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Ann Thorac Surg 1997;64:29
© 1997 The Society of Thoracic Surgeons
DR JOHN H. CALHOON (San Antonio, TX): That was a beautiful study, Dr Cope. You and Dr Kron have tried to answer a question we are all interested in. I would like to know why you would ligate the VV as you begin cooling as opposed to waiting until the end of the procedure?
I also would like to know whether you think it is really fair to compare mortality from the era before blood cardioplegia, and possibly from a different group of surgeons, to mortality at this point?
Nonetheless, this was a beautiful study that was presented very succinctly and nicely. Thank you.
DR CONSTANTINE MAVROUDIS (Chicago, IL): This is a nicely presented paper. I have a few questions. Were you able to identify any risk factors for the early group of patients, such as the type of cardioplegia or the conduct of cardiopulmonary bypass? Also, because some patients underwent cardiac catheterization, was there an adverse effect of preoperative cardiac catheterization on outcome? Do you have any experience using inhaled nitric oxide for these patients?
Leaving the VV open probably is a reasonable idea; however, I am not sure that this is the explanation for the better clinical results in the latter group of patients. You have shown that the VV closes spontaneously in all cases. What do you think is the mechanism of closure? Do you think that there might be ductal tissue within the VV?
DR JOHN W. HAMMON, JR (Winston-Salem, NC): Doctor Cope, that was a really good paper. I personally share your biases in the sense that I believe that in patients in whom the VV descends below the diaphragm, the anastomosis is really much easier to do when the VV is left intact. I believe as much as anything that it makes a better technical performance of the operation feasible.
John Kirklin put catheters in the left atrium in a number of patients in whom he left the VV intact, and in a few in whom he ligated it, and it did not produce any changes in the left atrial pressure after operation. So I am not sure that you can use the volume rationale for doing it, but I think it certainly does make the technical performance of the operation better, and you are to be commended for your excellent results.
DR COPE: I thank the three discussants. Those were all very insightful questions and comments.
Doctor Calhoon asks why we dissected and ligated the VV during the cooling phase. It can be done either during that phase or at the completion of the operation. You could argue that it is a time-saving issue to dissect and ligate the VV during the cooling period, and I do not know of any untoward sequelae or benefits to doing it either during cooling or at the completion of the procedure.
Second, Dr Calhoon asked about any issues in this study, such as the time factor, that may have affected mortality. We actually admit in the manuscript that it was a 21-year series and there may have been other factors affecting the improved mortality in more recent years of the study, such as advances in cardiac anesthesia or the use of blood cardioplegia. In terms of the latter, blood cardioplegia was used only for the last 6 cases of this series and most repairs actually were done using cold crystalloid cardioplegia for myocardial protection.
The other thing that changed during the series was the type of suture material used for the anastomosis. Before 1985, we used 5-0 or 6-0 polypropylene, usually in a continuous fashion, sometimes running the posterior wall and interrupting the anterior wall to allow for anastomotic growth. However, in 1986 and thereafter, we invariably used 6-0 polydioxanone in the interest of preventing the onset of late anastomotic stricture. One would not think that this would affect early mortality, which is what we are concerned with in this study.
Doctor Mavroudis also asks about any risk factors for increased mortality. In our retrospective review, we were not able to identify any other risk factors that we definitely could say would correlate with increased early mortality.
Cardiac catheterization was used to confirm any questionable anatomy and to identify or rule out pulmonary venous obstruction before operation. Six patients who did not undergo VV ligation underwent preoperative catheterization as compared with 12 patients who underwent VV ligation. It is true that early in the series there was a higher incidence of preoperative cardiac catheterization before the technology of echocardiography really took off, and most of the repairs done are performed only with preoperative confirmation of the diagnosis by echocardiography.
In terms of the question of whether cardiac catheterization affected mortality, I do not think so, because roughly the same percentage of patients in each group underwent cardiac catheterization.
In terms of the use of inhaled nitric oxide, we have used that therapy after operation in 1 patient who actually ended up having fixed pulmonary hypertension. He was supported on extracorporeal membrane oxygenation for about 21 days after operation, only to succumb to refractory pulmonary hypertension and right heart failure.
Doctor Mavroudis also asked about any other mechanisms for spontaneous VV closure. A study in Circulation in 1967 postulated that the high resistance of the hepatic bed eventually causes complete spontaneous closure of an unligated descending VV.
Finally, Dr Hammon, thank you for your comments. Again, I will reiterate that it is true that it is difficult to compare these groups because of the wide range of years in the study. The only way to prove definitively that there is a survival advantage to leaving the VV patent is through a carefully controlled, prospective study, in which the patients are followed up carefully after operation with echocardiography to evaluate the time course of spontaneous VV closure.
Related Article
Ann. Thorac. Surg. 1997 64: 23-28.
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