title: Endothelial progenitor cells in acute myocardial infarction and sleep-disordered breathing.
abstract: BACKGROUND
  Mobilization and functions of endothelial progenitor cells (EPCs) are increased in patients with acute myocardial infarction (AMI). Yet, sleep-disordered breathing (SDB) is highly prevalent in patients with AMI.
  
  
  OBJECTIVE
  To compare EPC numbers and functions in patients with AMI with SDB (AMI-SDB) and without SDB (AMI-only) and to determine the effects of intermittent hypoxia (IH) in vitro on EPC proliferative and angiogenic properties.
  
  
  METHODS
  Forty male patients with AMI underwent a whole-night sleep study using ambulatory monitoring. Nineteen had SDB (oxygen desaturation index > 5 events/h). AMI-SDB and AMI-only patients were matched by age, body mass index, blood chemistry, and comorbidities. Blood samples were analyzed by flow cytometry, endothelial cell colony-forming units (EC-CFU), paracrine measures, blood chemistry, and oxidative stress, inflammatory, and angiogenic markers. Effects of IH in vitro were studied in 12 healthy subjects.
  
  
  RESULTS
  Circulating EPCs (CD34(+)/KDR(+)), angiogenic T cells (CD3(+)/CD31(+)/CXCR4(+)), and vascular endothelial growth factor in monocytes were significantly higher in AMI-SDB patients, whereas plasma stromal cell-derived factor (SDF)-1α levels were significantly lower. Also, EC-CFU numbers and EC-CFU paracrine effects on endothelial tube formation were significantly higher in AMI-SDB compared with AMI-only patients. Similarly, in cell cultures from healthy subjects, EC-CFU numbers and their paracrine effects on endothelial tube formation were increased after exposure to IH in vitro compared with normoxia.
  
  
  CONCLUSIONS
  Coexistent mild to moderate SDB in patients with AMI increased the mobilization, proliferative and angiogenic capacities of EPCs, angiogenic T-cell numbers, and vascular endothelial growth factor expression in monocytes compared with patients with AMI without SDB. IH in vitro had similar effects on healthy EPC functions.
authors.affiliation: The Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
authors.forename: Slava
authors.initials: S
authors.lastname: Berger
authors.forename: Doron
authors.initials: D
authors.lastname: Aronson
authors.forename: Peretz
authors.initials: P
authors.lastname: Lavie
authors.forename: Lena
authors.initials: L
authors.lastname: Lavie
mesh_terms: D000328:Adult; D043303:Aryldialkylphosphatase / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002452:Cell Count; D054377:Chemokine CXCL12 / Q000097:blood; D015897:Comorbidity; D017077:Culture Media, Conditioned; D004730:Endothelium, Vascular / Q000166:cytology*; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008055:Lipids / Q000032:analysis; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology*; D018919:Neovascularization, Physiologic / Q000502:physiology; D012891:Sleep Apnea Syndromes / Q000453:epidemiology / Q000503:physiopathology*; D013234:Stem Cells / Q000502:physiology*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014463:Ultrasonography; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D055815:Young Adult
chemical_list: D054377:Chemokine CXCL12; D017077:Culture Media, Conditioned; D008055:Lipids; D017392:Thiobarbituric Acid Reactive Substances; D042461:Vascular Endothelial Growth Factor A; D002097:C-Reactive Protein; D043303:Aryldialkylphosphatase; D020780:Matrix Metalloproteinase 9