Stary H C
Louisiana State University School of Medicine, New Orleans.
Eur Heart J. 1990 Aug;11 Suppl E:3-19. doi: 10.1093/eurheartj/11.suppl_e.3.
We have studied the cell and matrix composition of normal intima and of atherosclerotic lesions in the coronary arteries of 691 subjects less than 40 years old. These arteries were obtained at autopsy and fixed by perfusion with glutaraldehyde under physiological pressure. A defined segment of the left coronary artery, known for its susceptibility to develop advanced lesions, was studied by light and electron microscopy. The initial intimal lesion occurred in infants and consisted in an increase in intimal macrophages and presence of isolated lipid-laden macrophages (foam cells). At puberty, more substantial accumulations of foam cells, accompanied now by lipid droplets in smooth muscle cells and by thinly scattered extracellular lipid (fatty streaks), were present. After puberty, an increasing number of subjects had intermediate lesions and atheroma. Intermediate lesions, characterized by greatly increased extracellular lipid, were the link between fatty streaks and atheroma. Atheroma was characterized by a massive core of extracellular lipid that damaged arterial structure by displacing normal intimal cells and matrix. In the third and more often in the fourth decade, some atheroma contained greatly increased collagen and smooth muscle cells above the lipid core (fibroatheroma). Collagenization and thickening were more marked when evidence of thrombotic deposits was present on the surface or within lesions. Smooth muscle cells were present in the intima of all subjects from birth. In early lesions, lipid in the intima was not associated with an increase in the number of smooth muscle cells. Smooth muscle cells were increased in lesions containing massive extracellular lipid, more so in those having, in addition, a thrombotic component; smooth muscle cells with massive basement membranes occurred in advanced lesions. Macrophages and macrophage foam cells were the cells that increased intimal cellularity at the onset of lesions. Other cell types associated with lesions were lymphocytes, mast cells, and plasma cells, but all of these were less numerous than either smooth muscle cells or macrophages. From birth, intima was always thicker opposite the flow divider wall of a bifurcation (eccentric thickening). When atherosclerotic lesions of any type were present in coronary arteries, the amount of lipid and accompanying cell reactions were greatest in eccentric thickening; intermediate lesions and atheroma were present only in eccentric thickening while fibroatheroma often extended beyond eccentric thickening.
我们研究了691名40岁以下受试者冠状动脉正常内膜和动脉粥样硬化病变的细胞及基质组成。这些动脉在尸检时获取，并在生理压力下通过戊二醛灌注固定。选取左冠状动脉中一段因易发生晚期病变而闻名的特定节段，通过光镜和电镜进行研究。初始内膜病变出现在婴儿期，表现为内膜巨噬细胞增多以及出现孤立的富含脂质的巨噬细胞（泡沫细胞）。青春期时，泡沫细胞大量积聚，同时平滑肌细胞内出现脂滴，细胞外脂质呈稀疏散在分布（脂肪条纹）。青春期后，越来越多的受试者出现中间病变和动脉粥样瘤。中间病变的特征是细胞外脂质大幅增加，是脂肪条纹和动脉粥样瘤之间的过渡阶段。动脉粥样瘤的特征是细胞外脂质形成巨大核心，通过取代正常内膜细胞和基质破坏动脉结构。在第三个十年，更常见于第四个十年，一些动脉粥样瘤在脂质核心上方含有大量增加的胶原蛋白和平滑肌细胞（纤维粥样瘤）。当病变表面或内部有血栓形成迹象时，胶原化和增厚更为明显。从出生起，所有受试者的内膜在分叉处的血流分流壁相对处总是更厚（偏心增厚）。当冠状动脉出现任何类型的动脉粥样硬化病变时，脂质含量及伴随的细胞反应在偏心增厚处最为显著；中间病变和动脉粥样瘤仅出现在偏心增厚处，而纤维粥样瘤常超出偏心增厚范围。
