Ann Thorac Surg 2002;73:343-344
© 2002 The Society of Thoracic Surgeons
a Department of Cardiovascular Diseases, King Faisal Specialist Hospital and Research Centre, MBC 16, P.O. Box 3354, Riyadh 11211, Saudi Arabia
To the Editor
With great interest, I read the article by Ehud Raanani and associates . In this article, the authors touch on two major issues. The first is the specific issue of the fate of the pulmonary homograft in the pulmonary position after the Ross procedure. The second is trying to identify predictors of late pulmonary homograft stenosis, which is a more general issue.
I agree with the authors that pulmonary homograft stenosis does exist following the Ross procedure. However, I do not feel that it represents a significant clinical problem. In our own experience of 292 Ross procedures, only 6 patients required surgical intervention for pulmonary stenosis (2%). This goes along with the authors own experience of 1 patient requiring change of the homograft twice; 6 other patients were balloon dilated, with 5 "moderate" reductions in gradient and 1 failure that subsequently required surgery.
Looking at this problem, I and my colleagues specifically studied 233 patients with detailed echocardiography. We found 28 patients (12%) with gradients greater than 40 mm Hg; those who required reoperation or balloon intervention were from this group, except for 1 patient who needed a tricuspid valve repair and, at surgery, was determined to have significant pulmonary stenosis. Very few patients developed electrocardiographic signs of right ventricular hypertrophy, dilation, or systolic dysfunction. What the authors reported about the stenosis being diffuse, rather than discrete, in the whole length of the homograft with calcification, is consistent with our findings. However, we have few patients with additional PR.
Our surgical approach has been to augment the area of pulmonary stenosis with a transannular bovine pericardial patch, which has been very successful thus far. We believe the PR will be well tolerated. The reason for this is our belief that these patients are already at a disadvantage, the most likely reason for development of the stenosis is immunologic, and that a second homograft will probably have the same fate.
As regards the second issue of risk factors for developing pulmonary stenosis, we believe that this is a complex issue since there are many variables that can enter the equation. The authors attempt to identify predictors is commendable, but I doubt that the findings will be of any clinical significance. For example, we use some fresh antibiotic preserved homografts and, to us, it seemed that this can be a risk factor for pulmonary stenosis. However, we did not see this when we looked at these same homografts being used in right-sided reconstruction in congenital heart disease. Our own bias is towards immunologic process and, as was eluded to, there is emerging evidence in the literature now supporting that concept to a certain extent. Anecdotally, we give our pediatric patients a small dose of 1 mg/kg body weight of cyclosporin hoping to halt this process. Our impression, and it is only an impression, is that it might be making a difference.
In conclusion, pulmonary stenosis after the Ross procedure is a frequent echocardiographic finding but of little clinical significance. One should not rush and intervene in those patients since this lesion can be tolerated for a long time and, actually, in many patients, is not progressive. Looking at right ventricular hypertrophy, ventricular dilatation and function is important in the decision for intervention. Exercise testing can help make that decision in borderline cases.
This article has been cited by other articles:
F. X. Schmid, A. Keyser, C. Wiesenack, S. Holmer, and D. E. Birnbaum
Stentless xenografts and homografts for right ventricular outflow tract reconstruction during the ross operation
Ann. Thorac. Surg., September 1, 2002; 74(3): 684 - 688.
[Abstract] [Full Text] [PDF]
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