Abstract

Porcine bioprosthetic valves are commonly used to replace the native cardiac valves when they become diseased and dysfunctional. One class of bioprosthesis consists of whole pig aortic valves, tanned in glutaraldehyde and mounted on plastic or wire frames. These devices work very well in the short term (< 5 years) but eventually begin to fail gradually and typically do not last more than 15 years [1]. Many have tried to elucidate a mechanism of bioprosthetic valve failure, but little progress has been made, until recently. Historically, calcification has been thought to be the primary mechanism of bioprosthetic valve failure [2]. Recently, however, it has become recognized that mechanical damage to bioprosthetic valves can occur independently from calcification [3]. This shift in opinion has been supported by a number of observations. For example, Purinya et. al. [4] have shown that after four years of implantation, bioprosthetic valve explants have lower failure stresses and fail at greater strains than fresh porcine bioprostheses. Similar observations have been made in valves fatigued in vitro [5]. Others have shown that these mechanical changes are accompanied by biochemical changes in the collagen fibers [6]. We have shown previously in preliminary studies that glycosaminoglycans (GAGs) are lost from implanted bioprosthetic valves [7]. Since GAGs are responsible for maintaining tissue viscoelasticity, loss of GAGs would have detrimental effects on tissue mechanics. In separate studies, we have demonstrated that damage to elastin can also have detrimental effects on tissue mechanics, and on valve durability as a whole [8].

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