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.
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.
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