Low CD34+ cell count and metabolic syndrome synergistically increase the risk of adverse outcomes

Metabolic syndrome (MetS) associates with endothelial dysfunction and a high risk of cardiovascular events and death. Circulating progenitor cells have been shown to contribute to endothelial homeostasis and repair . We aimed to test whether progenitor cell count is an independent event predictor an...

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Published inAtherosclerosis Vol. 207; no. 1; pp. 213 - 219
Main Authors Fadini, Gian Paolo, de Kreutzenberg, Saula, Agostini, Carlo, Boscaro, Elisa, Tiengo, Antonio, Dimmeler, Stefanie, Avogaro, Angelo
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier Ireland Ltd 01.11.2009
Elsevier
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ISSN0021-9150
1879-1484
1879-1484
DOI10.1016/j.atherosclerosis.2009.03.040

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Summary:Metabolic syndrome (MetS) associates with endothelial dysfunction and a high risk of cardiovascular events and death. Circulating progenitor cells have been shown to contribute to endothelial homeostasis and repair . We aimed to test whether progenitor cell count is an independent event predictor and modifies cardiovascular risk associated with MetS. On the basis of the expression of CD34, CD133 and KDR, 6 phenotypes of progenitor cells were counted using flow cytometry in 214 subjects with and without MetS. We recorded classical risk factors and MetS components, cumulative risk estimates, and high-sensitive C-reactive protein. Subjects were followed-up for a median of 34 months to collect total events, cardiovascular events and all-cause mortality. In the Cox proportional hazards regression analyses, we found that, unlike other phenotypes, reduced CD34+ cells predicted cardiovascular and total events and death, independently of all potential confounders. Remarkably, a low CD34+ cell count significantly increased the risk associated with MetS, as shown by synergy indexes. The level of circulating CD34+ cells is a novel independent risk biomarker and modulates outcomes in the MetS, suggesting that generic progenitor cells have a role in disease development or progression over the long-term.
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ISSN:0021-9150
1879-1484
1879-1484
DOI:10.1016/j.atherosclerosis.2009.03.040