| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||
Ann Thorac Surg 1996;62:1283
© 1996 The Society of Thoracic Surgeons
DR CARLO MARCELLETTI (Rome, Italy): I enjoyed this presentation very much; I think it brought an important message. I would like to add our experience to yours.
We talk about late failure differently from acute failure. In 6 of our patients, the Fontan had to be revised several years after the operation. Four patients had received an atrial pulmonary anastomosis, and 2 patients had had an atrial ventricular anastomosis. The symptoms were congestive heart failure in all of them. Three patients presented with life-threatening supraventricular arrhythmias and 2 patients with recurrent cyanosis. Our results are comparable with those presented by Dr Hanley, and we fully agree with the rationale that reduced atrial distention, reduced pressure within the coronary sinus, and an optimal pulmonary blood flow pattern within the connection are major factors in correcting the symptoms.
DR JOHN L. MYERS (Pittsburgh, PA): We have had a similar group of 7 patients with a mean age of 18 years (range, 6.9 to 31 years). The interval since the Fontan operation was 4.6 to 10.3 years (mean, 7.2 years). The mean postoperative length of stay was 8 days. The mean follow-up time is 26 months (range, 10 to 32 months). There is one feature about these patients that I would like to address. The markedly enlarged right atrium expands not only anteriorly and laterally, but also posteriorly, compressing the right pulmonary veins and also displacing the atrial septum leftward, reducing the left atrial cavity size. The conversion technique (to a total cavopulmonary connection) that we have used is very similar to what you and Dr Marcelletti have presented. It decompresses the right atrium by routing the blood from the inferior vena cava and the superior vena cava directly into the pulmonary arteries by means of a lateral baffle or tube graft. The atrial septum is excised. This decompression relieves the right pulmonary venous obstruction. The left atrial volume size is increased; therefore, there is a more compliant left atrial receiving chamber. We have been very pleased with our results. There have been no operative or late deaths. There was improvement in the New York Heart Association class in all of our patients, 2 of whom in class IV were actually referred for cardiac transplantation. Three patients improved from class II to class I, 1 patient from class III to class I, 1 patient from class IV to class II, and 2 patients from class IV to class II.
In your group of patients, you listed right pulmonary venous obstruction as one of the indications. My question for you is whether in fact you saw this in other patients, perhaps to a lesser degree. We believe that this is not an uncommon problem and is often not recognized in patients with the long-term atriopulmonary Fontan circulation.
DR HANLEY: Thank you. It is interesting to note that all three of the experiences mentioned here in discussion are very consistent.
To answer your question regarding pulmonary veins, yes, I believe that most patients with giant right atria have distorted right pulmonary veins if you look carefully. I listed only the 1 patient who had an actual hemodynamic pressure drop across his veins, which represents a severe degree of obstruction. There is a compensatory mechanism that prevents measurement of the hemodynamic pressure gradient across the veins until at a very late stage. As the pulmonary veins narrow, resistance changes cause a shift of blood toward the left lung and a reduction of flow to the right lung. The reduced flow does not allow detection of the obvious pressure gradient, which would be present if flow to the right lung were fixed. As a result, it may be very difficult to detect an obstruction until it is severe. The more subtle finding of the ribbon-like pulmonary veins behind the atrium is probably an important observation. I tend to agree with you that one does not need to prove hemodynamically that there is a gradient for the patient to gain improvement by reducing the right atrial size.
DR JACQUES A. van SON (Leipzig, Germany): This was an excellent presentation. My experience in this area consists of four conversions to an extracardiac conduit. As in your experience, the only patient who died had protein-losing enteropathy with extensive intestinal lymphangiectasis secondary to a 3-mm gradient across an atriopulmonary anastomosis. In fact, the conversion operation seemed to exacerbate the enteropathy despite the absence of any pressure gradient in the systemic venous conduit. I believe that the role of conversion in this subset of patients needs to be defined further. Would you still perform this operation in this subset of patients? And also, was the intracardiac tunnel in your series a classic lateral tunnel or a tube graft?
DR HANLEY: I think we have to be cautious in performing the Fontan revision in the group that is highly debilitated. They simply may not tolerate the insult of the operation itself. The experience, however, is very limited, essentially anecdotal, and I am not yet prepared to say that all patients in this category either should or should not undergo revision. The intracardiac tunnels were tube grafts in both cases.
Related Article
Ann. Thorac. Surg. 1996 62: 1276-1282.
| ||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
