Neopterin and Atherosclerotic Plaque Instability in Coronary and Carotid Arteries

  • Sugioka Kenichi
    Department of Internal Medicine and Cardiology, Osaka City University Graduate School of Medicine.
  • Naruko Takahiko
    Department of Cardiology, Osaka City General Hospital.
  • Matsumura Yoshiki
    Department of Internal Medicine and Cardiology, Osaka City University Graduate School of Medicine.
  • Shirai Nobuyuki
    Department of Internal Medicine and Cardiology, Osaka City University Graduate School of Medicine.
  • Hozumi Takeshi
    Department of Internal Medicine and Cardiology, Osaka City University Graduate School of Medicine.
  • Yoshiyama Minoru
    Department of Internal Medicine and Cardiology, Osaka City University Graduate School of Medicine.
  • Ueda Makiko
    Department of Pathology, Osaka City University Graduate School of Medicine.

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Abstract

Inflammation plays a key role in atherosclerosis and plaque vulnerability, and monocyte/macrophage activation contributes to these processes. Neopterin, a by-product of the guanosine triphosphate pathway, is produced by activated macrophages on stimulation with interferon-γ released from T lymphocytes, and is an activation marker for monocytes/macrophages. Coronary angiographic studies have shown a relationship between increased circulating levels of neopterin and the presence of complex coronary lesions in patients with unstable angina pectoris (UAP). Furthermore, in an immunohistochemical study performed using coronary atherectomy specimens, a significantly higher prevalence of neopterin-positive macrophages was found in culprit lesions in patients with UAP than in those with stable angina pectoris (SAP). We recently clarified that the presence of complex carotid plaques detected by carotid ultrasound was related to increased circulating levels of neopterin, and immunohistochemical localization of neopterin was observed in complex carotid lesions obtained from carotid endarterectomy in patients with SAP. These findings suggest that neopterin is an important biomarker of plaque instability in both coronary and carotid atherosclerotic lesions.

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