title: Vascular endothelial function and circulating endothelial progenitor cells in patients with cardiac syndrome X.
abstract: BACKGROUND
  Endothelial dysfunction and microvascular abnormalities have been reported in patients with cardiac syndrome X (CSX), but the underlying mechanisms are unclear. Recent insights suggest that the injured endothelial monolayer is regenerated by circulating bone marrow-derived endothelial progenitor cells (EPCs).
  
  
  OBJECTIVE
  To test the hypothesis that the biology of altered EPCs might contribute to the pathophysiology of CSX.
  
  
  METHODS
  34 subjects (mean (SD) age: 62 (7) years) were enrolled in the study, including 12 patients with CSX, 12 stable subjects with coronary artery disease (CAD) and 10 healthy controls. The number and adhesive function of EPCs were measured in peripheral-blood samples from these study participants.
  
  
  RESULTS
  The baseline characteristics in patients with CSX and CAD were enhanced Framingham risk scores, more hypertension and lower high-density lipoproteins than the controls. Patients with CSX and CAD had significantly decreased endothelium-dependent flow-mediated vasodilation (FMD) compared with normal controls (normal controls vs CSX vs CAD: 10.6% (3.5%) vs 6.1% (1.8%) vs 4.1% (1.9%), p<0.001), but the difference was not found in endothelium-independent nitroglycerine-mediated vasodilation (p = 0.159). Reduced numbers of colony-forming units (CFU) of EPCs were noted in patients with CSX and CAD (normal vs CSX vs CAD: 41 (9) vs 30 (7) vs 14 (7) CFU/well, p<0.001). Levels of EPCs were shown to be associated with FMD (r = 0.557, p = 0.001) and high-density lipoprotein (r = 0.339, p = 0.049). Also, attenuated fibronectin adhesion function of EPCs was found in patients with CSX and CaD compared with normal subjects (104 (12) vs 80 (20) vs 65 (13)/well, p<0.001).
  
  
  CONCLUSIONS
  This study clearly showed for the first time that compared with normal subjects, patients with CSX have decreased levels and adhesive function of circulating EPCs. These findings may explain the underlying mechanisms which contribute to the endothelial dysfunction and microvascular abnormalities observed in patients with CSX.
authors.affiliation: Institute of Clinicial Medicine and [corrected] Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan.
authors.forename: Po-Hsun
authors.initials: PH
authors.lastname: Huang
authors.forename: Yung-Hsiang
authors.initials: YH
authors.lastname: Chen
authors.forename: Yuh-Lien
authors.initials: YL
authors.lastname: Chen
authors.forename: Tao-Cheng
authors.initials: TC
authors.lastname: Wu
authors.forename: Jaw-Wen
authors.initials: JW
authors.lastname: Chen
authors.forename: Shing-Jong
authors.initials: SJ
authors.lastname: Lin
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis; D002448:Cell Adhesion; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D003327:Coronary Disease / Q000097:blood / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000187:drug effects / Q000502:physiology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D015444:Exercise; D005260:Female; D006801:Humans; D008297:Male; D017566:Microvascular Angina / Q000097:blood / Q000503:physiopathology*; D008875:Middle Aged; D013234:Stem Cells / Q000187:drug effects / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014664:Vasodilation
chemical_list: D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein