title: Long-term effects of novel biolimus eluting DEVAX AXXESS plus nitinol self-expanding stent in a porcine coronary model.
abstract: OBJECTIVE
  The purpose of this study was to evaluate the long-term effects of the DEVAX AXXESS biolimus eluting stent (BES) in a porcine coronary model, compared with those of bare metal stent (BMS) and polymer only stent (POS) controls.
  
  
  BACKGROUND
  Excessive neointimal growth has been identified as a major cause of late failure of percutaneous coronary interventions. The effect of drug eluting from self-expanding stents for prevention of neointimal hyperplasia has not been studied before. The DEVAX AXXESS is a self-expanding nickel titanium stent, coated with antiproliferative compound-biolimus.
  
  
  METHODS
  Twenty juvenile farm swine, 25-35 kg in weight, 3-6 months in age were used. Each animal received a stent to the left anterior descending artery, left circumflex or right coronary arteries as permitted per anatomy. The chronic vascular response after BES implantation was compared with that after BMS and POS implantation at 28, 90, and 180 days follow-up.
  
  
  RESULTS
  The 28-day outcome by quantitative coronary angiography (QCA) showed significant increase in minimal luminal diameter (MLD) in the BES (MLD: 2.90 +/- 0.97, 2.39 +/- 0.90, 1.59 +/- 0.91; P = 0.009) compared with BMS and POS, respectively. By histomorphometric analysis, there was also a corresponding significant reduction in neointimal tissue proliferation in the BES (average neointimal area: 2.78 +/- 0.07, 5.46 +/- 0.66, 8.42 +/- 0.85; P = 0.002) compared with that in BMS and POS controls, respectively at 28-days follow-up. At 90 and 180 days, the mean neointimal area was not significantly different between the BES and the controls.
  
  
  CONCLUSIONS
  BES favorably modulates the neointimal tissue formation for 28 days, in the porcine coronary model. Long-term inhibition of neointimal hyperplasia is not sustained most likely because of the delayed cellular proliferation and inflammation in the vessel wall.
authors.affiliation: Division of Cardiology, Department of Medicine, University of Texas Health Science Center in San Antonio, Texas 78229-3900, USA.
authors.forename: Mehmet
authors.initials: M
authors.lastname: Cilingiroglu
authors.forename: Jim
authors.initials: J
authors.lastname: Elliott
authors.forename: Devang
authors.initials: D
authors.lastname: Patel
authors.forename: Furman
authors.initials: F
authors.lastname: Tio
authors.forename: Holly
authors.initials: H
authors.lastname: Matthews
authors.forename: Melissa
authors.initials: M
authors.lastname: McCasland
authors.forename: Brett
authors.initials: B
authors.lastname: Trauthen
authors.forename: John
authors.initials: J
authors.lastname: Elicker
authors.forename: Steven R
authors.initials: SR
authors.lastname: Bailey
mesh_terms: D000497:Alloys; D000818:Animals; D020099:Coated Materials, Biocompatible / Q000008:administration & dosage*; D017023:Coronary Angiography; D006965:Hyperplasia; D007166:Immunosuppressive Agents / Q000008:administration & dosage; D023421:Models, Animal; D011091:Polyesters; D011474:Prosthesis Design; D020123:Sirolimus / Q000008:administration & dosage; D015607:Stents; D013552:Swine; D013997:Time Factors; D017539:Tunica Intima / Q000473:pathology
chemical_list: D000497:Alloys; D020099:Coated Materials, Biocompatible; D007166:Immunosuppressive Agents; D011091:Polyesters; C505727:poly(epsilon-caprolactone-co-lactide); C013616:nitinol; D020123:Sirolimus