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J Thorac Cardiovasc Surg 2007;133:1342-1343
© 2007 The American Association for Thoracic Surgery
Surgery for Congenital Heart Disease |
First, in the patients who required more than one PTFE monocusp valve, what was the cause of failure and the median and mean time to replacement? In addition, how did you choose in this group of patients whether they would have repeat PTFE monocusp valve replacement versus an RV-PA conduit?
Second, 15% of the patients had implantation of the PTFE monocusp after RV-PA conduit. Oftentimes when homograft conduits fail, they exhibit shrinkage and calcification. Your own data suggested that there was a mean gradient of 78 mm Hg in these gradients consistent with shrinkage, calcification, or outgrowth. How did you decide which patients with previous artery to PA conduits would benefit from a PTFE monocusp valve in this group?
Third, in your slide listing indications for PTFE monocusp redo, you listed 10 patients with trace-to-mild PI as the reason. Many of the valved conduits that we use have trace-to-mild PI immediately after they are placed and the chest is closed. Why would trace-to-mild PI of the PTFE monocusp or any other valve other than for the reason of infection ever be an indication for redo?
Dr Brown. Thank you, Dr Cohen. Those are all excellent questions. To answer your first question, in patients who underwent more than one PTFE monocusp, the cause of failure in almost all situations, as pointed out in the curves, was PI. Only a handful of patients had stenosis.
The second part of that is, how did you choose in which patients you would repeat a PTFE monocusp and in which ones would you use a conduit? To answer that question, if they previously had a conduit, we were not going to put in a second homograft conduit because we know a second homograft conduit fails faster than the first one. Therefore, if a patient had a failed conduit we would put in a PTFE monocusp and then roof that over with another PTFE patch. That is how we decided. However, after 2001, when the Contegra conduit came along, we had a choice of either doing a PTFE monocusp reconstruction of that RVOT or putting in a Contegra conduit. I have to admit our results with the Contegra conduit look pretty promising thus far, and we are leaning in that direction in those whose initial repairs have failed.
To answer your second question, in the 15% of patients who had PTFE monocusp after RVOT conduits, the answer is almost the same. We continue to try to use the PTFE monocusp in patients in whom it makes sense, but when we have a conduit now that is as good as the Contegra conduit, we are inclined to use more Contegras when a reoperation is necessary. We usually reserve the PTFE monocusp for primary repairs.
Finally, you are absolutely right about the patients with trace PI. That is never an indication for replacement of a conduit or a reconstruction of the RVOT. We just listed those in the slide. Those were the few patients who had significant stenosis. They also had mild PI, but we listed those diagnoses separately. We did not reoperate on patients with trace PI because we know that almost all pulmonary valves, pulmonary conduits, have some leakage early in the postoperative period.
DOCTOR. I would like your comment on a couple issues. Obviously, this is a big issue for congenital heart surgeons. We are replacing the RVOT weekly in our patients. The issue that I have seen, though, is that over the past few years our indications for reinterventions seemed to be changed. Can you comment about that over the time frame of your study?
Second, we are on the verge of these readily deployable percutaneous valve replacements that are probably going to be most successful in the pulmonary outflow tract first before they are deployed in other regions. Does that influence your current reconstruction? In other words, if a 20-year-old patient is referred to you, what kind of valve replacement do you do so that he or she can be set up for subsequent percutaneous valve replacements?
Dr Brown. Those are both excellent questions. First of all, the way we are deciding to intervene has to do with magnetic resonance imaging. We are studying all of our patients who have dilated RVs with magnetic resonance images, comparing the end-diastolic volumes of the RV with the LV. Right now we are using the Emory formula. If the RV volume is twice that of the LV, we know it is time to intervene even though the patient is asymptomatic because atrial arrhythmias are likely to develop shortly after those ventricles begin to dilate more than that and significant tricuspid insufficiency is likely to occur. We would like to try to intervene before they get those arrhythmias or the tricuspid valve begins to fail. We are doing more RVOT reconstructions than we have ever done in the past and we, like you, are doing them weekly.
Percutaneous pulmonary valves are available in Europe now. More than 110 have been used in London. Yes, we would prefer to put a nonstented valve in the pulmonary position initially because that will make it easier for a stent-deployed valve later on. We are using more stentless valves in the adult patient population. I think there is a little caution here, though, that at least the Contegra conduit is what they use for the stent-mounted valves for the pulmonary position. At least there are some early data that suggest when those valves are mounted inside a stent they do not last nearly as long as if they were surgically implanted. We are going to have to watch that patient population very closely, because I know that at least 10% of the stent-mounted valves have failed within a 2-year period and we do not see that with a surgically inserted Contegra valve. We will need a little more follow-up.
Related Article
J. Thorac. Cardiovasc. Surg. 2007 133: 1336-1343.
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