title: Coronary intimal proliferation after balloon injury and stenting in swine: an animal model of restenosis.
abstract: OBJECTIVE
  This study was designed to compare the proliferative response in coronary arteries after tantalum stent placement or balloon injury in a normolipemic swine model of restenosis.
  
  
  BACKGROUND
  Restenosis remains a significant complication of percutaneous transluminal coronary angioplasty. Efforts to study restenosis have been hampered by the lack of a suitable animal model.
  
  
  METHODS
  In an attempt to create lesions resembling those of human restenosis, normolipemic swine underwent injury of either the left anterior descending or the left circumflex coronary artery with either balloon inflation or deployment of a tantalum stent. At 4 weeks, they were killed and the injured vessels processed for histopathologic analysis. Intimal area, lumen area and maximal intimal thickness were measured. The degree of stenosis was expressed as residual lumen area (lumen area/intimal area ratio).
  
  
  RESULTS
  Vessels injured by either method demonstrated significant intimal smooth muscle proliferation leading to reduction in lumen area. In the 18 stented vessels residual lumen area measured 0.64 +/- 0.18 and maximal intimal thickness measured 0.6 +/- 0.3 mm; in the 15 balloon-injured vessels these values were 0.75 +/- 0.18 and 0.4 +/- 0.3 mm, respectively (p less than 0.05). In addition, most stented vessels had reactive inflammatory infiltrates surrounding the stent wires composed of lymphocytes, histiocytes and many eosinophils.
  
  
  CONCLUSIONS
  These data indicate that coronary artery injury in swine with either balloon inflation or stenting leads to intimal smooth muscle cell proliferation similar to that seen in human restenosis. The degree of intimal proliferation appears to be greater after stenting than after balloon injury. Intracoronary stenting in swine is associated with a marked inflammatory reaction around the stent wires. These models may be helpful in planning systemic and local antirestenosis strategies.
authors.affiliation: Andreas Gruentzig Cardiovascular Center, Department of Medicine (Cardiology), Emory University School of Medicine, Atlanta, Georgia 30322.
authors.forename: S P
authors.initials: SP
authors.lastname: Karas
authors.forename: M B
authors.initials: MB
authors.lastname: Gravanis
authors.forename: E C
authors.initials: EC
authors.lastname: Santoian
authors.forename: K A
authors.initials: KA
authors.lastname: Robinson
authors.forename: K A
authors.initials: KA
authors.lastname: Anderberg
authors.forename: S B
authors.initials: SB
authors.lastname: King
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D003327:Coronary Disease / Q000473:pathology / Q000628:therapy; D003331:Coronary Vessels / Q000293:injuries* / Q000473:pathology; D006965:Hyperplasia; D009131:Muscle, Smooth, Vascular / Q000293:injuries* / Q000473:pathology; D012008:Recurrence; D015607:Stents; D013552:Swine