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Eur J Cardiothorac Surg 2005;27:122-127
© 2005 Elsevier Science NL

Upregulation of endothelial adhesion molecules in hearts with congestive and ischemic cardiomyopathy: immunohistochemical evaluation of inflammatory endothelial cell activation

^a Division for Thoracic-, and Cardiovascular Surgery, Hannover Medical School, Carl-Neuberg-Straße 1, 30625 Hannover, Germany
^b Leibnitz Research Laboratories for Biotechnology and Artificial Organs (LEBAO), Hannover, Germany

Received 23 March 2004; received in revised form 14 June 2004; accepted 20 September 2004.

^* Corresponding author. Tel.: +49 511 532 2393; fax: +49 511 532 5404. (E-mail: wilhelmi{at}thg.mh-hannover.de).

Objective: In recent years many data emphasized, that inflammatory reactions seem to be involved in the pathogenesis of ischemic (ICM) and congestive (CCM) heart disease. Since, it is well known that endothelial adhesion molecules play a pivotal role in the initiation and maintenance of inflammatory reactions we therefore, evaluated the endothelial expression of a wide variety of different adhesion molecules in hearts suffering from ICM and CCM. Methods: Tissue samples from coronary arteries, and left and right ventricle myocardium originating form heart with ICM and CCM were evaluated. Tissue samples from healthy human donor hearts, which were not transplanted, served as controls. Evaluated adhesion molecule expression: selectin-family ELAM-1, CD62, immunoglobulin-supergene-family PECAM-1, ICAM-1, VCAM-1, integrin-family VLA-1,-2,-3,-4,-5, and -6, complementary-adhesion-molecules CD34, CD44 and the von-Willebrand-factor (vWF). Results: While endocardial surfaces and coronary arteries revealed only little differences when comparing tissue samples originating from healthy donor hearts and those suffering from ICM and CCM, significant differences were found within the myocardial microvasculature. Both kinds of diseased hearts showed stronger expressions for CD62, ELAM-1, ICAM-1 and VCAM-1 (only CCM) than controls. More and above, integrin molecules showed differential expressions too. Whereas, VLA-1 showed stronger expressions in diseased hearts, VLA-3,-5, and -6 were expressed much weaker in those hearts. Complementary adhesion molecules (CD34/CD44) did not show significant differences and the vWF was not found in any sample. Conclusions: Inflammatory reactions play a pivotal role in the propagation and maintenance of both these cardiac detoriating diseases.

Key Words: Cardiomyopathy • Congestive heart disease • Ischemic heart disease • Immunology • Adhesion molecules • Endothelial cells

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