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 in | Atherosclerosis Vol. 207; no. 1; pp. 213 - 219 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier Ireland Ltd
01.11.2009
Elsevier |
Subjects | |
Online Access | Get full text |
ISSN | 0021-9150 1879-1484 1879-1484 |
DOI | 10.1016/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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0021-9150 1879-1484 1879-1484 |
DOI: | 10.1016/j.atherosclerosis.2009.03.040 |