Human atherosclerotic disease can be resolved into eight types of lesion, each characterized by its composition and structure and the absence or degree of intimal injury. The eight types have been arranged in the sequence in which they may progress in complexity from the initial change in childhood or youth to the clinical endpoints in older persons. While lesions at first increase primarily by intra- and extracellular accumulation of lipid, this in itself rarely accounts for symptomatic obstruction. Lipidic lesions become symptomatic primarily by means of successively superimposed deposits of thrombotic material. Non-homogeneity of hemodynamic forces within the length of an artery account for local differences in intima thickness (adaptive intimal thickening) and, in persons with risk factors, differences in susceptibility to lesion formation. According to the degree to which they can accumulate or retain lipid and bring about secondary mechanisms, specific locations of the arterial tree have been designated as atherosclerosis-resistant, atherosclerosis-prone and progression-prone.