RT Journal Article
SR Electronic
T1 Neopterin is associated with plaque inflammation and destabilisation in human coronary atherosclerotic lesions
JF Heart
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP 1537
OP 1541
DO 10.1136/hrt.2006.109736
VO 93
IS 12
A1 T Adachi
A1 T Naruko
A1 A Itoh
A1 R Komatsu
A1 Y Abe
A1 N Shirai
A1 H Yamashita
A1 S Ehara
A1 M Nakagawa
A1 C Kitabayashi
A1 Y Ikura
A1 M Ohsawa
A1 M Yoshiyama
A1 K Haze
A1 M Ueda
YR 2007
UL http://heart.bmj.com/content/93/12/1537.abstract
AB 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).Patients and 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.