title: Pathology of substitute heart valves: new concepts and developments.
abstract: All types of contemporary cardiac valve substitutes suffer deficiencies and complications that limit their success. Mechanical and bioprosthetic valves are intrinsically obstructive, especially in small sizes. Mechanical valves are associated with thromboembolic problems; the chronic anticoagulation used in virtually all mechanical valve recipients causes hemorrhage in some. Calcification limits the success of porcine and pericardial bioprostheses, allograft valves, and the yet experimental trileaflet polymeric prostheses. The predominant mechanism of calcification in porcine, pericardial, and allograft valves is cell mediated, being nucleated at the membranes and in organelles of the transplanted cells. In polymeric leaflet valves, calcification is both extrinsic (in adherent thrombus) and intrinsic (subsurface and acellular in the solid elastomer). Nevertheless, except for a few notable exceptions, contemporary mechanical valves are durable. Other important potential complications of prosthetic and bioprosthetic valves include paravalvular leak, endocarditis, or extrinsic interference with function. Moreover, aortic valvular allografts undergo progressive noncalcific degeneration, tearing, sagging, and/or retraction. Studies of retrieved long-term cryopreserved allograft explants demonstrate severe degeneration, with distortion of normal architectural detail, loss of endothelial and deep connective tissue cells, and variable inflammatory cellularity. Thus, they are morphologically nonviable valves, whose structural basis for function seems primarily related to the largely preserved collagen, and they are unlikely to have the capacity to grow, remodel, or exhibit active metabolic functions. Since calcification intrinsic to the cusps is the major pathologic process necessitating bioprosthetic valve reoperations, efforts to prevent formation of mineral deposits are active.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pathology, Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts 02115.
authors.forename: F J
authors.initials: FJ
authors.lastname: Schoen
authors.forename: R J
authors.initials: RJ
authors.lastname: Levy
mesh_terms: D001705:Bioprosthesis / Q000009:adverse effects; D002114:Calcinosis / Q000517:prevention & control; D006350:Heart Valve Prosthesis / Q000009:adverse effects; D006351:Heart Valves / Q000473:pathology / Q000637:transplantation*; D006801:Humans; D011474:Prosthesis Design; D011475:Prosthesis Failure; D014184:Transplantation, Homologous / Q000009:adverse effects