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Volume 205, Issue 1, Pages 272-278 (July 2009)


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Risk factor correlates of platelet and leukocyte markers assessed by flow cytometry in a population-based sample

Aaron R. FolsomaCorresponding Author Informationemail address, Nena Aleksicb, Antonio Sanhuezac, Eric Boerwinkled

Received 30 April 2008; received in revised form 6 November 2008; accepted 11 November 2008. published online 05 January 2009.

Abstract 

Background

Platelet and leukocyte products are involved in atherothrombosis. However, the determinants of platelet and leukocyte markers assessed by flow cytometry have not been documented in a population-based sample.

Methods and results

We performed flow cytometry on blood from participants (n=1894) in the Atherosclerosis Risk in Communities (ARIC) Carotid MRI Study. Cellular aggregates and multiple platelet and leukocyte markers, such as myeloperoxidase in granulocytes and toll-like receptor-4, CD14, and CD45 in monocytes, were quantified. Their cross-sectional associations with demographic and risk factors were assessed using multiple linear regression. Mean values of most cellular markers and aggregates were considerably higher in blacks than whites (p<0.01). There were some differences in cellular markers between men and women, but little association with age. LDL-cholesterol was associated positively with several markers (toll-like receptor-4 and myeloperoxidase in granulocytes and CD162 in lymphocytes). Cholesterol-lowering therapy tended to show opposite associations. Smokers had much higher granulocyte myeloperoxidase than nonsmokers. However, most other correlations between risk factors and cellular markers were nonsignificant.

Conclusions

Race/ethnicity, sex, and to a lesser degree LDL-cholesterol and cholesterol-lowering therapy, but few other risk factors, were correlated with markers of cellular activation in this population-based study.

a Division of Epidemiology & Community Health, School of Public Health, University of Minnesota, 1300 South Second Street, Suite 300, Minneapolis, MN 55454-1015, USA

b Division of Hematology, University of Texas Health Science Center, Houston, TX, USA

c Collaborative Studies Coordinating Center, Department of Biostatistics, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

d Human Genetics Center and Institute of Molecular Medicine, University of Texas Health Science Center, Houston, TX, USA

Corresponding Author InformationCorresponding author. Tel.: +1 612 626 8862 fax: +1 612 624 0315.

PII: S0021-9150(08)00783-1

doi:10.1016/j.atherosclerosis.2008.11.005


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