PATHOLOGY OF THE PERICARBON(R) BOVINE PERICARDIAL XENOGRAFT IMPLANTEDIN HUMANS

Citation
M. Valente et al., PATHOLOGY OF THE PERICARBON(R) BOVINE PERICARDIAL XENOGRAFT IMPLANTEDIN HUMANS, Journal of heart valve disease, 7(2), 1998, pp. 180-189
Citations number
27
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
09668519
Volume
7
Issue
2
Year of publication
1998
Pages
180 - 189
Database
ISI
SICI code
0966-8519(1998)7:2<180:POTPBP>2.0.ZU;2-M
Abstract
Background and aims of the study: Pericarbon(R) is a new-generation bo vine pericardial bioprosthesis designed to withstand mechanical wear. Following optimal in vitro testing and animal experiments, clinical tr ials were initiated in many European centers and explants sent to our department Par pathological evaluation. This included gross, radiograp hic, histologic and ultrastructural investigations. Methods: Between 1 986 and 1996, 24 bioprostheses (eight aortic, II mitral, two mitro-aor tic, one tricuspid) were collected from 22 patients (10 males and 12 f emales; mean age 57.0 +/- 18.9 years) either at autopsy (nine) or reop eration (15). Results: Ten bioprostheses explanted <2 months after sur gery were either normal or failed because of surgical problems or non- structural causes. Among the other 14 bioprostheses (mean placement 41 .9 +/- 23.6 months; range: 7 to 90 months), structural deterioration o ccurred in seven and was due to dystrophic calcification with stenosis in five (three aortic, two Mitral), mixed lesion in one (mitral), and incompetence in one by calcium-related commissural tear (mitral). At the ultrastructural level, calcification was detected either on cell d ebris or upon collagen fibers. No bioprosthesis failed because of fibr ous tissue overgrowth. Of the remaining seven bioprostheses, vegetativ e endocarditis occurred in two, thrombosis in one, and aseptic paraval vular leak in one; whereas three showed no signs of dysfunction. Concl usions: This pathologic experience with the Pericarbon valve showed ca lcification to be the main cause of late structural failure, causing m ainly cusp stiffness and bioprosthesis stenosis. Tissue rupture or abr upt dysfunction never occurred. Thus, prevention of mineralization rem ains the main challenge.