Abstract

Diffuse intimal thickening (DIT) has appeared in human coronary arteries in infants. Eccentric intimal thickening (EIT) is raised from DIT, and may develop to atheromatous intimal thickening (plaque). In order to clarify histological changes according to the development from DIT to EIT or plaque, coronary arteries obtained from 95 male autopsy cases were histometrically and immunohistochemically investigated. Histometrival studies were carried out on the main trunk of the right coronary artery (segment 1: seg. 1) and the left descending artery (seg. 6). Thickness of the intima was measured in all cases. In cases over 30 years of age, volume fractions (Vfs) of smooth muscle cells (SMCs), foam cells, blood cells, collagen, elastic fibers, extracellular matrix (ECM) and atheroma in the intima and as well as the number and density of intimal SMCs were analyzed by a point counting method. Immunohistochemical studies were carried out on 12 cases for which postmortem time was less than 4 hrs. The thickness of DIT in both seg. 1 and 6 increased with age. Histometrically collagen fibers were the most major component in these segments, and the collagen Vf also increased with age. Vfs of SMCs, elastic fibers, and ECM decreased with age. The density of SMCs in the intima decreased rapidly in the fourth and fifth decades, and then reafter decreased more slowly. EIT in both seg. 1 and 6 also thickened with age, and the rate of increase was higher than that of DIT. Collagen Vf was the largest, and was most similar to DIT. Atheromas were more frequently seen in seg. 6. Although the number of SMCs in EIT was two times larger than that of DIT in each decade, the density of SMCs in EIT was lower than that of DIT. The density of SMCs in plaque was lower than that of EIT. In contrast, the collagen Vf was higher than that of EIT. In immunohistochernical studies, alot of anti-muscle or anti-macrophage positive foam cells were identified in plaques. Some of them were positively stained with anti-prolyl hydroxylase. The anti-prolyl hydroxylase positive cells were more in plaque than DIT. Anti-β lipoproteins and anti-collagen type I reacted more intensely in plaque than DIT. From these results, EIT could turn into plague because of the accumulation of collagen fibers, and lipid infiltration leading to atheroma formation. In conclusion, in the human coronary artery, EIT, DIT and plaque thickened mainly because of the accumulation of collagen fibers, not by SMCs proliferation, particularly after the fourth decade.

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