Upregulation of endothelial adhesion molecules in hearts with congestive and ischemic cardiomyopathy: immunohistochemical evaluation of inflammatory endothelial cell activation.
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.
Wilhelmi
Mathias H
MH
Division for Thoracic-, and Cardiovascular Surgery, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. wilhelmi@thg.mh-hannover.de
Leyh
Rainer G
RG
Wilhelmi
Michaela
M
Haverich
Axel
A
D015703:Antigens, CD / Q000378:metabolism; D009202:Cardiomyopathies / Q000378:metabolism*; D002311:Cardiomyopathy, Dilated / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D003331:Coronary Vessels / Q000378:metabolism; D019040:E-Selectin / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D016023:Integrins / Q000032:analysis; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D019007:P-Selectin / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D014841:von Willebrand Factor / Q000032:analysis
D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D016023:Integrins; D019007:P-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1