title: Low CD34+ cell count and metabolic syndrome synergistically increase the risk of adverse outcomes.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Clinical and Experimental Medicine, University of Padova, Medical School, Padova, Italy. gianpaolofadini@hotmail.com
authors.forename: Gian Paolo
authors.initials: GP
authors.lastname: Fadini
authors.forename: Saula
authors.initials: S
authors.lastname: de Kreutzenberg
authors.forename: Carlo
authors.initials: C
authors.lastname: Agostini
authors.forename: Elisa
authors.initials: E
authors.lastname: Boscaro
authors.forename: Antonio
authors.initials: A
authors.lastname: Tiengo
authors.forename: Stefanie
authors.initials: S
authors.lastname: Dimmeler
authors.forename: Angelo
authors.initials: A
authors.lastname: Avogaro
mesh_terms: D000071916:AC133 Antigen; D015703:Antigens, CD / Q000097:blood; D018952:Antigens, CD34 / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000276:immunology* / Q000401:mortality; D016022:Case-Control Studies; D002452:Cell Count; D018450:Disease Progression; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000276:immunology* / Q000401:mortality; D008875:Middle Aged; D010455:Peptides / Q000097:blood; D010641:Phenotype; D011237:Predictive Value of Tests; D016016:Proportional Hazards Models; D012372:ROC Curve; D018570:Risk Assessment; D012307:Risk Factors; D013234:Stem Cells / Q000276:immunology*; D013997:Time Factors; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000097:blood
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D015415:Biomarkers; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides; D040301:Vascular Endothelial Growth Factor Receptor-2