Pathological analyses of long-term intracoronary Palmaz-Schatz stenting - Is its efficacy permanent

被引:76
作者
Inoue, K
Abe, K
Ando, K
Shirai, S
Nishiyama, K
Nakanishi, M
Yamada, T
Sakai, K
Nakagawa, Y
Hamasaki, N
Kimura, T
Nobuyoshi, M
Miyamoto, TA
机构
[1] Kokura Mem Hosp, Dept Lab Med, Kokurakita Ku, Kitakyushu, Fukuoka 8028555, Japan
[2] Kokura Mem Hosp, Dept Cardiol, Kokurakita Ku, Kitakyushu, Fukuoka 8028555, Japan
[3] Kyoto Univ, Dept Cardiovasc Surg, Kyoto, Japan
关键词
stents; inflammation; atherosclerosis; pathology;
D O I
10.1016/s1054-8807(03)00132-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: 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. Methods and Results: 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) greater than or equal to 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) greater than or equal to 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. Conclusions: 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. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:109 / 115
页数:7
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