Plasma soluble intercellular adhesion molecule-1 levels in coronary circulation in patients with unstable angina - 08/09/11
, Hirofumi Yasue, MD a, Yuji Miyao, MD a, Tomohiro Sakamoto, MD a, Hirofumi Soejima, MD a, Koichi Nishiyama, MD a, Koichi Kaikita, MD a, Hisakazu Suefuji, MD a, Kenji Misumi, MD a, Keiji Takazoe, MD a, Kiyotaka Kugiyama, MD a, Michihiro Yoshimura, MD aAbstract |
It has been suggested that active inflammation plays an important role in the pathogenesis of acute coronary syndromes, including unstable angina. Intracellular adhesion molecule-1 (ICAM-1) is a major ligand on the endothelial cells for adherence of the activated polymorphonuclear leukocytes. Recently, it has been demonstrated that the soluble form of ICAM-1 has been detected in human serum and has been increased in many other inflammatory or autoimmune disorders. To evaluate the involvement of ICAM-1 in unstable angina, we examined plasma soluble ICAM-1 (sICAM-1) levels in coronary circulation. The plasma sICAM-1 levels in the coronary sinus and aortic root were simultaneously examined in 20 patients with unstable angina, 19 patients with stable exertional angina, and 16 control subjects. The plasma levels of sICAM-1 were measured by enzyme-linked immunosorbent assay. The mean plasma sICAM-1 levels (nanograms per milliliter) both in the coronary sinus and aortic root were significantly higher (p <0.01) in patients with unstable angina than in those with stable exertional angina and in control subjects (217 ± 14 vs 126 ± 8; 120 ± 10 in the coronary sinus, 202 ± 13 vs 125 ± 9; 123 ± 10 in the aortic root). Furthermore, the mean value was higher in the coronary sinus than in the aortic root in patients with unstable angina. There were no significant differences in the values between in the coronary sinus and aortic root in patients with stable exertional angina and control subjects. Thus, sICAM-1 release is increased, especially in coronary circulation in unstable angina.
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| ☆ | This study was supported in part by Research Grant for Cardiovascular Disease (7A-3 and 9A-3) from the Ministry of Health and Welfare, Smoking Research Foundation Grant for Biomedical Reseach, Tokyo, Japan, and a grant from Japan Cardiovascular Research Foundation, Osaka, Japan. |
Vol 83 - N° 1
P. 38-42 - janvier 1999 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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