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Ann Thorac Surg 1996;62:455
© 1996 The Society of Thoracic Surgeons
DR PAUL L. STELZER (New York, NY): It is an honor to discuss this fine report from Oklahoma, where I had the privilege of scrubbing with Dr Elkins on the very first pulmonary autograft done in this country almost 10 years ago.
Long ago Donald Ross observed that the only two failure modes of the autograft valve were endocarditis and regurgitation, the latter being technical in origin. Doctor Elkins has confirmed these observations and further defined the causes of regurgitation in terms of patient-specific factors. These factors must be addressed at the time of the initial operation. The size of the recipient site relative to the autograft is very important. Major discrepancy or distensibility of either the annulus or the sinotubular ridge can produce regurgitation and must be addressed with appropriate support such as a strip of Teflon felt, with or without tailoring techniques.
Systemic inflammatory disease such as lupus or rheumatic disease can affect the transposed pulmonary valve, resulting in regurgitation. An ill-defined eosinophilic inflammatory root disease that I encountered 5 years ago did the same thing.
The pulmonary valve can also be bicuspid or otherwise unsuitable. One patient with very big, floppy leaflets represents the only technical failure in my series of 78 autografts (all done as total root replacement) over the last 6 years in New York with 167 patient-years of follow-up. When these conditions are encountered, alternatives to the Ross procedure should be considered.
I have two questions. Do right ventricular outflow tract obstructive problems occur only in children with small sizes? Also, because 1 of 4 patients having autograft repairs had to come back for re-replacement, how do you determine which valve can be repaired and which should be replaced?
DR ELKINS: In terms of the echocardiographic evaluation of the pulmonary valve, this clearly is a technique that is learned by the echocardiographer who is interested in the surgical care of these patients. For instance, we have one echocardiographer who works primarily at our adult hospital; using transesophageal echocardiography at the operation, he has been very successful in (1) delineating whether or not we are dealing with a three-leaflet pulmonary valve and (2) identifying whether there is any abnormality that would identify or suggest that you should not use the pulmonary valve. That has taken a lot of interest and a lot of close personal association between the two of us because we are very interested in this group of patients. I think the average echocardiographer can provide you very little information about the pulmonary valve because it is difficult to look at with either transthoracic or transesophageal technique.
In terms of the failure of the pulmonary homograft reconstruction, there has been absolutely no relationship in our series between age and requirement for replacement. Certainly in the series of patients reported from the Mayo Clinic and the series of patients reported from David Clarke's group in Colorado, age has been a significant factor in accelerated degeneration of the pulmonary homograft used for right ventricular outflow tract reconstruction. All occurred before 1 year of age. This has not been true of the people who have had pulmonary autografts. And I know of at least 10 or 15 surgeons across the country who have a sizable experience with pulmonary autografts and have had similar experience to ours.
In our patients we have replaced all of the failed pulmonary homografts. One patient had a patch angioplasty done at his home institution; however, this lasted for about 3 years and required re-replacement at that time. And as I mentioned, our 6 patients who have had replacement of their pulmonary homograft have all had satisfactory results except for 1.
Related Article
Ann. Thorac. Surg. 1996 62: 450-455.
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