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Paclitaxel stent coating inhibits neointimal hyperplasia at 4 weeks in a porcine model of coronary restenosis

Despite limiting elastic recoil and late vascular remodeling after angioplasty, coronary stents remain vulnerable to restenosis, caused primarily by neointimal hyperplasia. Paclitaxel, a microtubule-stabilizing drug, has been shown to inhibit vascular smooth muscle cell migration and proliferation c...

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Published in:Circulation (New York, N.Y.) N.Y.), 2001-05, Vol.103 (18), p.2289-2295
Main Authors: HELDMAN, Alan W, CHENG, Linda, BUNGE, Katherine E, KINSELLA, James L, SOLLOTT, Steven J, LAKATTA, Edward G, BRINKER, Jeffrey A, HUNTER, William L, FROEHLICH, Jeffrey P, JENKINS, G. Mark, HELLER, Phillip F, KIM, Dong-Woon, WARE, Melvin JR, NATER, Cynthia, HRUBAN, Ralph H, REZAI, Banafsheh, ABELLA, Benjamin S
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Language:English
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Summary:Despite limiting elastic recoil and late vascular remodeling after angioplasty, coronary stents remain vulnerable to restenosis, caused primarily by neointimal hyperplasia. Paclitaxel, a microtubule-stabilizing drug, has been shown to inhibit vascular smooth muscle cell migration and proliferation contributing to neointimal hyperplasia. We tested whether paclitaxel-coated coronary stents are effective at preventing neointimal proliferation in a porcine model of restenosis. Palmaz-Schatz stents were dip-coated with paclitaxel (0, 0.2, 15, or 187 microgram/stent) by immersion in ethanolic paclitaxel and evaporation of the solvent. Stents were deployed with mild oversizing in the left anterior descending coronary artery (LAD) of 41 minipigs. The treatment effect was assessed 4 weeks after stent implantation. The angiographic late loss index (mean luminal diameter) decreased with increasing paclitaxel dose (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.103.18.2289