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Cardiovascular Research 1999 42(3):823; doi:10.1016/S0008-6363(99)00065-6
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Procoagulant and proinflammatory activity in acute coronary syndromes

U Ikeda*, Y Hojo, T Katsuki and K Shimada

Department of Cardiology, Jichi Medical School, Minamikawachi-Machi, Tochigi, 329-0498 Japan

uikeda{at}jichi.ac.jp

* Corresponding author. Tel.: +81-285-58-7344 fax: +81-285-44-5317

Received 15 December 1998; accepted 15 December 1998

To the Editor:

We read with interest the recent paper by Manten et al. [1] concerning the enhanced proinflammatory activity in acute coronary syndromes. They found that plasma interleukin-6 (IL-6) levels were significantly higher in patients with the acute phase of coronary artery disease than in patients with stable angina. On the other hand, plasma IL-8 levels were not different between stable and unstable coronary artery disease. We previously reported the plasma IL-6 levels become elevated in patients with acute myocardial infarction [2] and IL-6 mRNA is expressed in human atherosclerotic lesions [3]. Therefore, we propose that the main source of plasma IL-6 in unstable coronary artery disease is the vascular tissue, although Manten et al. did not discuss it.

Recently, we measured the levels of IL-6, IL-8 and von Willebrand factor (vWF), a marker of endothelial injury, in the coronary sinus blood of patients with stable angina. Blood samples were taken from the coronary sinus immediately before and after, and 4 and 24 hours after percutaneous transluminal coronary angioplasty (PTCA) (group A; n=52) or diagnostic coronary angiography (group B; n=7). Levels of IL-6 and vWF in the coronary sinus blood did not change in group B after coronary angiography. Conversely, in group A, the levels of IL-6 and vWF increased significantly 4 hours after the procedure from the baseline value of 3.34±0.56 to 8.20±0.63 pg/ml (P<0.01) and 113±6.2 to 130±7.3% (P<0.01), respectively, and reached peak values at 24 hours (13.2±1.20 pg/ml and 139±7.4%, both P<0.01 versus baseline). Furthermore, there was a significant positive correlation between IL-6 and vWF levels at both 4 (r=+0.38, P<0.01) and 24 hours (r=+0.43, P<0.01). On the other hand, there was no significant increases in IL-8 levels in both two groups. These observations suggest that the mechanism of increased IL-6 after PTCA as well as in acute coronary syndromes is related to local vascular injury.

Although Manten et al. found an increase in plasma IL-6 levels in patients with the acute phase of coronary artery disease, we suspect that if blood samples were drawn from the coronary sinus, rather than the peripheral vein, more definite conclusions regarding the involvement of inflammatory cytokines in the pathogenesis of acute coronary syndromes could be obtained.


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  1. Manten A., de Winter R.I., Minnema M.C., ten Cate H., Lijmer J.G., Adams R., Peters R.J.G., van Deventer S.J.H. Procoagulant and proinflammatory activity in acute coronary syndromes. Cardiovasc Res (1998) 40:389–395.[Abstract/Free Full Text]
  2. Ikeda U., Okawa F., Seino Y., Yamamoto K., Hidaka Y., Kasahara T., Kawai T., Shimada K. Serum interleukin 6 levels become elevated in acute myocardial infarction. J Mol Cell Cardiol (1992) 24:579–584.[CrossRef][Web of Science][Medline]
  3. Seino Y., Ikeda U., Ikeda M., Yamamoto K., Misawa Y., Hasegawa T., Kano S., Shimada K. Interleukin-6 gene transcripts are expressed in human atherosclerotic lesions. Cytokine (1994) 6:87–91.[CrossRef][Web of Science][Medline]

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This Article
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