Histochemical observation was conducted on arterial lesion in 4 cases of Marfan's syndrome and electron microscopic observation was also carried out on the aorta and gastroepiploic artery in 2 of the 4 cases. Acid mucopolysaccharide (AMPS) noted In cystic medionecrosis demonstrated meshwork of spheres and threads, and showed the same structure as the ground substances widely distributed in the mesenchymal connective tissues including normal arteries and as AMPS in cystic medionecrosis‐like lesions such as arteriosclerosis, mesoaortitis syphilitica, and aortitis syndrome (Takayasu's disease). In histochemical observation, there was found no distinct qualitative difference between AMPS in Marfan's syndrome and that in controls. The overaccumulation of AMPS is not a direct cause of vascular lesions in Marfan's syndrome. The pattern of degeneration of elastic fibers was peculiar to Marfan's syndrome but it also resembled senile change. Degeneration of elastic fibers was accompanied by regeneration in the same area. There was observed no electron microscopic anomaly in collagen fibers nor was found anomaly of fibrlllogenesis in media smooth muscle cells. From the point of view of cell pathology, attribution of the cause of vascular lesion merely to some enzyme deficiency results in much contradiction.

In various arterial lesions including atherosclerotic lesions, the main morphological change involves smooth muscle cells. The potential sensitivity is different among the arterial smooth muscle cells, venous smooth muscle cells and smooth muscle cells of other organs. The modified smooth muscle cells characterized by the increase of rough endoplasmic reticula are considered to express their latent ability to synthesize collagen fibers, elastic fibers and other ground substances. The foam cells noted in atherosclerosis and fatty streak consist of lipid accumulated smooth muscle cells and hematogenous macrophages. Lipid metabolism and synthesis in the latter differ from those in the former. The ratio of the two kinds of foam cells in atheroma or fatty streak varies by the stage of the lesion. It is possible to suppose that there exists a factor which would selectively attack the media smooth muscle cells of small arteries or arterioles. This is observed electron microscopically as focal cytoplasmic necrosis (cytoplasmolysis) of smooth muscle cells and plays an important role in the histogenesis of fibrinoid necrosis. In case of experimental periarteritis nodosa the early stage begins with cytoplasmolysis of smooth muscle cells and marked increase of rough endoplasmic reticula in adjacent smooth muscle cells.

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