title: Methotrexate loaded SAE coated coronary stents reduce neointimal hyperplasia in a porcine coronary model.
abstract: OBJECTIVE
  To evaluate the effect of stent based methotrexate delivery on neointimal hyperplasia.
  
  
  METHODS
  Stainless steel coronary stents and biological polymer coated (SAE) stents were randomly implanted in coronary arteries of pigs with a stent to artery ratio of 1.1:1. The pigs were killed after five days (10 stents) or four weeks (20 stents). Second, stainless steel coronary stents were dip coated in a 10 mg/ml methotrexate-SAE polymer solution, resulting in a total load of 150 microg methotrexate/stent. SAE coated stents and methotrexate loaded stents were randomly implanted in porcine coronary arteries with a stent to artery ratio of 1.2:1 and followed up to four weeks.
  
  
  RESULTS
  SAE coated stents and bare stents elicited a similar tissue response at five days. At four weeks, neointimal hyperplasia induced by the coated stents was less pronounced than with the bare stents (1.32 (0.66) v 1.73 (0.93) mm2, p > 0.05). In vitro drug release studies showed that 50% of the methotrexate was released in 24 hours, and all drug was released within four weeks. No impact on vascular smooth muscle cell proliferation or viability was observed in in vitro cell cultures. At four weeks the arteries with methotrexate loaded stents had decreased peristrut inflammation and neointimal hyperplasia (1.22 (0.34) v 2.25 (1.28) mm2, p < 0.01).
  
  
  CONCLUSIONS
  SAE coating had an excellent biocompatibility with vascular tissue. Stent based delivery of methotrexate in the SAE coating effectively reduced neointimal hyperplasia in a porcine coronary stent model, potentially due to reduced peristrut inflammation.
authors.affiliation: Department of Cardiology, Department of Pathology, University Hospitals, Leuven, Belgium.
authors.forename: Y
authors.initials: Y
authors.lastname: Huang
authors.forename: K
authors.initials: K
authors.lastname: Salu
authors.forename: X
authors.initials: X
authors.lastname: Liu
authors.forename: S
authors.initials: S
authors.lastname: Li
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: E
authors.initials: E
authors.lastname: Verbeken
authors.forename: J
authors.initials: J
authors.lastname: Bosmans
authors.forename: I
authors.initials: I
authors.lastname: De Scheerder
mesh_terms: D000818:Animals; D001672:Biocompatible Materials; D002455:Cell Division; D002470:Cell Survival; D003331:Coronary Vessels / Q000473:pathology*; D004343:Drug Implants; D005260:Female; D006965:Hyperplasia / Q000517:prevention & control; D007166:Immunosuppressive Agents / Q000008:administration & dosage*; D008297:Male; D008727:Methotrexate / Q000008:administration & dosage*; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011897:Random Allocation; D015607:Stents; D034421:Sus scrofa; D017539:Tunica Intima / Q000473:pathology*
chemical_list: D001672:Biocompatible Materials; D004343:Drug Implants; D007166:Immunosuppressive Agents; D008727:Methotrexate