title: Late-phase inflammatory response as a feature of in-stent restenosis after drug-eluting stent implantation.
abstract: OBJECTIVE
  The aim of this study was to compare pathological features among in-stent restenosis lesions after drug-eluting stent (DES) placement, those after bare metal stent (BMS) placement, and de-novo atherosclerotic lesions.
  
  
  BACKGROUND
  Restenosis after stenting is an over-reaction of the wound-healing response after vascular injury, which is characterized by a sequence of inflammation, granulation, extracellular matrix remodeling, and smooth muscle cell proliferation and migration. Recent advances in DES technology could considerably succeed in inhibiting this sequence of events. Thus, we hypothesized that the mechanism of in-stent restenosis after DES stenting might be different from that after BMS stenting as well as atherosclerosis.
  
  
  METHODS
  Tissues obtained by directional atherectomy (DES: seven specimens, BMS: 17 specimens, and de-novo: 15 specimens) were immunostained for T lymphocytes (CD45), macrophages (CD68), smooth muscle cells (α-smooth muscle actin), endothelial cells (von Willebrand factor), and activated platelets (P-selectin).
  
  
  RESULTS
  The accumulation of T lymphocytes tended to increase and that of macrophages increased significantly in the DES lesions compared with BMS lesions. No significant differences were observed for the other parameters evaluated.
  
  
  CONCLUSIONS
  Pathological features of restenotic tissues after DES implantation showed a stronger inflammatory response compared with those after BMS implantation. Thus, the mechanism of restenosis after DES implantation may be different from that observed after BMS implantation.
authors.affiliation: Department of Cardiovascular, Dokkyo Medical University School of Medicine, Mibu, Tochigi, Japan.
authors.forename: Shuichi
authors.initials: S
authors.lastname: Yoneda
authors.forename: Shichiro
authors.initials: S
authors.lastname: Abe
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Kanaya
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Oda
authors.forename: Setsu
authors.initials: S
authors.lastname: Nishino
authors.forename: Michiya
authors.initials: M
authors.lastname: Kageyama
authors.forename: Isao
authors.initials: I
authors.lastname: Taguchi
authors.forename: Nobuhide
authors.initials: N
authors.lastname: Masawa
authors.forename: Teruo
authors.initials: T
authors.lastname: Inoue
mesh_terms: D000199:Actins / Q000032:analysis; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D017225:Atherectomy, Coronary; D016009:Chi-Square Distribution; D003324:Coronary Artery Disease / Q000276:immunology* / Q000473:pathology / Q000628:therapy*; D023903:Coronary Restenosis / Q000276:immunology* / Q000473:pathology; D003331:Coronary Vessels / Q000276:immunology* / Q000473:pathology; D054855:Drug-Eluting Stents; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000032:analysis*; D017493:Leukocyte Common Antigens / Q000032:analysis; D008264:Macrophages / Q000276:immunology*; D008297:Male; D008670:Metals; D008875:Middle Aged; D019007:P-Selectin / Q000032:analysis; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects* / Q000295:instrumentation*; D011474:Prosthesis Design; D012307:Risk Factors; D013601:T-Lymphocytes / Q000276:immunology*; D016896:Treatment Outcome; D014841:von Willebrand Factor / Q000032:analysis; D000097382:CD68 Molecule
chemical_list: D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D018836:Inflammation Mediators; D017493:Leukocyte Common Antigens; D008670:Metals; D019007:P-Selectin; D014841:von Willebrand Factor; C541116:ACTA2 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C546937:SELP protein, human; C516769:PTPRC protein, human