title: Elevated circulating inflammatory markers in female patients with cardiac syndrome X.
abstract: BACKGROUND
  The pathophysiological mechanism in cardiac syndrome X has been suggested as impairment in normal endothelial function of the coronary microvasculature, resulting in inadequate flow reserve. However, despite the extensive studies, the precise mechanisms in cardiac syndrome X remain unclear.
  
  
  OBJECTIVE
  The present study was, therefore, to investigate whether inflammatory cells and markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) might be involved in the pathogenesis of cardiac syndrome X.
  
  
  METHODS
  Thirty-six female patients with cardiac syndrome X and 30 sex-matched normal controls were prospectively enrolled in this study. Blood samples were drawn for measuring white blood and monocyte cells, inflammatory markers such as CRP and IL-6, and data were compared between patients with cardiac syndrome X and normal controls.
  
  
  RESULTS
  The data showed that increased numbers of white blood and monocyte cells were found in patients with cardiac syndrome X compared with normal controls (white blood cells: 7072+/-1146/mm(3) vs. 6138+/-1079/mm(3); monocyte cells: 612+/-186/mm(3) vs. 539+/-190/mm(3)p<0.05, respectively). Moreover, patients with cardiac syndrome X were detected to have significantly higher plasma CRP and IL-6 levels in comparison with patients with normal controls (CRP: 0.48+/-0.26 mg/L vs. 0.22+/-0.15 mg/L; IL-6: 13.4+/-1.2 pg/dl vs. 6.2+/-0.6 pg/dl, p<0.01, respectively). The multivariate analysis showed that CRP was the independent variable most strongly associated with cardiac syndrome X.
  
  
  CONCLUSIONS
  Our data suggested that low-grade, chronic inflammation might contribute to the development of cardiac syndrome X manifested by increased plasma levels of inflammatory cells and inflammatory markers.
authors.affiliation: Department of Cardiology, Fu Wai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100037, PR China. lijnjn@yahoo.com.cn
authors.forename: Jian-Jun
authors.initials: JJ
authors.lastname: Li
authors.forename: Chen-Gang
authors.initials: CG
authors.lastname: Zhu
authors.forename: Jin-Lo
authors.initials: JL
authors.lastname: Nan
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: Zi-Cheng
authors.initials: ZC
authors.lastname: Li
authors.forename: He-Song
authors.initials: HS
authors.lastname: Zeng
authors.forename: Zhan
authors.initials: Z
authors.lastname: Gao
authors.forename: Xue-Wen
authors.initials: XW
authors.lastname: Qin
authors.forename: Chao-Yang
authors.initials: CY
authors.lastname: Zhang
mesh_terms: D000328:Adult; D001772:Blood Cell Count; D002097:C-Reactive Protein / Q000032:analysis*; D002908:Chronic Disease; D003326:Coronary Circulation; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D017566:Microvascular Angina / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D002097:C-Reactive Protein