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J Thorac Cardiovasc Surg 1994;108:988-990
© 1994 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Surgery
University of Alabama at Birmingham
Birmingham, AL 35294-0007
To the Editor:
The usefulness of allograft aortic and pulmonary valves in the surgical management of aortic valve and aortic root disease, as well as for correction of complex congenital heart disease, is undeniable As well as an ongoing evolution in the technique of allograft valve insertion to accommodate all types of aortic valve and aortic root disease, there has been considerable focus on biologic characteristics of valve leaflets. Of particular interest has been the investigation of allograft leaflet viability and how this may be associated with valve durability. This has resulted in the incorporation of words such as viable, nonviable, and allovitalallograft valves into the allograft lexicon reflecting the putative nexus between viability and durability.
The article by Lupinetti and colleagues
1 has convincingly demonstrated the loss of endothelial cells from human allograft aortic and pulmonary valve leaflets. In their letter to the Editor, Mohan and colleagues 2 vigorously argue that with their "better" [sic] cryopreservation, loss of endothelial cells is neither inevitable nor desirable. How important, then, are endothelial cell viability and for that matter fibroblast viability? This discussion will focus on two important and topical aspects of the allograft valve—valve failure and valve viability.
The usual view of allograft valve failure is of the development of progressive aortic regurgitation resulting from the mutually exclusive mechanisms of geometric distortion, leaflet degeneration, and progressive aortic root dilatation. However, the end points of reoperationand development of progressive aortic regurgitation(so-called assumed leaflet failure) are insensitive methods of determining the mechanism of allograft valve failure. Furthermore, when allograft valves are being compared, attempting to find common unifying theories to explain differences in durability, such as leaflet viability or insertion technique, ignores the complex way in which allograft valves may fail.
Allograft valve endocarditis and paravalvular leak are uncommon occurrences and, although they may result in aortic regurgitation that may be progressive and severe enough to necessitate reoperation, they will not be considered as mechanisms of allograft valve failure.
There are a number of important mechanisms of allograft valve failure, and of equal importance is the way in which these mechanisms may interact.
The elegant mathematical modeling by Christie and Barratt-Boyes, 3 which demonstrates the progressive development of aortic regurgitation after insertion of an allograft as a result of the changing mechanical properties of the leaflets over time (loss of leaflet extensibility in the radial direction), provides cogent evidence for an important mechanism of allograft valve failure. This loss of allograft leaflet radial extensibility is in fact an exaggeration of the normal change in the mechanical properties of leaflet tissue resulting from the aging process. Although this modeling was performed by incorporating the mechanical properties derived from antibiotic-sterilized leaflet tissue, I believe that the finding of progressive loss of leaflet coaption caused by reduction of radial extensibility is a feature observed in explanted cryopreserved allograft leaflets.
Cryopreserved valves may also fail uncommonly as the result of a degenerative processof the leaflets characterized by leaflet thinning, tearing, and perforation. 4 Also, leaflet calcification may occur. 5 Both these features (especially leaflet perforation and tearing) were prominent mechanisms of failure of the now obsolete chemically and irradiated allograft valves. 6
Geometric distortionafter insertion of an allograft valve is an important mechanism of valve failure. Although the subcoronary technique has been the traditional method of insertion, there are concerns that distortion and progressive regurgitation may be more likely with this technique than with the cylindrical or aortic root replacement technique. 7-9
Allograft valves may fail as the result of progressive dilatation of the aortic root, and this has been reflected in the finding by multivariable analysis of larger aortic root size as a risk factor for the development of aortic regurgitation. 10
It should be intuitive that these mechanisms of allograft valve failure are interrelated and are influenced by a number of known risk factors for allograft valve failure. Perhaps then a less compartmentalized view of allograft valve failure is required to incorporate these interrelationships.
Fig. 1 represents an attempt to portray the interrelationship between these mechanisms of allograft failure and risk factors. For example, older donor age 11 as a risk factor for allograft valve failure may be explained by preimplantation loss of radial extensibility. If this older donor valve was implanted by a subcoronary rather than a cylindrical technique, then any geometric distortion, exacerbated by further loss of radial extensibility, may quite significantly reduce the likelihood of adequate long-term leaflet coaption. It is not difficult to imagine other combinations of mechanisms of valve failure and risk factors. The point to be made is that allograft valve failure is complex and multifactorial and not amenable to oversimplified explanations such as presence or absence of viable leaflet cells or the type of insertion technique.
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12 and the demonstration that these autograft leaflets can grow 13 does suggest that autogenous valve tissue with intact endothelial and fibroblast cells has distinct advantages over allograft valve tissue. But as far as allograft valve tissue is concerned, the use of the appellation viableis conjectural. The demonstration that fibroblasts of homogenized recently cryopreserved aortic valve tissue can incorporate tritiated glycine into collagen 14 does not necessarily translate into the long-term postimplantation ability to repair leaflet wear and tear injury, which is implied by the term viable. Although persistence of donor fibroblasts has been demonstrated, 11 the histologic picture of explanted cryopreserved allografts (including allografts explanted for reasons other than degeneration) is one of acellularity or patchy cellularity and rare cellular leaflets. 15,16
Perhaps the disappearance of these cells is related to a possible immunologic response together with damage caused by ischemic injury after procurement 17 and cryopreservation. However, given the other important mechanical ways in which allograft valves may fail, the presence or absence of a few surviving fibroblast cells long term after implantation is likely to be of little importance. From time to time, mention is made, in passing, of treating allograft valve recipients with immunosuppressants on the basis of the unproved hypothesis that valve viability will substantially improve durability. If the need to avoid the disadvantages and potential complications of anticoagulation is an indication for use of an allograft valve, it is hard to see how immunosuppression could be any less of a potential risk than anticoagulation.
Although dissecting out precise mechanisms of valve failure may be difficult for the reasons previously outlined, there is some evidence that cryopreservation is currently the best method of storing allograft valves. However, the reasons probably have more to do with preventing matrix damage by, for example, minimizing autolytic processes than by preservation of viability.
As far as endothelial cell viability of the allograft valve is concerned, its role in valve durability is at least as uncertain as that of fibroblast viability. An equally plausible argument could be made for the benefits of retention of the endothelium (minimizing host blood cell attachment and perhaps injury to the matrix) as opposed to the disadvantages of the retention of the endothelium (augmentation of the host immune response).
Despite all the variables associated with allograft valve failure, Mohan and colleagues 2 have identified maintenance of endothelial cell viability as a particularly important goal, and worthy of a categorical letter to the Editor. Unfortunately, there is currently no clinical information to support this position. Using the occurrence of "accelerated thrombosis, calcification, and infection of commercial bioprosthetic valves" 2 that are without an endothelial lining as justification for preserving the endothelium of allografts is not sufficient.
I would be disappointed if this discussion was construed as deprecatory of investigations into the biology of allograft valves. However, I do believe that the enthusiasm for valve viability should be considered in the overall context of allograft valve failure.
References
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