The prevention and treatment of spontaneous atherosclerotic lesions presents one of the most challenging clinical problems to internists, surgeons, and pathologists, since our knowledge of the pathogenesis of the basic alterations of the arterial wall is at present fragmentary and ill-defined.
Since the early work of Anitschkov2 on the production of experimental lesions in the rabbit, after prolonged dietary hypercholesterolemia, that have some resemblance to those found in man, and the high concentration of cholesterol in the early spontaneous plaque, a natural relation between disturbances in lipid metabolism and atherogenesis has been suspected.5,6,14
Recent emphasis on studies of local factors in this disease has been the direct result of efforts to reconcile extensive data on aberrations of the blood lipid spectrum with the histochemical and morphological changes encountered in early atheroma, since a satisfactory correlation between specific lipid changes and the degree of atherosclerosis present in many clinical