The pathophysiology of atherosclerosis is a complex biologic process which involves severe perturbations in cellular and hormonal interactions as well as in lipoprotein and arachidonic acid metabolism. Platelets, endothelial cells, monocytes, and smooth muscle cells as well as fibroblasts exhibit critical interactions which have been proposed as the prerequisite for the development of the arteriosclerotic lesion [1]. Secretion of the potent chemotactic and mitogenic platelet-derived growth factor by activated platelets as well as monocytes and endothelial cells results in phospholipase activation, subsequent release of arachidonic acid, and the synthesis of eicosanoids which promote platelet aggregation, cause vascular constriction, and exhibit potent chemotactic properties.