ABSTRACT
Growing evidence indicates that atherosclerosis is a dynamic process, with an important inflammatory component. In patients, quantitative differences in the inflammatory component have been observed in acute coronary syndromes compared with stable atherosclerosis, suggesting that the inflammation plays a role in the pathogenesis of atherosclerosis. The process of atherosclerosis as proposed by Ross (I) is a "response to injury." In this theory, atherosclerosis is the result of an excessive inflammatory-fibroproliferative response to different forms of injury to the arterial wall. The process, once initiated, is regulated and sustained by a number of inflammatory mediators, such as cytokines, adhesion molecules, and growth factors, and involves all the cellular elements with inflammatory properties, such as T lymphocytes, macrophages, neutrophils, and mast cells, as well as activated endothelial cells and smooth muscle cells. Cytokines, adhesion molecules, and other inflammatory mediators typical of immune interactions, have also been found to be increased in the peripheral circulation of patients with atherosclerosis, suggesting that at least some of the mechanisms are not confined to the arterial wall, but may have a systemic "reverberation."
