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Coronary leukocyte activation in relation to progression of coronary artery disease |
Marijke A. de Vries1,*( ),Arash Alipour1,Erwin Birnie2,Andrew Westzaan1,Selvetta van Santen1,Ellen van der Zwan3,Anho H. Liem4,Noëlle van der Meulen1,Manuel Castro Cabezas1 |
1. Department of Internal Medicine, Centre for Diabetes and Vascular Medicine 2. Department of Statistics and Education 3. Department of Clinical Chemistry 4. Department of Cardiology, Sint Franciscus Gasthuis, Rotterdam, P.O. Box 10900, 3004 BA, The Netherlands |
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Abstract Leukocyte activation has been linked to atherogenesis, but there is little in vivo evidence for its role in the progression of atherosclerosis. We evaluated the predictive value for progression of coronary artery disease (CAD) of leukocyte activation markers in the coronary circulation. Monocyte and neutrophil CD11b, neutrophil CD66b expression and intracellular neutrophil myeloperoxidase (MPO) in the coronary arteries were determined by flow cytometry in patients undergoing coronary angiography. The primary outcome included fatal and nonfatal myocardial infarction or arterial vascular intervention due to unstable angina pectoris. In total 99 subjects who were included, 70 had CAD at inclusion (26 patients had single-vessel disease, 18 patients had two-vessel disease and 26 patients had three-vessel disease). The median follow-up duration was 2242 days (interquartile range: 2142–2358). During follow-up, 13 patients (13%) developed progression of CAD. Monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO measured in blood obtained from the coronary arteries were not associated with the progression of CAD. These data indicate that coronary monocyte CD11b, neutrophil CD11b and CD66b expression and intracellular MPO do not predict the risk of progression of CAD.
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Keywords
coronary artery disease
inflammation
integrin
myeloperoxidase
leukocyte activation
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Corresponding Author(s):
Marijke A. de Vries
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Just Accepted Date: 14 January 2016
Online First Date: 18 February 2016
Issue Date: 31 March 2016
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