Complement Activation Is Involved in the Structural Deterioration of Bovine Pericardial Bioprosthetic Heart Valves
| Autor: | Daniel Loisance, Lecerf L, Madeleine Moczar, Maryvonne Ginat |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Adult
medicine.medical_specialty Neutrophil granulocyte Biomedical Engineering Biophysics Bioengineering Matrix (biology) Fibrin Biomaterials Internal medicine medicine Animals Humans Complement Activation Aged Bioprosthesis biology Chemistry Elastase Chemotaxis General Medicine Middle Aged Heart Valves Blood proteins Cell biology Complement system medicine.anatomical_structure Heart Valve Prosthesis biology.protein Cardiology Cattle Collagen Antibody Pericardium |
| Zdroj: | ASAIO JOURNAL. 42:M375-380 |
| ISSN: | 1058-2916 |
| Popis: | Disintegrated collagen fibers surrounded with protein deposits are a morphologic feature in torn, folded, and disrupted cusps of pericardial prostheses explanted for clinical dysfunction. New technologies for valve bioprostheses with improved durability require further investigation of molecular mechanisms initiating the deterioration of bioprosthetic valves. The authors' aim was to obtain experimental evidence of biologic factors contributing to the degradation of the bioprosthetic matrix. Clinically failed Mitroflow (22), Hancock (3), Ionescu-Shiley (2), and Sorin (1) valves were explanted after 69-170 months. Non calcific deterioration of the prosthetic matrix was studied with labeled antibodies to plasma proteins and cells. IgG, and complement proteins C1q, C3, and C4 were accumulated close to dissociated collagen bundles (26/28) throughout the prostheses. Fibrin was identified on the cuspal surface and in the deep disrupted areas. The fibrin peptides and proteolytic breakdown products of the complement components, the latter consistent with complement activation and chemotaxis for monocytes, were shown by immunoenzymic assay on Western blots from the valve extracts. The complement activation triggered by the IgG aggregates generates bioactive peptide signals that can activate macrophages (22/28) and neutrophil granulocyte elastase (22/24) able to cooperate with the mechanical stress in the breakdown of the chemically processed, non hemocompatible, and non-self macromolecular matrix. |
| Databáze: | OpenAIRE |
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