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      Valved Conduit with Glutaraldehyde-Fixed Bovine Pericardium Treated by Anticalcification Protocol

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          A preclinical study was conducted for evaluating a valved conduit manufactured with a glutaraldehyde (GA)-fixed bovine pericardium treated using an anticalcification protocol.


          Bovine pericardia were decellularized, fixed with GA in an organic solvent, and detoxified. We prepared a valved conduit using these bovine pericardia and a specially designed mold. The valved conduit was placed under in vitro circulation by using a mock circulation model, and the durability under mechanical stress was evaluated for 2 months. The valved conduit was implanted into the right ventricular outflow tract of a goat, and the hemodynamic, radiologic, histopathologic, and biochemical results were obtained for 6 months after the implantation.


          The in vitro mock circulation demonstrated that valve motion was good and that the valved conduit had good gross and microscopic findings. The evaluation of echocardiography and cardiac catheterization demonstrated the good hemodynamic status and function of the pulmonary xenograft valve 6 months after the implantation. According to specimen radiography and a histopathologic examination, the durability of the xenografts was well preserved without calcification at 6 months after the implantation. The calcium and inorganic phosphorus concentrations of the explanted xenografts were low at 6 months after the implantation.


          This study demonstrated that our synergistic employment of multiple anticalcification therapies has promising safety and efficacy in the future clinical study.

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          Most cited references 35

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          Calcification of tissue heart valve substitutes: progress toward understanding and prevention.

          Calcification plays a major role in the failure of bioprosthetic and other tissue heart valve substitutes. Tissue valve calcification is initiated primarily within residual cells that have been devitalized, usually by glutaraldehyde pretreatment. The mechanism involves reaction of calcium-containing extracellular fluid with membrane-associated phosphorus to yield calcium phosphate mineral deposits. Calcification is accelerated by young recipient age, valve factors such as glutaraldehyde fixation, and increased mechanical stress. Recent studies have suggested that pathologic calcification is regulated by inductive and inhibitory factors, similar to the physiologic mineralization of bone. The most promising preventive strategies have included binding of calcification inhibitors to glutaraldehyde fixed tissue, removal or modification of calcifiable components, modification of glutaraldehyde fixation, and use of tissue cross linking agents other than glutaraldehyde. This review summarizes current concepts in the pathophysiology of tissue valve calcification, including emerging concepts of endogenous regulation, progress toward prevention of calcification, and issues related to calcification of the aortic wall of stentless bioprosthetic valves.
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            Prosthetic heart valves.

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              Osteopontin inhibits mineral deposition and promotes regression of ectopic calcification.

              Ectopic calcification, the abnormal calcification of soft tissues, can have severe clinical consequences especially when localized to vital organs such as heart valves, arteries, and kidneys. Recent observations suggest that ectopic calcification, like bone biomineralization, is an actively regulated process. These observations have led a search for molecular determinants of ectopic calcification. A candidate molecule is osteopontin (OPN), a secreted phosphoprotein invariantly associated with both normal and pathological mineral deposits. In the present study, OPN was found to be a natural inhibitor of ectopic calcification in vivo. Glutaraldehyde-fixed aortic valve leaflets showed accelerated and fourfold to fivefold greater calcification after subcutaneous implantation into OPN-null mice compared to wild-type mice. In vitro and in vivo studies suggest that OPN not only inhibits mineral deposition but also actively promotes its dissolution by physically blocking hydroxyapatite crystal growth and inducing expression of carbonic anhydrase II in monocytic cells and promoting acidification of the extracellular milieu. These findings suggest a novel mechanism of OPN action and potential therapeutic approach to the treatment of ectopic calcification.

                Author and article information

                Korean J Thorac Cardiovasc Surg
                Korean J Thorac Cardiovasc Surg
                The Korean Journal of Thoracic and Cardiovascular Surgery
                The Korean Society for Thoracic and Cardiovascular Surgery
                August 2014
                05 August 2014
                : 47
                : 4
                : 333-343
                [1 ]Xenotransplantation Research Center, Seoul National University Hospital Clinical Research Institute
                [2 ]Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, Seoul National University College of Medicine
                [3 ]Department of Pediatrics, Seoul National University Hospital, Seoul National University College of Medicine
                Author notes
                Corresponding author: Yong Jin Kim, Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Korea, (Tel) 82-2-2072-3638 (Fax) 82-2-745-5209 (E-mail) kyj@
                Copyright © 2014 by The Korean Society for Thoracic and Cardiovascular Surgery. All rights Reserved.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Basic Research


                calcification, heart valves, bioprosthesis, bioengineering, biomaterials, xenograft


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