title: Relationship between neointimal regrowth and mechanism of acute lumen gain during the treatment of in-stent restenosis with or without supplementary intravascular radiation.
abstract: We investigated whether neointimal regrowth is related to the mechanism of acute lumen gain during the treatment of in-stent restenosis (ISR) lesions both with and without adjunct intravascular brachytherapy. From the WRIST (Washington Radiation for In-Stent Restenosis Trial) cohort, 54 ISR patients ((192)Ir, 29; placebo, 25) were treated with nonrepeat stenting percutaneous interventions (excimer laser, rotational atherectomy, and/or balloon angioplasty) prior to (192)Ir or placebo therapy. Using Simpson's method, serial volumetric intravascular ultrasound (IVUS) analyses (pre- and posttreatment and 6-month follow-up) were analyzed to obtain stent, lumen, and intimal hyperplasia (IH) volumes that were then adjusted for stent length to create stent, lumen, and IH volume indexes. In the placebo group, the acute reduction of neointima (1.6 +/- 1.4 mm(3)/mm) was counteracted by intimal regrowth (2.1 +/- 1.7 mm(3)/mm). The amount of intimal regrowth correlated directly with the intimal reduction due to the intervention (r = 0.76; P < 0.001), but not with the amount of additional stent expansion. In the (192)Ir-treated group, intimal regrowth was significantly less than in the placebo group (-0.3 +/- 0.1 vs. 2.1 +/- 1.7 mm(3)/mm; P < 0.001) despite a similar initial intimal reduction (1.3 +/- 0.9 vs. 1.6 +/- 1.4 mm(3)/mm; P = NS). No correlation was found between intimal reduction at the time of the procedure and intimal regrowth in the (192)Ir group. In this study, neointimal regrowth following treatment of ISR lesions correlates directly with the extent of acute intimal volume reduction, but not with the extent of additional stent expansion. This relation is not seen in ISR segments treated with radiation, where intimal regrowth is substantially inhibited.
authors.affiliation: Center for Research in Cardiovascular Interventions, Stanford University Medical Center, Stanford, California 94305, USA.
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Morino
authors.forename: Thosaphol
authors.initials: T
authors.lastname: Limpijankit
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Honda
authors.forename: Manoon
authors.initials: M
authors.lastname: Somrantin
authors.forename: Ron
authors.initials: R
authors.lastname: Waksman
authors.forename: Heidi N
authors.initials: HN
authors.lastname: Bonneau
authors.forename: Paul G
authors.initials: PG
authors.lastname: Yock
authors.forename: Gary S
authors.initials: GS
authors.lastname: Mintz
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Fitzgerald
mesh_terms: D000368:Aged; D001918:Brachytherapy; D015331:Cohort Studies; D023903:Coronary Restenosis / Q000473:pathology* / Q000532:radiotherapy*; D003331:Coronary Vessels / Q000000981:diagnostic imaging; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015607:Stents; D017539:Tunica Intima / Q000473:pathology*; D018084:Ultrasonography, Interventional; D014654:Vascular Patency