Bioprosthetic heart valves : ultrastructure and calcification

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dc.contributor.advisorZilla, Peteren_ZA
dc.contributor.authorZhang, Yinxingen_ZA
dc.date.accessioned2018-01-24T11:47:12Z
dc.date.available2018-01-24T11:47:12Z
dc.date.issued1998en_ZA
dc.descriptionSumaary in English.en_ZA
dc.descriptionIncludes bibliographical references.en_ZA
dc.description.abstractBackground: Due to the geographic distance between abattoirs and commercial valve plants delays between harvest and fixation usually range from 48 to 72 hours. In order to assess the pre-fixation tissue damage arising from the hypoxic period and the resulting calcific degeneration after implantation, we used an ultrastructural damage score and transmission electron microscopy. Materials and Methods: In a step by step manner, three major issues were clarified: 1) The degree of pre-fixation tissue damage was determined in the four most widely used commercially produced tissue heart valves. Since stentless bioprostheses represent the latest promising trend in the development of biological heart valves, stentless models of the following makes were compared: Baxter, Medtronic, St. Jude and Biocor. Due to the fact that the aortic wall component of these valves proved most resistant to all anticalcification treatments, aortic wall tissue stood in the centre of our analyses. 2) Subsequently, three main determinants of the fixation process namely: delay, temperature and fixative-concentration were varied with the goal of significantly improving the ultrastructural preservation of the bioprosthetic tissue. 3) Eventually, the influence of improved ultrastructural preservation on calcific degeneration was evaluated under in vivo conditions in the non-human primate and the rat model. Results: The comparison of the four most commonly used stentless bioprosthetic heart valves revealed a disturbing degree of tissue damage in all valves. Using a damage score from 1 to 21 (21 being the worst), aortic wall tissue of commercial valves ranged from 10 to 18 and that of leaflet tissue from 12 to 20. When fixation conditions were permutated, tissue damage could almost be abolished by immediate fixation (within 30 minutes of slaughter), low-temperature fixation(4°C) and high glutaraldehyde concentrations (> 1 %). Our in vivo experiments confirmed that commercially used fixation (delayed fixation, room-temperature and I ow concentrations of glutaraldehyde) with its concomitant high degree of tissue damage results in high levels of calcification. Apart from a distinctly improved calcification potential in ultrastructurally well preserved tissue, there was also an inverse correlation between tissue calcification and the concentration of glutaraldehyde used for fixation. Conclusion: We could demonstrate that commercially produced bioprosthetic heart valves uniformly show badly damaged tissue and that tissue damage contributes to the calcific degeneration of these valves. We were also able to determine ideal fixation conditions which in turn significantly reduced tissue calcification.en_ZA
dc.identifier.apacitationZhang, Y. (1998). <i>Bioprosthetic heart valves : ultrastructure and calcification</i>. (Thesis). University of Cape Town ,Faculty of Health Sciences ,Division of Cardiology. Retrieved from http://hdl.handle.net/11427/26921en_ZA
dc.identifier.chicagocitationZhang, Yinxing. <i>"Bioprosthetic heart valves : ultrastructure and calcification."</i> Thesis., University of Cape Town ,Faculty of Health Sciences ,Division of Cardiology, 1998. http://hdl.handle.net/11427/26921en_ZA
dc.identifier.citationZhang, Y. 1998. Bioprosthetic heart valves : ultrastructure and calcification. University of Cape Town.en_ZA
dc.identifier.ris TY - Thesis / Dissertation AU - Zhang, Yinxing AB - Background: Due to the geographic distance between abattoirs and commercial valve plants delays between harvest and fixation usually range from 48 to 72 hours. In order to assess the pre-fixation tissue damage arising from the hypoxic period and the resulting calcific degeneration after implantation, we used an ultrastructural damage score and transmission electron microscopy. Materials and Methods: In a step by step manner, three major issues were clarified: 1) The degree of pre-fixation tissue damage was determined in the four most widely used commercially produced tissue heart valves. Since stentless bioprostheses represent the latest promising trend in the development of biological heart valves, stentless models of the following makes were compared: Baxter, Medtronic, St. Jude and Biocor. Due to the fact that the aortic wall component of these valves proved most resistant to all anticalcification treatments, aortic wall tissue stood in the centre of our analyses. 2) Subsequently, three main determinants of the fixation process namely: delay, temperature and fixative-concentration were varied with the goal of significantly improving the ultrastructural preservation of the bioprosthetic tissue. 3) Eventually, the influence of improved ultrastructural preservation on calcific degeneration was evaluated under in vivo conditions in the non-human primate and the rat model. Results: The comparison of the four most commonly used stentless bioprosthetic heart valves revealed a disturbing degree of tissue damage in all valves. Using a damage score from 1 to 21 (21 being the worst), aortic wall tissue of commercial valves ranged from 10 to 18 and that of leaflet tissue from 12 to 20. When fixation conditions were permutated, tissue damage could almost be abolished by immediate fixation (within 30 minutes of slaughter), low-temperature fixation(4°C) and high glutaraldehyde concentrations (> 1 %). Our in vivo experiments confirmed that commercially used fixation (delayed fixation, room-temperature and I ow concentrations of glutaraldehyde) with its concomitant high degree of tissue damage results in high levels of calcification. Apart from a distinctly improved calcification potential in ultrastructurally well preserved tissue, there was also an inverse correlation between tissue calcification and the concentration of glutaraldehyde used for fixation. Conclusion: We could demonstrate that commercially produced bioprosthetic heart valves uniformly show badly damaged tissue and that tissue damage contributes to the calcific degeneration of these valves. We were also able to determine ideal fixation conditions which in turn significantly reduced tissue calcification. DA - 1998 DB - OpenUCT DP - University of Cape Town LK - https://open.uct.ac.za PB - University of Cape Town PY - 1998 T1 - Bioprosthetic heart valves : ultrastructure and calcification TI - Bioprosthetic heart valves : ultrastructure and calcification UR - http://hdl.handle.net/11427/26921 ER - en_ZA
dc.identifier.urihttp://hdl.handle.net/11427/26921
dc.identifier.vancouvercitationZhang Y. Bioprosthetic heart valves : ultrastructure and calcification. [Thesis]. University of Cape Town ,Faculty of Health Sciences ,Division of Cardiology, 1998 [cited yyyy month dd]. Available from: http://hdl.handle.net/11427/26921en_ZA
dc.language.isoengen_ZA
dc.publisher.departmentDivision of Cardiologyen_ZA
dc.publisher.facultyFaculty of Health Sciencesen_ZA
dc.publisher.institutionUniversity of Cape Town
dc.subject.otherCardiovascular Researchen_ZA
dc.titleBioprosthetic heart valves : ultrastructure and calcificationen_ZA
dc.typeMaster Thesis
dc.type.qualificationlevelMasters
dc.type.qualificationnameMSc (Med)en_ZA
uct.type.filetypeText
uct.type.filetypeImage
uct.type.publicationResearchen_ZA
uct.type.resourceThesisen_ZA
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