Inoue Katsumi, Abe Kenichi, Ando Kenji, Shirai Shinichi, Nishiyama Kei, Nakanishi Michio, Yamada Takashi, Sakai Koyu, Nakagawa Yoshihisa, Hamasaki Naoya, Kimura Takeshi, Nobuyoshi Masakiyo, Miyamoto Tadaomi Alfonso
Department of Laboratory Medicine, Kokura Memorial Hospital, 1-1 Kifune-machi, Kokurakita-ku, Kitakyushu, 802-8555, Japan.
Cardiovasc Pathol. 2004 Mar-Apr;13(2):109-15. doi: 10.1016/S1054-8807(03)00132-7.
Angiographic regression of luminal narrowing occurs 6 months to 3 years poststenting. However, after 4 years lesions progressed gradually and late restenosis was observed in 28% of 179 Palmaz-Schatz-stented lesions during the past 10 years. Elucidating its pathogenesis is pivotal to developing preventive strategies.
Histopathological and immunohistochemical studies were performed in 19 stented coronary arteries obtained from 19 patients autopsied after noncardiac death 2-7 years poststenting. The quality/severity of chronic inflammatory cells (T lymphocytes, macrophages and multinucleated giant cells) infiltration around the stent struts that is observed even in the absence of restenosis depended on the time elapsed from stenting: a) 2 years postprocedure, in spite of angiographic regression during the first year and pathologically expressed as maturation of the neointimal scar, there was chronic inflammatory response evidence: neovascularization and lymphocyte infiltration, b) > or = 3 years: the neointimal smooth muscle cells were sparse with abundant proliferation of collagen fibers. Presence of slight helper/inducer T lymphocytes and mild macrophage infiltration around the stent struts was evident immunohistochemically, c) > or = 4 years: prominent infiltration by lipid-laden macrophages with strong collagen-degrading matrix metalloproteinase immunoreactivity was observed around the struts. In two of these arteries, the surface contacting the stent was focally disrupted and covered by nonocclusive mural thrombi.
Stainless steel stents evoke a remarkable foreign-body inflammatory reaction to the metal. These persistent peri-strut chronic inflammatory cells may accelerate new indolent atherosclerotic changes and consequent plaque vulnerability.
支架置入术后6个月至3年，管腔狭窄会出现血管造影退缩。然而，4年后病变逐渐进展，在过去10年中，179例置入Palmaz-Schatz支架的病变中有28%出现了晚期再狭窄。阐明其发病机制对于制定预防策略至关重要。
对19例患者在支架置入术后2至7年因非心脏原因死亡后进行尸检所获得的19条冠状动脉进行了组织病理学和免疫组织化学研究。即使在没有再狭窄的情况下，观察到的支架支柱周围慢性炎症细胞（T淋巴细胞、巨噬细胞和多核巨细胞）浸润的质量/严重程度取决于支架置入后的时间：a）术后2年，尽管第一年血管造影显示有退缩且病理表现为新生内膜瘢痕成熟，但仍有慢性炎症反应证据：新生血管形成和淋巴细胞浸润；b）≥3年：新生内膜平滑肌细胞稀少，胶原纤维大量增生。免疫组织化学显示支架支柱周围存在少量辅助/诱导性T淋巴细胞和轻度巨噬细胞浸润；c）≥4年：在支柱周围观察到富含脂质的巨噬细胞显著浸润，伴有强烈的胶原降解基质金属蛋白酶免疫反应性。在其中两条动脉中，与支架接触的表面局部破坏，并被非闭塞性壁血栓覆盖。
不锈钢支架会引发对金属的显著异物炎症反应。这些持续存在的支柱周围慢性炎症细胞可能会加速新的隐匿性动脉粥样硬化改变以及随之而来的斑块易损性。
