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Biomaterials-Associated Pathology of Cardiac Valve Prostheses: Clinical Explant Analysis and Studies of Tissue Valve Calcification

Published online by Cambridge University Press:  22 February 2011

Frederick J. Schoen  and
Robert J. Levy
Frederick J. Schoen
Affiliation:
Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Ngston, MA 02115 Departments of Pathology and Pediatrics, Harvard Medical School, Boston, MA 02115
Robert J. Levy
Affiliation:
Department of Cardiology, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115 Departments of Pathology and Pediatrics, Harvard Medical School, Boston, MA 02115
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Abstract

Studies of the pathology of explanted clinical and experimental valve specimens were done to determine the role of biomaterials in the failure of heart valve prostheses. From 7/80 through 12/84, 129 patients had valve prostheses removed at our hospital. Thrombosis/thromboembolism was the most frequent cause of the 39 mechanical valve failures (23%). Structural failure (poor durability) caused 12%. In contrast, with tissue-derived bioprostheses (90 patients), primary tissue degenerative failure was frequent (70%), and was usually associated with calcification (CALC). Infection caused 19% of all valve failures with a frequency not differing among valve types. Other causes of failure were not biomaterials-related. Thus, although frank materials degradation necessitates only a minority of mechanical valve removals, the suboptimal biologic properties of contemporary heart valve biomaterials contribute to some frequent complications (such as thrombosis/thromboembolism). Furthermore, degeneration due to mineralization is the overwhelming mode of failure of bioprosthetic valves.

To understand and potentially eliminate bioprosthetic valve CALC, the kinetics, morphology and host and implant determinants of this process were studied using subcutaneous implants in rats. In this model, in which the pathologic features were similar to those of actual experimental and clinical valve replacements, CALC of glutaraldehyde-treated porcine aortic valve and bovine pericardium began within 48 hours following implantation; mineral levels were comparable to those in failed clinical valves after 84–126 days. Calcific deposits were initially associated with connective tissue cells, but later involved collagen. Systemically-administered ethane-hydroxy-diphosphonate (EHDP), a drug used to treat some forms of metabolic bone disease, inhibited CALC by 97%, but caused significant bone growth retardation. However, EHDP given by site-specific controlled-release largely mitigated CALC at only 1% of the total effective systemic dose, but without adverse effects.

Type
Research Article
Information
MRS Online Proceedings Library (OPL) , Volume 55: Symposium G – Biomedical Materials , 1985 , 29
Copyright
Copyright © Materials Research Society 1986

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References

REFERENCES

1. Rahimtoola, S.H., J. Am. Coll. Cardiol. 1, 199 (1983).CrossRefGoogle Scholar
2. Cohn, L.H., Chest 85, 387 (1984).Google Scholar
3. Schoen, F.J., -Titus, J.L., Lawrie, G.M., Ann. Biomed. Eng. 10, 97 (1982).Google Scholar
4. McClung, J.A., Stein, J.H., Ambrose, J.A., et al, Prog. Cardiovasc. Dis. 26, 237 (1983).Google Scholar
5. Roberts, W.C., Bulkley, B.H., Morrow, A.G., Prog. Cardiovasc. Dis. 15, 539, (1973).Google Scholar
6. Schoen, F.J., Titus, J.L., Lawrie, G.M., J. Am. Med. Ass. 249, 899 (1983).Google Scholar
7. Schoen, F.J., Levy, R.J., Cardiol. Clin. 2, 717 (1984).Google Scholar
8. Bortolotti, U., Milano, A., Mazzucco, A., et al, J. Thorac. Cardiovasc. Surg. 90, 564 (1985).Google Scholar
9. Schoen, F.J., Hobson, C.E., Hum. Pathol. 16, 549 (1984).Google Scholar
10. Starr, A., J. Am. Coll. Cardiol. 6, 899 (1985).Google Scholar
11. Schoen, F.J., Cohn, L.H., in Biological and Bioprosthetic Valves, edited by Bodnar, E., Yacoub, M.H. (Yorke Publishers, New York, 1986).; F.J Schoen, R.J. Levy, Biological and Bioprosthetic Valves, edited by E. Bodnar, M.H. Yacoub (Yorke Publishers, New York, 1986)., in press.Google Scholar
12. Ishihara, T., Ferrans, V.J., Boyce, S.W., et al, Am. J. Cardiol. 48, 665, (1981).Google Scholar
13. Ferrans, V.J., Boyce, S.W., Billingham, M.E., et al, Am. J. Cardiol. 46, 721 (1980).Google Scholar
14. Valente, M., Bortolotti, U., Thiene, G., Am. J. Pathol. 119, 12 (1985).Google Scholar
15. Thubrikar, M.J., Deck, J.D., Aouad, J., J. Thorac. Cardiovasc. Surg. 86, 115, (1983).Google Scholar
16. Barnhart, G.R., Jones, M., Ishihara, T., et al, Am. J. Pathol. 106, 136, (1983).Google Scholar
17. Levy, R.J., Zenker, J.A., Bernhard, W.F., Ann. Thorac. Surg. 36, 187 (1983).Google Scholar
18. Schoen, F.J., Levy, R.J., Nelson, A.C., et al, Lab. Invest. 52, 523 (1985).Google Scholar
19. Levy, R.J., Schoen, F.J., Howard, S.L., Am. J. Cardiol. 52, 629 (1983).Google Scholar
20. Levy, R.J., Schoen, F.J., Levy, J.T., et al, Am. J. Pathol. 113, 143 (1983).Google Scholar
21. Fishbein, M.C., Levy, R.J., Ferrans, V.J., et al, J. Thorac. Cardiovasc. Surg. 83, 602 (1982).Google Scholar
22. Levy, R.J., Schoen, F.J., Sherman, F.S., et al, Am. J. Pathol. (1985), in press.Google Scholar
23. Levy, R. J., Hawley, M.A., Schoen, F.J., et al, Circulation 71, 349 (1985).Google Scholar
24. Levy, R.J., Wolfrum, J., Schoen, F.J., et al, Science 228, 190 (1985).Google Scholar