title: Neopterin is associated with plaque inflammation and destabilisation in human coronary atherosclerotic lesions.
abstract: BACKGROUND
  Previous studies have shown that recent activation of the inflammatory response in coronary atherosclerotic lesions contributes to rapid progressive plaque destabilisation. Neopterin, a by-product of the guanosine triphosphate pathway, is produced by activated macrophages and serves as an activation marker for monocytes/macrophages.
  
  
  OBJECTIVE
  To elucidate the role of neopterin in coronary plaque destabilisation by immunohistochemical study of the presence of neopterin in coronary atherectomy specimens obtained from patients with stable angina pectoris (SAP) and unstable angina pectoris (UAP).
  
  
  METHODS
  All patients underwent atherectomy of the primary atherosclerotic lesions responsible for SAP (n = 25) and UAP (n = 25). Frozen samples were studied with antibodies against smooth muscle cells, macrophages, T cells, neutrophils and neopterin.
  
  
  RESULTS
  In 22/25 patients with UAP, abundant neopterin-positive macrophages were found at the sites of coronary culprit lesions. However, in 25 lesions from patients with SAP, only 11 lesions showed neopterin positivity. Quantitatively, the neopterin-positive macrophage score was significantly higher (p<0.001) in patients with UAP than in patients with SAP. Moreover, the neopterin-positive macrophage score showed a significant positive correlation with the number of neutrophils or T cells, respectively (neutrophils, r = 0.55, p<0.001; T cells, r = 0.70, p<0.001).
  
  
  CONCLUSIONS
  Neopterin can be considered as one of the significant factors in the process of plaque inflammation and destabilisation in human coronary atherosclerotic lesions. Its exact role in the process needs to be investigated further.
authors.affiliation: Department of Cardiology, Osaka City General Hospital, 2-13-22, Miyakojima-hondori, Miyakojima-ku, Osaka 534-0021, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Adachi
authors.forename: T
authors.initials: T
authors.lastname: Naruko
authors.forename: A
authors.initials: A
authors.lastname: Itoh
authors.forename: R
authors.initials: R
authors.lastname: Komatsu
authors.forename: Y
authors.initials: Y
authors.lastname: Abe
authors.forename: N
authors.initials: N
authors.lastname: Shirai
authors.forename: H
authors.initials: H
authors.lastname: Yamashita
authors.forename: S
authors.initials: S
authors.lastname: Ehara
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: C
authors.initials: C
authors.lastname: Kitabayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Ikura
authors.forename: M
authors.initials: M
authors.lastname: Ohsawa
authors.forename: M
authors.initials: M
authors.lastname: Yoshiyama
authors.forename: K
authors.initials: K
authors.lastname: Haze
authors.forename: M
authors.initials: M
authors.lastname: Ueda
mesh_terms: D000787:Angina Pectoris / Q000378:metabolism* / Q000473:pathology; D000789:Angina, Unstable / Q000378:metabolism* / Q000473:pathology; D003324:Coronary Artery Disease / Q000378:metabolism* / Q000473:pathology; D003331:Coronary Vessels / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D019798:Neopterin / Q000378:metabolism*
chemical_list: D019798:Neopterin