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Title
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Stent-mediated methylprednisolone delivery reduces macrophage contents and in-stent neointimal formation
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Author
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Abstract
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| Objective Corticosteroids have a wide range of biological effects. Stent-based methylprednisolone delivery could effectively suppress peri-strut inflammation and neointima induced by a polymer matrix. We tested the safety and efficacy of local stent-mediated methylprednisolone delivery using a biological coating on in-stent neointimal formation in a porcine coronary stent model. Methods Stainless steel coronary stents were dip-coated in a biological polymer/ methylprednisolone solution, resulting in total load of 530 mu g methylprednisolone per stent. In-vitro drug release was performed. Stainless steel bare stents, polymer-only and methylprednisolone-coated stents (MID) were implanted in coronary arteries of pigs with a stent/artery ratio of 1.2:1. Histopathologic evaluation, morphometry and immunohistochemistic staining were analyzed at 4-week follow-up. Results In-vitro drug release studies showed sustained release up to 10 weeks. In vivo the vascular response of polymer-only-coated stents was comparable with the bare stents. No increased peri-strut inflammation and neointimal hyperplasia were observed. The in-stent neointimal formation of methylprednisolone-coated stents was significantly reduced compared with the bare and polymer-only-coated stents (bare, 1.92 +/- 0.73; polymer-only, 2.14 +/- 1.50; MP, 1.01 +/- 0.47 mm(2), P= 0.019). The macrophage content of methylprednisolone-coated stents (bare, 30.74 +/- 48.67; polymer-only, 19.55 +/- 24.60; MP, 1.16 +/- 3.33/mm(2), P=0.072) was dramatically decreased. However, there were no significant difference among the three group in terms of the proliferating cells expressed by proliferation cell nuclear antigens. Conclusion Stent-based local methylprednisolone delivery could effectively decrease both vascular macrophage infiltration and in-stent neointimal hyperplasia. (c) 2005 Lippincott Williams & Wilkins. |
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Language
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English
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Source (journal)
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Coronary artery disease. - Philadelphia, Pa
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Publication
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Philadelphia, Pa
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2005
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ISSN
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0954-6928
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DOI
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10.1097/00019501-200506000-00005
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Volume/pages
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16
:4
(2005)
, p. 237-243
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ISI
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000230133600005
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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