title: Pathological analyses of long-term intracoronary Palmaz-Schatz stenting; Is its efficacy permanent?
abstract: 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.
  
  
  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) > 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.
  
  
  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.
authors.affiliation: Department of Laboratory Medicine, Kokura Memorial Hospital, 1-1 Kifune-machi, Kokurakita-ku, Kitakyushu, 802-8555, Japan. kmhptca@nn.iij4u.or.jp
authors.forename: Katsumi
authors.initials: K
authors.lastname: Inoue
authors.forename: Kenichi
authors.initials: K
authors.lastname: Abe
authors.forename: Kenji
authors.initials: K
authors.lastname: Ando
authors.forename: Shinichi
authors.initials: S
authors.lastname: Shirai
authors.forename: Kei
authors.initials: K
authors.lastname: Nishiyama
authors.forename: Michio
authors.initials: M
authors.lastname: Nakanishi
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamada
authors.forename: Koyu
authors.initials: K
authors.lastname: Sakai
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Nakagawa
authors.forename: Naoya
authors.initials: N
authors.lastname: Hamasaki
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kimura
authors.forename: Masakiyo
authors.initials: M
authors.lastname: Nobuyoshi
authors.forename: Tadaomi Alfonso
authors.initials: TA
authors.lastname: Miyamoto
mesh_terms: D000368:Aged; D023903:Coronary Restenosis / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D005549:Foreign-Body Reaction / Q000209:etiology / Q000473:pathology; D006083:Graft Occlusion, Vascular / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D008297:Male; D013193:Stainless Steel / Q000009:adverse effects*; D015607:Stents / Q000009:adverse effects*; D013997:Time Factors
chemical_list: D013193:Stainless Steel