Abstract
Several observations argue against Ross's hypothesis (Jan. 14 issue)1 that atherosclerosis is an inflammatory disease. Oxidized low-density lipoprotein (LDL) is widely distributed in the fetal aorta,2 but atherosclerotic plaques are not present until the third or fourth decade of life. This observation argues against a theory of atherogenesis based on in vitro data ascribing inflammatory activity to oxidized LDL. The presence of foamy macrophages in a fatty streak does not make the lesion inflammatory. The supposed entry of circulating monocytes into the developing fatty streak, which could be a basis for characterizing that lesion as “inflammatory,” is even in doubt. My colleagues and I have examined microscopically aortas from many young people, and we have never seen a monocyte that is adherent to the aortic endothelium.