Frederick J. Schoen, MD, PhD, Robert J. Levy, MD

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Calcification of Tissue Heart Valve Substitutes: Progress Toward Understanding and Prevention Frederick J. Schoen, MD, PhD, Robert J. Levy, MD The Annals of Thoracic Surgery Volume 79, Issue 3, Pages 1072-1080 (March 2005) DOI: 10.1016/j.athoracsur.2004.06.033 Copyright © 2005 The Society of Thoracic Surgeons Terms and Conditions

Fig 1 Extended hypothetical model for the calcification of bioprosthetic tissue. This model considers host factors, implant factors, and mechanical damage and relates initial sites of mineral nucleation to increased intracellular calcium in residual cells and cell fragments in bioprosthetic tissue. The ultimate result of calcification is valve failure, with tearing or stenosis. The key contributory role of existing phosphorus in membrane phospholipids and nucleic acids in determining the initial sites of crystal nucleation is emphasized, and a possible role for the independent mineralization of collagen is acknowledged. Mechanical deformation probably accelerates to both nucleation and growth of calcific crystals. Modified by permission from Schoen FJ: Interventional and surgical cardiovascular pathology: clinical correlations and basic principles. Philadelphia: WB Saunders, 1989. The Annals of Thoracic Surgery 2005 79, 1072-1080DOI: (10.1016/j.athoracsur.2004.06.033) Copyright © 2005 The Society of Thoracic Surgeons Terms and Conditions