title: Pressure rinsing of coronary stents immediately before implantation reduces inflammation and neointimal hyperplasia.
abstract: OBJECTIVE
  This study evaluates whether rinsing stents with high pressure immediately before implantation minimizes stent-induced inflammation and neointimal formation.
  
  
  BACKGROUND
  Several reports indicate that manual stent manipulation before implantation results in foreign body contamination and increased neointimal hyperplasia.
  
  
  METHODS
  A stent-cleaning chamber was developed to rinse stents at a sustained hydrodynamic pressure of 4 atm for 10 s. Commercial pre-mounted stents were examined with different levels of manipulation: 1) untouched stents: no stent manipulation before implantation; 2) handled stents: manual stent re-crimping on the balloon; 3) rinsed stents: pressure-rinsed with the stent-cleaning chamber. In vitro surface analysis was evaluated by scanning electron microscopy. Neointimal hyperplasia and inflammation around stent struts were also assessed in the pig in-stent restenosis model.
  
  
  RESULTS
  In vitro analysis revealed fewer contaminants on rinsed stents compared with untouched (p = 0.01) and handled stents (p < 0.001). In vivo, neointimal thickness, neointimal area and vessel percent stenosis were significantly reduced in rinsed, compared with not-rinsed, stents (p = 0.002, p = 0.007, p = 0.008 respectively). In addition, a significant reduction in the inflammatory infiltrate around struts was observed in untouched, compared with handled, stents (p = 0.04) and in rinsed, compared with not-rinsed, stents (p < 0.001). Regression analysis accounting for injury and neointimal thickness showed significant differences in slopes between "handled + not-rinsed" and "handled + rinsed" stents (p = 0.004), and between "untouched + not-rinsed" and "untouched + rinsed stents" (p = 0.037).
  
  
  CONCLUSIONS
  Rinsing stents under high pressure immediately before coronary implantation results in less inflammation around struts and thinner neointima at 28 days in this pig model.
authors.affiliation: Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
authors.forename: A
authors.initials: A
authors.lastname: Bayes-Genis
authors.forename: A R
authors.initials: AR
authors.lastname: Camrud
authors.forename: M
authors.initials: M
authors.lastname: Jorgenson
authors.forename: J
authors.initials: J
authors.lastname: Donovan
authors.forename: K L
authors.initials: KL
authors.lastname: Shogren
authors.forename: D R
authors.initials: DR
authors.lastname: Holmes
authors.forename: R S
authors.initials: RS
authors.lastname: Schwartz
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D005549:Foreign-Body Reaction / Q000473:pathology / Q000517:prevention & control; D006083:Graft Occlusion, Vascular / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D007249:Inflammation / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D008854:Microscopy, Electron; D011312:Pressure; D055672:Static Electricity; D015607:Stents / Q000009:adverse effects*; D013552:Swine