Ann Thorac Surg 2001;71:59-60
© 2001 The Society of Thoracic Surgeons
Invited commentary: original article: cardiovascular
Invited commentary
David R. Clarke, MDa
a Cardiothoracic Surgery, The Children’s Hospital, 1056 E 19th Ave, Box B-200, Denver, CO 80218, USA
e-mail: clarke.david{at}tchden.org
This article by Forbess and colleagues provides an accurate description of the fate of patients who receive homograft valve conduits to reconstruct the right ventricular outflow tract. However, the authors’ evaluation of the presented data limits the reader’s ability to understand the mechanisms responsible for failure. Defining homograft failure as reoperation for homograft replacement or patient death introduces an endpoint not always related to problems with the graft. This is particularly true in the case of complex repairs in infants. Also, the fact that no homograft was replaced for isolated regurgitation might indicate that follow up was not long enough for patients to exhibit secondary signs of right ventricular failure. This could easily bias the data by increasing the relative importance of homograft size and growth rate as risk factors.
Although the statistical methods used in this study appear valid, one can’t help but wonder if the identification of homograft size as the only significant risk factor in the multivariate analysis doesn’t represent an over simplification. In group 1 patients who are less than 1 year old at surgery, why do some failures occur at a few months, another cohort fail at about 3 years, and several are still free from failure at five years postoperatively? Could it be that this is all accounted for by various sizes (6 mm to 17 mm range) implanted in various infants or is it just as likely that early failure is mostly patient mortality, 3 year failure is active immune mediated degeneration leading to a shrunken, fibrocalcific, tubular graft, and later failure is primarily growth related with a relatively stable valved conduit? If this logic is applied to groups 2 and 3, it makes sense that mortality within the first few months after surgery becomes much less likely in the older age groups and that active immune mediated degeneration might be somewhat less aggressive leading to a more gentle slope on the failure curve.
The difference in survival between aortic and pulmonary homografts in the entire group was not supported by data from the groups less than 10 years of age at operation and is not reported for group 1 alone. This is difficult to interpret because of the large number of pulmonary and small number of aortic grafts, particularly in group 3 where the ratio was 82:4 respectively. It is interesting however, that aortic survival is 100 percent at two years follow up. Could this be secondary to less regurgitation and better cardiac output particularly in complex infants where pulmonary vascular resistance is often elevated?
Although this is a well done study and provides some useful general information concerning the fate of patients who receive cryopreserved homografts to reconstruct the right ventricular outflow tract, the conclusions might over simplify the problem. One must remember these grafts contain viable cells at implantation and thus must be considered "transplants". Is it possible that a few of these patients might be lucky enough to have a continuously viable and growing valved conduit? Would immunosuppressive therapy increase homograft survival? These are questions that must be considered.
Related Article
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Cryopreserved homografts in the pulmonary position: determinants of durability
- Joseph M. Forbess, Ashish S. Shah, James D. St. Louis, James J. Jaggers, and Ross M. Ungerleider
Ann. Thorac. Surg. 2001 71: 54-59.
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