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Thromb Haemost 2015; 113(03): 605-616
DOI: 10.1160/TH14-02-0151
Blood Cells, Inflammation and Infection
Schattauer GmbH

Coronary artery endothelial cells and microparticles increase expression of VCAM-1 in myocardial infarction

Christopher E. Radecke
1   Department of Biomedical Engineering, University of California, Davis, Davis, California, USA
,
Alexandra E. Warrick
2   Division of Cardiovascular Medicine, University of California, Davis, Medical Center. Sacramento, California, USA
,
Gagan D. Singh
2   Division of Cardiovascular Medicine, University of California, Davis, Medical Center. Sacramento, California, USA
,
Jason H. Rogers
2   Division of Cardiovascular Medicine, University of California, Davis, Medical Center. Sacramento, California, USA
,
Scott I. Simon
1   Department of Biomedical Engineering, University of California, Davis, Davis, California, USA
,
Ehrin J. Armstrong
3   Division of Cardiology, University of Colorado, Denver, Colorado, USA
4   VA Eastern Colorado Healthcare System, Denver, Colorado, USA
› Institutsangaben Financial support: This study was made possible with assistance from AHA 11CRP7260031 Clinical Research Program, NIH RO1 HL082689, and the University of California San Francisco-Gladstone Institute of Virology & Immunology Center for AIDS Research (CFAR), an NIH-funded program (P30AI027763).
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Publikationsverlauf

Received: 18. Februar 2014

Accepted after major revision: 10. Oktober 2014

Publikationsdatum:
17. November 2017 (online)

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Summary

Coronary artery disease (CAD) is characterised by progressive atherosclerotic plaque leading to flow-limiting stenosis, while myocardial infarction (MI) occurs due to plaque rupture or erosion with abrupt coronary artery occlusion. Multiple inflammatory pathways influence plaque stability, but direct assessment of endothelial inflammation at the site of coronary artery stenosis has largely been limited to pathology samples or animal models of atherosclerosis. We describe a technique for isolating and characterising endothelial cells (ECs) and EC microparticles (EMPs) derived directly from the site of coronary artery plaque during balloon angioplasty and percutaneous coronary intervention. Coronary artery endothelial cells (CAECs) were identified using imaging flow cytometry (IFC), and individual CAEC and EMP expression of the pro-atherogenic adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) was assessed immediately following angioplasty. Patients with MI registered 73 % higher VCAM-1 expression on their CAECs and 79 % higher expression on EMPs compared to patients with stable CAD. In contrast, VCAM-1 expression was absent on ECs in the peripheral circulation from these same subjects. VCAM-1 density was significantly higher on CAECs and EMPs among patients with MI and positively correlated with markers of myocardial infarct size. We conclude that increased VCAM-1 expression on EC and formation of EMP at the site of coronary plaque is positively correlated with the extent of vascular inflammation in patients with myocardial infarction.

Keywords

Acute myocardial infarction - adhesion molecules - VCAM-1 - endothelial cells - inflammation - microparticles

 

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