INCREASED PLASMA SOLUBLE INTERCELLULAR ADHESION MOLECULE-1 LEVELS IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION
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- KAIKITA Koichi
- Division of cardiology, Kumamoto University School of Medicine
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- OGAWA Hisao
- Division of cardiology, Kumamoto University School of Medicine
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- YASUE Hirofumi
- Division of cardiology, Kumamoto University School of Medicine
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- SAKAMOTO Tomohiro
- Division of cardiology, Kumamoto University School of Medicine
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- MIYAO Yuji
- Division of cardiology, Kumamoto University School of Medicine
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- SUEFUJI Hisakazu
- Division of cardiology, Kumamoto University School of Medicine
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- SOEJIMA Hirofumi
- Division of cardiology, Kumamoto University School of Medicine
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- TAYAMA Shinji
- Division of cardiology, Kumamoto University School of Medicine
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- HAYASAKI Kazuya
- Division of Cardiology, Saiseikai Kumamoto Hospital
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- HONDA Takashi
- Division of Cardiology, Saiseikai Kumamoto Hospital
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- KUMIJIKKOKU Shuichi
- Division of Cardiology, Saiseikai Kumamoto Hospital
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抄録
Intercellular adhesion molecule-1 (ICAM-1) is a major ligand for 2 members of the CD18 family of leukocyte integrin adhesion molecules and mediates adhesion between leukocytes and stimulated endothelial cells. We examined plasma soluble ICAM-1 (sICAM-1) levels in 30 patients with acute myocardial infarction (AMI) within 6 h of symptom onset, 21 patients with unstable angina (UA), 35 patients with stable exertional angina (SEA) and 21 control subjects. Plasma sICAM-1 levels (ng/ml) were significantly higher in both the acute and chronic phases of AMI and in the UA group than in the SEA and the control groups (195±14, 198±16 in the acute and chronic phases of AMI, 188±11 in the UA group vs 142±7 in the SEA group, 141±10 in the control group, p<0.01). Plasma sICAM-1 levels were significantly higher in AMI patients when preceded by unstable angina than when not preceded by unstable angina at any point over the time course except 1 week after admission (p<0.01 vs admission, 12 h, 2 days, 3 days, 5 days, 2 weeks, 3 weeks. p<0.05 vs 24 h). These results suggest that the increase in sICAM-1 is associated with repeated episodes of myocardial ischemia and reperfusion not leading to myocardial necrosis. The increase in sICAM-1 may play an important role as an inflammatory component in the pathogenesis of the ischemic myocardium.
収録刊行物
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- Japanese circulation journal
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Japanese circulation journal 61 (9), 741-748, 1997-08-20
社団法人日本循環器学会
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詳細情報 詳細情報について
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- CRID
- 1573950401963427584
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- NII論文ID
- 110002564855
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- NII書誌ID
- AA00690731
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- ISSN
- 00471828
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- 本文言語コード
- en
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- データソース種別
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- CiNii Articles