there is morphological evidence that there is deposition of thrombus (for discussion see Chapter 4) and 111In-labelled platelet imaging experiments in patients document platelet uptake onto atherosclerotic plaques (Davis et al, 1978).