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Circulation. 2000;101:e86

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(Circulation. 2000;101:e86.)
© 2000 American Heart Association, Inc.


Circulation Electronic Pages

Cardiac Interleukin-6 in Ischemic Myocardium

Tsugiyasu Kanda, MD

Department of General Medicine

Isao Kobayashi, MD

Department of Laboratory Medicine

Ryozo Nagai, MD

Second Department of Internal Medicine Gunma University School of Medicine, Maebashi, Japan


*    Introduction
 
To the Editor:

We read with great interest the recent report of Gwechenberger et al1 demonstrating that cardiac myocytes in the viable border zone of myocardial infarction exhibited reperfusion-dependent expression of interleukin (IL)-6 mRNA within 1 hour in a canine model of ischemia and reperfusion. These authors point to the first direct histological demonstration of IL-6 mRNA, and they suggest the enhanced expression of IL-6 may exert primary effects on myocardial function, such as reduced contractility, positive protein balance (hypertrophy), and antiapoptosis. We agree with their hypothesis, but this is not the first demonstration of IL-6 expression in the infarcted heart in vivo.

In our report,2 we demonstrated that IL-6 protein was immunohistochemically expressed in the hypertrophied myocardium of patients who died 1 to 7 days after myocardial infarction. The greatest expression of IL-6 was confirmed in the adjacent myocardium in patients who died 3 to 4 days after the onset (2.7±0.4; P<0.05) compared with those who died within 1 to 2 days (1.0±0.3). The diameter of IL-6–positive myocytes was significantly (P<0.05) increased in patients who died within 1 to 2 days (1.6±0.2), 3 to 4 days (1.8±0.3), or 5 to 8 days (2.0±0.2) after the onset of myocardial infarction. Moreover, the IL-6–positive myocytes were adjacent to the infarcted area, such as in the border zone, and coexpressed with atrial natriuretic peptide (ANP). Our study demonstrated that ischemic myocytes surrounding infarcted myocardium definitely expressed IL-6 proteins in their cytoplasm in the first 7 days after infarction.

Although . . . [Full Text of this Article]

Mark L. Entman, MD; Marianne Gwechenberger, MD; Keith A. Youker, PhD; Nikolaos G. Frangogiannis, MD; Lloyd H. Michael, PhD

Department of Medicine, Section of Cardiovascular Sciences, The DeBakey Heart Center, Baylor College of Medicine, Houston, Tex

Leonardo H. Mendoza; C. Wayne Smith, MD

Section of Leukocyte Biology, Department of Pediatrics, Texas Children’s Hospital, Baylor College of Medicine, Houston, Tex