title: Local arterial responses to 32P beta-emitting stents.
abstract: OBJECTIVE
  32P beta-emitting stents reduce neointimal growth in rabbit iliac arteries for at least 12 months after deployment but are associated with incomplete healing. The aim of this study was to quantitate arterial cellularity, with emphasis on the inflammatory response following radioactive stenting.
  
  
  METHODS
  32P beta-emitting stents were placed in rabbit iliac arteries and analyzed at 3 months (6 and 24 microCi), and 6 and 12 months (6, 24, and 48 microCi). Arterial cellular proliferation and cell densities of smooth muscle cells (SMC), mononuclear cells (macrophages and lymphocytes), and neutrophils (PMN) were determined.
  
  
  RESULTS
  Total intimal cell density was greatest in control stents at all three time points, composed mostly of SMCs. SMC density associated with radioactive stents increased from 3 to 12 months but was significantly less than control nonradioactive stents. There was a 4-fold increase in cellular proliferation in the 24 and 48 microCi group vs. control stents. In the media, SMC density of radioactive stent groups was significantly reduced vs. control stents at all three time points, for all three activities. At 3, 6 and 12 months, there was a dose-dependent increase in intimal inflammatory cell density, which consisted mostly of macrophages. For 6-microCi stents inflammation peaked at 3 months and decreased thereafter. Inflammation for 24-microCi stents peaked at 6 months and then decreased at 12 months. Inflammation associated with 48-microCi stents remained high at 6 and 12 months. Focal atherosclerotic change was seen in 11% of stents in the 24-microCi group, and 37% and 50% in the 48-microCi group at 6 and 12 months, respectively.
  
  
  CONCLUSIONS
  Intimal SMC density remains suppressed out to 12 months after placement of 32P beta-emitting stents. However, inflammation and cell proliferation remain increased and may potentially result in greater neointimal formation over time.
authors.affiliation: Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
authors.forename: M
authors.initials: M
authors.lastname: John
authors.forename: S
authors.initials: S
authors.lastname: Shroff
authors.forename: A
authors.initials: A
authors.lastname: Farb
authors.forename: R
authors.initials: R
authors.lastname: Virmani
mesh_terms: D000818:Animals; D002452:Cell Count; D002455:Cell Division / Q000502:physiology* / Q000528:radiation effects*; D007083:Iliac Artery / Q000166:cytology* / Q000502:physiology / Q000528:radiation effects*; D008214:Lymphocytes / Q000502:physiology / Q000528:radiation effects; D008264:Macrophages / Q000502:physiology / Q000528:radiation effects; D008297:Male; D009504:Neutrophils / Q000502:physiology / Q000528:radiation effects; D010761:Phosphorus Radioisotopes; D011817:Rabbits; D015607:Stents; D013997:Time Factors; D017539:Tunica Intima / Q000503:physiopathology / Q000528:radiation effects*
chemical_list: D010761:Phosphorus Radioisotopes