Role of inflammation in allogeneic and xenogeneic heart valve degeneration: immunohistochemical evaluation of inflammatory endothelial cell activation.
OBJECTIVE
Biological heart valve prostheses undergo degenerative changes which lead ultimately to dysfunction or even complete destruction. The study aim was to evaluate immunological factors and their potential role in biological heart valve destruction.


METHODS
Allogeneic (n = 10) and xenogeneic (n = 3) aortic valve prostheses, as well as aortic valves retrieved from transplanted human hearts which had to be replaced due to chronic graft rejection (n = 4), were analyzed. Aortic valves from human donor hearts (n = 4) served as controls. Evaluated adhesion molecule expression included: selectin family ELAM-1, CD62; integrin family VLA-1, -2, -3, -4, -5 and -6; immuoglobulin supergene family PECAM-1, ICAM-1 and -2, and class I heavy chain proteins; complementary adhesion molecules CD34, CD44 and von Willebrand factor.


RESULTS
ELAM-1, ICAM-1 and -2, CD34, CD44 and class I heavy chain proteins, which play significant roles during inflammatory processes, showed stronger expression patterns in allogeneic and xenogeneic aortic heart valve prostheses compared to native or chronically rejected valves. Furthermore, allogeneic and xenogeneic valves showed a strong thrombogenicity which stained positive for von Willebrand factor outside endothelial cells on these valves. Integrin molecules as well as CD62 showed only mild differences.


CONCLUSIONS
Immunological reactions play a pivotal role in the degeneration of biological heart valve prostheses. As immunosuppressive therapy after heart valve replacement is not a viable option, novel approaches in 'tissue engineering' may help to avoid tissue degeneration while preserving the advantage of biological tissue origin.
Wilhelmi
Mathias H
MH
Division for Thoracic-, and Cardiovascular Surgery, Hanover Medical School, Hanover, Germany.
Mertsching
Heike
H
Wilhelmi
Michaela
M
Leyh
Rainer
R
Haverich
Axel
A
D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000096:biosynthesis / Q000276:immunology; D018952:Antigens, CD34 / Q000096:biosynthesis / Q000276:immunology; D001021:Aortic Valve / Q000166:cytology / Q000276:immunology* / Q000601:surgery*; D001705:Bioprosthesis; D015815:Cell Adhesion Molecules / Q000096:biosynthesis / Q000276:immunology; D019040:E-Selectin / Q000096:biosynthesis / Q000276:immunology; D042783:Endothelial Cells / Q000276:immunology / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis / Q000276:immunology; D006084:Graft Rejection / Q000276:immunology / Q000378:metabolism; D016027:Heart Transplantation; D006349:Heart Valve Diseases / Q000276:immunology* / Q000378:metabolism; D006350:Heart Valve Prosthesis; D006801:Humans; D018960:Hyaluronan Receptors / Q000096:biosynthesis / Q000276:immunology; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D016023:Integrins / Q000096:biosynthesis / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000276:immunology; D008875:Middle Aged; D014181:Transplantation Immunology / Q000276:immunology; D014184:Transplantation, Homologous; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis / Q000276:immunology; D014841:von Willebrand Factor / Q000096:biosynthesis / Q000276:immunology
D015703:Antigens, CD; D018952:Antigens, CD34; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D016326:Extracellular Matrix Proteins; D018960:Hyaluronan Receptors; C065289:ICAM2 protein, human; D016023:Integrins; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1