ABSTRACT
The lesions of atherosclerosis take different forms depending upon their anatomic site; the age, genetic, and physiological status of the affected individual; and the so-called risk factors to which each individual may have been exposed. The examination of atherosclerotic lesions with modern techniques of cell and molecular biology has revealed that each lesion contains significant elements of a specialized chronic inflammatory fibroproliferative response. These consist of accumulated monocyte/macrophages and T lymphocytes followed by smooth-muscle proliferation; the formation by the proliferated cells of large amounts of connective tissue matrix, including collagen, elastic fibers, and proteoglycans; and the accumulation of intracellular and extracellular lipid.[1,2] In each instance, the relative degree to which each of the cells responds to different atherogenic stimuli determines the unique combination of these three elements that defines the type and extent of the resulting lesion.
