Early Lesions of Atherosclerosis in the Human Carotid and Cerebral Arteries

Abstract

Fatty streak, fat-free edema and thrombus as early lesions in genesis of atherosclerosis have been discussed. In this paper early lesions of atherosclerosis in human carotid and cerebral arteries are investigated.
Both fatty streak (accumulation of foam cells in the intima) and fat-free edema in the intima can become early lesions.
Groups of foam cells which accumulate in the intima disintegrate and undergo to atheroma (cell disintergration type atheroma, OONEDA). Collagenous and elastic fibers between foam cells disappear.
Fat-free edema is followed by proliferation of intimal smooth muscle cells which produce collagenous and elastic fibers, and results in fibrosis in the intima. Collagenous fibers in the depths of the thickened intima can be seen to lighten in color and swell in varying degree. Electron microscopic examination reveals that many small lipid droplets, fine electron-dense materials similar to blood plasma protein and cell debris deposit between collagenous fibrils, as a result of which the fibrils split apart. Subsequently swollen fibers break down and undergo to atheroma (fiber disintegration type atheroma, OONEDA).
Foam cells, fat-free edema and fatty swelling of collagenous fibers are often seen in the intima of which vascular permeability has been increased. Opening of intercellular junctions, degeneration, necrosis and desquamation of the endothelial cells are responsible for increase of endothelial permeability and can be frequently observed in areas where are marginal areas of the thickened intima and junctional areas between layers of the stratified thickened intima.