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(Circulation. 2006;114:261-264.)
© 2006 American Heart Association, Inc.

Editorial

Bioprosthetic Valves and Laudable Inflammation?

Richard A. Hopkins, MD

From the Department of Cardiothoracic Surgery, Brown University and Rhode Island Hospital, Providence.

Correspondence to Richard Hopkins, MD, Karlson Professor and Chief Cardiothoracic Surgery, Brown University Medical School, Rhode Island Hospital, 2 Dudley St, MOC #500, Providence, RI 02905. E-mail rahopkins@lifespan.org

Key Words: Editorials • inflammation • prosthesis • tissue • transplantation • valves

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In this issue of Circulation, Dr Manji and colleagues¹ from the University of Alberta (Canada) report a series of animal experiments designed to test the mythic role of gluteraldehyde in preventing recognition of bioprosthetic heart valve antigenicity with subsequent rejection and failure. Gluteraldehyde–cross-linked xenograft tissues (initially porcine) have been used in the manufacturing of stented (and now stentless) heart valves since 1970. Original theories for the clinical efficacy of gluteraldehyde were based on its ability to irreversibly cross-link collagen and thus to increase mechanical strength and durability over fresh untanned cardiovascular tissues. Porcine valve leaflets, bovine pericardium, equine pericardium, and bovine jugular vein, among other structures, have been treated this way for clinical applications. Since its introduction, however, limitations and unexpected consequences of gluteraldehyde and similar chemical treatments have been recognized clinically. As pointed out by the authors, durability is quite variable, tending to be better in older patients whereas younger patients suffer early deterioration, calcification, and fibrocalcific failure.^2,3 The good news has been that the failures tend to be progressive rather than catastrophic, leading to semielective reoperations. Additionally, the xenograft bioprostheses have been extremely helpful in avoiding warfarin in the very young and the very old, reducing the risk of thromboembolism. The traditional explanation for the fibrocalcific degeneration of the nonvital gluteraldehyde-treated bioprosthetic heart valves has been a combination of physical and chemical effects leading to calcification and a fixation of the structural proteins that prevent protein recycling and renewal. Mechanical theories of fatigue-induced wear resulting in calcification . . . [Full Text of this Article]

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