Journal of Vascular Research

Research Paper

Circulating Endothelial Progenitor Cells and Coronary Collaterals in Patients with Non-ST Segment Elevation Myocardial Infarction

Lev E.I.a · Kleiman N.S.a · Birnbaum Y.b · Harris D.c · Korbling M.c · Estrov Z.c

Author affiliations

aThe Methodist DeBakey Heart Center and Baylor College of Medicine, Houston, Tex., bDivision of Cardiology, The University of Texas Medical Branch at Galveston, Galveston, Tex., cDepartment of Leukemia, The University of Texas M.D. Anderson Cancer Center, Houston, Tex., USA

Keywords: Endothelial progenitor cellsMyocardial infarctionCollateral circulation

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J Vasc Res 2005;42:408–414
https://doi.org/10.1159/000087370

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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: April 07, 2005
Accepted: May 19, 2005
Published online: September 28, 2005
Issue release date: September – October

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 3

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: https://www.karger.com/JVR

Abstract

Background: Endothelial progenitor cells (EPCs) are bone marrow-derived cells that are augmented in response to ischemia and incorporated into neovascularization sites. We sought to determine whether circulating EPCs are related to collateral formation following non-ST segment elevation myocardial infarction (NSTEMI). Methods: Twenty patients who underwent percutaneous coronary intervention (PCI) within a week of NSTEMI were divided into two groups: patients without collaterals (coll–, n = 10) and patients with Rentrop grade 3–4 collaterals (coll+, n = 10). Blood samples were drawn before PCI and 24 ± 2 h after PCI. EPC colonies were grown from peripheral blood mononuclear cells, characterized, and counted. Using flow cytometry the percentage of cells coexpressing vascular endothelial growth factor receptor-2 and CD133 was determined. Results: The coll+ group had higher degree of culprit vessel stenosis and lower initial thrombolysis in myocardial infarction flow grade. The relative number of EPCs before PCI was significantly higher in the coll+ group than in the coll– group (1.49 ± 0.9% vs. 0.77 ± 0.4%, p = 0.045). There were no significant intergroup differences in the number of EPC colony-forming cells. The number of EPC colonies increased in the coll– group after PCI (9.5 ± 4.8 to 14.0 ± 5.9/106 cells, p = 0.01). Conclusions: This study supports an association between circulating EPC levels and collateral formation in patients with an NSTEMI.

© 2005 S. Karger AG, Basel



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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: April 07, 2005
Accepted: May 19, 2005
Published online: September 28, 2005
Issue release date: September – October

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 3

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: https://www.karger.com/JVR

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2005, Vol.42, No. 5

September – October

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