title: Eosinophilic infiltration in restenotic tissue following coronary stent implantation.
abstract: OBJECTIVE
  The aim of our study was to compare the histopathological features of restenotic tissue after balloon angioplasty and after stent placement. We emphasized on specific types of inflammatory cells to evaluate the type of tissue immune response in both situations.
  
  
  METHODS
  A total of 32 patients underwent elective directional coronary atherectomy; 16 patients had restenosis after balloon angioplasty, 16 patients had in-stent restenosis (ISR). Atherectomy specimens were stained with antibodies against T cells, eosinophils, smooth muscle cell actin, macrophages and with antibodies against T cell activation markers. Quantitative morphometric analysis was performed using image analysis software.
  
  
  RESULTS
  In-stent restenotic tissue contained more smooth muscle cells (P < 0.001), anti-CD3 positive T cells (P < 0.001) and eosinophils (P = 0.012). Anti-CD40L positive activated T cells were more numerous in ISR lesions (P = 0.003) and were frequently clustered around stent imprints in the tissue. Five ISR specimens contained grossly visible stent fragments amidst the restenotic tissue. In all cases of balloon restenosis, T cells and eosinophils (if present) were concentrated around lipid rich tissue.
  
  
  CONCLUSIONS
  Our study indicates involvement of inflammatory responses in both types of restenosis, with significantly more eosinophils encountered in case of in-stent restenosis. In contrast with clustering of inflammatory cells around stent struts after stent placement, the inflammatory cells in balloon restenosis were located in association with lipid rich tissue, suggesting different inflammatory triggers in balloon restenosis and in-stent restenosis.
authors.affiliation: Department of Cardiology, B2-115, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. z.h.rittersma@amc.uva.nl
authors.forename: Saskia Z H
authors.initials: SZ
authors.lastname: Rittersma
authors.forename: Martijn
authors.initials: M
authors.lastname: Meuwissen
authors.forename: Chris M
authors.initials: CM
authors.lastname: van der Loos
authors.forename: Karel T
authors.initials: KT
authors.lastname: Koch
authors.forename: Robbert J
authors.initials: RJ
authors.lastname: de Winter
authors.forename: Jan J
authors.initials: JJ
authors.lastname: Piek
authors.forename: Allard C
authors.initials: AC
authors.lastname: van der Wal
mesh_terms: D000368:Aged; D017225:Atherectomy, Coronary; D019917:Blood Vessel Prosthesis Implantation / Q000009:adverse effects*; D017252:CD3 Complex / Q000276:immunology; D023201:CD40 Ligand / Q000276:immunology; D023903:Coronary Restenosis / Q000150:complications / Q000473:pathology* / Q000601:surgery; D004802:Eosinophilia / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011475:Prosthesis Failure; D012720:Severity of Illness Index; D015607:Stents / Q000009:adverse effects*; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D017252:CD3 Complex; D023201:CD40 Ligand