title: Long-term vascular responses to Resolute® and Xience V® polymer-based drug-eluting stents in a rabbit model of atherosclerosis.
abstract: OBJECTIVE
  To assess the late postinterventional response to iliac stenting in atheromatous rabbits using the Xience V everolimus-eluting stent (Xience V EES; Abbott Vascular) and the Resolute zotarolimus-eluting stent (Resolute ZES; Medtronic Vascular) with the MultiLink Vision bare metal stent (BMS; Abbott Vascular) as a reference.
  
  
  BACKGROUND
  Xience V EES and Resolute ZES were developed to overcome shortcomings of first-generation DES.
  
  
  METHODS
  Functional and microscopic changes were assessed by organ bath experiments and histopathologic examination. Gene expression was investigated using RT-PCR.
  
  
  RESULTS
  After 91 days, re-endothelialization was nearly complete (BMS: 93 ± 3%; Resolute ZES: 92 ± 2%; Xience V EES: 94 ± 3%; P = 0.10). Neointima thickness was similar in Resolute ZES (0.17 ± 0.08 mm) and BMS (0.17 ± 0.09 mm), and reduced in Xience V EES (0.03 ± 0.01 mm; P < 0.0001). Xience V EES had less peri-strut inflammation compared with BMS (P = 0.001) and Resolute ZES (P = 0.0001), while arterial segments distal to Xience V EES were more sensitive to acetylcholine than those distal to BMS and Resolute ZES (P = 0.02). Lectin-like oxidized receptor-1 was overexpressed in stented arteries (P < 0.001), whereas thrombomodulin was downregulated in Resolute ZES (P = 0.01) and BMS (P = 0.02) compared to unstented arteries of rabbits on regular chow. No significant changes were seen for vascular cell adhesion molecule-1, nitric oxide synthase 3, or endothelin-1.
  
  
  CONCLUSIONS
  At 3-month follow-up, nearly complete re-endothelialization was achieved for all stent groups. Xience V EES induced greater suppression of neointimal growth and peri-strut inflammation, higher vasorelaxation to acetylcholine, and expression of thrombomodulin at the level of unstented controls.
authors.affiliation: Laboratory for Cellular and Molecular Cardiology, Department of Cardiology, Antwerp University Hospital, Antwerp, Belgium; Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Antwerp, Belgium.
authors.forename: Vicky Y
authors.initials: VY
authors.lastname: Hoymans
authors.forename: Christophe J
authors.initials: CJ
authors.lastname: VAN Dyck
authors.forename: Steven E
authors.initials: SE
authors.lastname: Haine
authors.forename: Geert
authors.initials: G
authors.lastname: Frederix
authors.forename: Erik
authors.initials: E
authors.lastname: Fransen
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Timmermans
authors.forename: Christiaan J
authors.initials: CJ
authors.lastname: Vrints
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000800:Angioplasty, Balloon; D000818:Animals; D050197:Atherosclerosis / Q000473:pathology / Q000628:therapy*; D004195:Disease Models, Animal; D015536:Down-Regulation; D054855:Drug-Eluting Stents; D004730:Endothelium, Vascular / Q000473:pathology; D000068338:Everolimus / Q000008:administration & dosage*; D007083:Iliac Artery / Q000473:pathology*; D007249:Inflammation / Q000473:pathology; D058426:Neointima / Q000473:pathology; D011817:Rabbits; D051127:Scavenger Receptors, Class E / Q000378:metabolism; D020123:Sirolimus / Q000008:administration & dosage / Q000031:analogs & derivatives*; D018180:Thrombomodulin / Q000378:metabolism; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D051127:Scavenger Receptors, Class E; D018180:Thrombomodulin; D014665:Vasodilator Agents; D000068338:Everolimus; C489443:zotarolimus; D000109:Acetylcholine; D020123:Sirolimus