From the clinical point of view the most important end results of atherosclerosis are stenosis and occlusion of the affected artery. A prerequisite for this is a degree of plaque growth sufficient to encroach significantly on the integrity of the vessel lumen. It is clear that in the earlier phases of the natural history of an atherosclerotic plaque, this growth is mediated via the proliferation of modified smooth muscle cells in the affected area of the arterial intima and by the elaboration of extra-cellular connective tissue elements such as collagen, elastin and glycoso-amino-glycans of which these cells are capable (l, 2, 3). Experimental data now exist which suggest that one of the factors stimulating this form of localized connective tissue proliferation is platelet adhesion and aggregation and the evidence for this will be reviewed briefly in a later section of this paper. Of equal, perhaps greater importance, is the proposition that mural thrombi occur in relation to established atherosclerotic plaques and that the thrombi may become incorporated into the substances of the arterial wall with a subsequent increase in plaque thickness.