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Estrogen‐eluting, phosphorylcholine‐coated stent implantation is associated with reduced neointimal formation but no delay in vascular repair in a porcine coronary model
Author(s) -
New Gishel,
Moses Jeffrey W.,
Roubin Gary S.,
Leon Martin B.,
Colombo Antonio,
Iyer Sriram S.,
Tio Fermin O.,
Mehran Roxana,
Kipshidze Nicholas
Publication year - 2002
Publication title -
catheterization and cardiovascular interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 116
eISSN - 1522-726X
pISSN - 1522-1946
DOI - 10.1002/ccd.10339
Subject(s) - restenosis , medicine , stent , estrogen , neointimal hyperplasia , angioplasty , cardiology , neointima , urology , surgery
Estrogen can inhibit intimal proliferation and accelerate endothelial regeneration after angioplasty. This suggests that estrogen may prevent in‐stent restenosis. Unlike other therapies to prevent restenosis, estrogen may also not delay endothelial regrowth, thereby avoiding the risk of late stent thrombosis. The purpose of this work was to determine the effect of a 17β‐estradiol–eluting stent on neointimal formation in a porcine model. Each artery of six pigs was randomized to either a control, low‐dose, or high‐dose 17β‐estradiol–eluting stent. All animals were sacrificed at 30 days for histopathological analysis. There was a 40% reduction in intimal area in the high‐dose stents compared with control stents (2.54 ± 1.0 vs. 4.13 ± 1.1 mm 2 , for high dose vs. control, respectively; P < 0.05). There was complete endothelial regeneration at 30 days and similar inflammatory response to stenting on histopathology in all the stent groups. This is the first study to show that 17β‐estradiol–eluting stents are associated with reduced neointimal formation without affecting endothelial regeneration in the pig model of in‐stent restenosis. Estrogen‐coated stents may have a potential benefit in the prevention and treatment of in‐stent restenosis. Cathet Cardiovasc Intervent 2002;57:266–271. © 2002 Wiley‐Liss, Inc.