title: Extent and distribution of in-stent intimal hyperplasia and edge effect in a non-radiation stent population.
abstract: Intimal hyperplasia within the body of the stent is the primary mechanism for in-stent restenosis; however, stent edge restenosis has been described after brachytherapy. Our current understanding about the magnitude of in vivo intimal hyperplasia and edge restenosis is limited to data obtained primarily from select, symptomatic patients requiring repeat angiography. The purpose of this study was to determine the extent and distribution of intimal hyperplasia both within the stent and along the stent edge in relatively nonselect, asymptomatic patients scheduled for 6-month intravascular ultrasound (IVUS) as part of a multicenter trial: Heparin Infusion Prior to Stenting. Planar IVUS measurements 1 mm apart were obtained throughout the stent and over a length of 10 mm proximal and distal to the stent at index and follow-up. Of the 179 patients enrolled, 140 returned for repeat angiography and IVUS at 6.4 +/- 1.9 months and had IVUS images adequate for analysis. Patients had 1.2 +/- 0.6 Palmaz-Schatz stents per vessel. There was a wide individual variation of intimal hyperplasia distribution within the stent and no mean predilection for any location. At 6 months, intimal hyperplasia occupied 29.3 +/- 16.2% of the stent volume on average. Lumen loss within 2 mm of the stent edge was due primarily to intimal proliferation. Beyond 2 mm, negative remodeling contributed more to lumen loss. Gender, age, vessel location, index plaque burden, hypercholesterolemia, diabetes, and tobacco did not predict luminal narrowing at the stent edges, but diabetes, unstable angina at presentation, and lesion length were predictive of in-stent intimal hyperplasia. In a non-radiation stent population, 29% of the stent volume is filled with intimal hyperplasia at 6 months. Lumen loss at the stent edge is due primarily to intimal proliferation.
authors.affiliation: Cardiovascular Research Institute, Washington Hospital Center, Washington, DC 20010, USA. njw1@mhg.edu
authors.forename: N J
authors.initials: NJ
authors.lastname: Weissman
authors.forename: R L
authors.initials: RL
authors.lastname: Wilensky
authors.forename: J F
authors.initials: JF
authors.lastname: Tanguay
authors.forename: A L
authors.initials: AL
authors.lastname: Bartorelli
authors.forename: J
authors.initials: J
authors.lastname: Moses
authors.forename: D O
authors.initials: DO
authors.lastname: Williams
authors.forename: S
authors.initials: S
authors.lastname: Bailey
authors.forename: J L
authors.initials: JL
authors.lastname: Martin
authors.forename: M R
authors.initials: MR
authors.lastname: Canos
authors.forename: H
authors.initials: H
authors.lastname: Rudra
authors.forename: J J
authors.initials: JJ
authors.lastname: Popma
authors.forename: M B
authors.initials: MB
authors.lastname: Leon
authors.forename: A V
authors.initials: AV
authors.lastname: Kaplan
authors.forename: G S
authors.initials: GS
authors.lastname: Mintz
mesh_terms: D003327:Coronary Disease / Q000473:pathology* / Q000628:therapy; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006965:Hyperplasia / Q000209:etiology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D011446:Prospective Studies; D012008:Recurrence; D015607:Stents / Q000009:adverse effects; D017539:Tunica Intima / Q000473:pathology*