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Levels of circulating cells do not predict coronary in-stent restenosis
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Author
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Abstract
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Background: Angiographic and clinical parameters are poor predictors of in-stent restenosis. Bone marrowederived CD34(+) cells that coexpress a receptor for vascular endothelial growth factor (kinase insert domain receptor [KDR]) are committed to endothelial lineage. Mobilization and infusion of CD34(+)/ KDR+ cells accelerates reendothelialization and reduces neointimal thickness in vascular injury models. Bioengineered stents capturing CD34(+) cells also show expedited re-endothelialization. We examined whether circulating CD34(+)/ KDR+ cell counts can be used to predict restenosis in a baremetal stent (BMS). Methods: CD34(+)/KDR+ cells were counted by flow cytometry in 124 nondiabetic patients before BMS implantation and the relation to instent late luminal loss (LLL) was examined by angiography at 6 months (primary end point). Neointima was also quantified as the maximum percentage area stenosis (M%AS) and percentage volume intima hyperplasia (%VIH) on intravascular ultrasonography (secondary end points). Results: Multiple linear regression analysis, taking into account implanted stent length and diameter, revealed no relation between CD34(+)/ KDR+ cell counts and LLL (partial regression coefficient b = 0.11; 95% confidence interval [CI], -0.19-0.42; P = 0.46). Similarly, no relation between CD34(+)/KDR+ cell counts and M%AS or %VIH could be demonstrated. Moreover, the increase in CD34(+)/KDR+ cell counts over 6 months was unrelated to LLL (b = -0.15; 95% CI, 0.42-0.12; P = 0.28), M%AS, and %VIH. Conclusions: Although our study does not exclude a pathophysiologic role for CD34(+)/KDR+ cells in the formation of neointima, cell counts before percutaneous coronary intervention proved to be unrelated to LLL or intravascular ultrasonographically derived restenosis parameters in coronary BMSs at 6 months. |
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Language
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English
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Source (journal)
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Canadian journal of cardiology. - Oakville, Ont.
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Publication
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Oakville, Ont.
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2014
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ISSN
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0828-282X
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DOI
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10.1016/J.CJCA.2013.10.012
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Volume/pages
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30
:1
(2014)
, p. 102-108
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ISI
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000329072300016
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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