Neointimal tissue response at sites of coronary stenting in humans - Macroscopic, histological, and immunohistochemical analyses
Neointimal tissue response at sites of coronary stenting in humans - Macroscopic, histological, and immunohistochemical analyses
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DOI：
10.1161/01.cir.98.3.224
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发表时间：
1998-07-21
期刊：
影响因子：
37.8
通讯作者：
Becker, AE
中科院分区：
文献类型：
--
作者：
Komatsu, R;Ueda, M;Becker, AE
背景-动物实验研究表明冠状动脉支架植入术可诱导新生内膜增生。然而，在人类冠状动脉支架植入术后的组织病理学事件还没有进行系统的studyed.Methods和结果，我们研究了11个支架冠状动脉（9 Palmaz-Schatz支架，1 Wiktor支架，1 ACS多链接支架）从11例患者谁已经死亡2天至21个月后支架。我们着重于修复过程的大体、组织学和免疫组化方面。2例患者出现再狭窄症状。连续切片用抗平滑肌细胞（SMC）、巨噬细胞和内皮细胞的抗体染色。在支架植入后第9天和第12天，支架部位显示血栓形成，早期新生内膜由大量巨噬细胞和铜肌动蛋白阴性梭形细胞组成。从64天开始，所有支架植入部位均显示出明显的新生内膜层，尽管程度不同。在nonrestenotic病变，新生内膜增厚显着小于再狭窄病变，但没有质的差异;新生内膜含有巨噬细胞，但主要是由α-肌动蛋白阳性SMCs. Conclusions，这些观察结果强烈支持的概念，即在人类的新生内膜增殖是一个过程中的分期再分化的SMCs，这可能会导致支架内狭窄。此外，支架再狭窄部位新生内膜增生旺盛，巨噬细胞聚集，广泛新生血管形成，提示附壁血栓机化的作用。
Background-Experimental animal studies have shown that coronary stenting induces neointimal proliferation. However, the histopathological events after coronary stenting in humans have not been studied systematically.Methods and Results-We investigated 11 stented coronary arteries (9 Palmaz-Schatz stents, 1 Wiktor stent, and 1 ACS Multi-Link stent) obtained from 11 patients who had died 2 days to 21 months after stenting. We focused on gross, histological, and immunohistochemical aspects of the repair processes. Two patients developed symptoms of restenosis. Serial sections were stained with antibodies against smooth muscle cells (SMCs), macrophages, and endothelial cells. At 9 and 12 days after stenting, the stent sites showed thrombus formation with early formation of neointima composed of abundant macrophages and cu-actin-negative spindle cells. From 64 days on, all sites with stenting showed a distinct layer of neointima, albeit to varying degrees. In nonrestenotic lesions, neointimal thickening was markedly less than in restenotic lesions but without qualitative differences; the neointima contained macrophages but was composed predominantly of alpha-actin-positive SMCs.Conclusions-These observations strongly support the concept that neointimal proliferation in humans Is a process of staged redifferentiation of SMCs, which may cause in-stent stenosis. Moreover, the exuberant neointimal proliferation with accumulation of macrophages and extensive neovascularization at sites of stent restenosis suggests a role for organization of mural thrombus.