LIPID AND CELLULAR-CONSTITUENTS OF UNSTABLE HUMAN AORTIC PLAQUES

Unstable plaques are undergoing thrombosis which, in most instances, i s due to fissuring and rupture of the plaque cap. This process (deep i ntimal injury) is a complication of plaques with a lipid-rich core. Th e cap tear allows blood to enter the core from the lumen, leading init ially to intraplaque thrombosis and, subsequently, in some cases intra luminal thrombosis. Cap tears reflect the interplay between the force exerted on the tissue and its inherent mechanical strength. Factors wh ich elevate and concentrate circumferential wall stress on the cap dur ing systole include an increasing proportion of the total plaque volum e occupied by the lipid core, thinning of the cap and a loss of intern al collagen struts within the core. Factors which lead to an inherent reduction in the mechanical strength of cap tissue include a reduction in collagen and glycosaminoglycan concentrations, an increase in the number and density of macrophages, and a concomitant reduction in smoo th muscle cells in the cap tissue. It is therefore possible to define a vulnerable plaque as one in which the lipid core is disproportionate ly large, the cap thin, and in which monocytes preponderate over smoot h muscle cells.