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Ann Thorac Surg 2003;76:1383-1388
© 2003 The Society of Thoracic Surgeons
a Division of Cardiovascular Surgery, Keio University, Tokyo, Japan
* Address reprint requests to Dr Aeba, Division of Cardiovascular Surgery, Keio University, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan.
e-mail: aeba{at}sc.itc.keio.ac.jp
Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons in San Diego, CA, Jan 31–Feb 2, 2003.
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Abstract |
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METHODS: Between 1985 and 1990, a nonvalved Dacron woven-fabric graft conduit was placed between the left ventricular apex and pulmonary artery in 5 patients (mean age, 6.2 ± 1.7 years) who were then followed for at least 10 years.
RESULTS: No iatrogenic heart blocks or mitral regurgitation developed. All patients were complaint-free during the follow-up period, although 1 patient who was clinically well died suddenly in the 10th follow-up year. Cardiac catheterization in the 10th follow-up year indicated a pressure gradient of 21 ± 6 mm Hg across the conduit, and angiography revealed that the conduit diameter was 91% ± 6% of the original conduit diameter.
CONCLUSIONS: The reportedly poor early and late outcomes that occur after a conventional repair of congenitally corrected transpositions of the great arteries associated with ventricular septal defect and pulmonary outflow tract obstruction, which places an extracardiac conduit between the left ventricle and the pulmonary artery, may be partially neutralized by relocating the inflow position to the apex.
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Introduction |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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All operations were performed through a midline sternotomy with cardiopulmonary bypass, moderate systemic hypothermia, and cardioplegic heart arrest. All of the VSDs were single and large, located at an inlet position (adjacent to the tricuspid and mitral valves), and committed to the pulmonary valve, which was obstructive. Closure of the VSD was performed through the right atriotomy and mitral valve. An equine pericardial patch was tailored and secured with interrupted polyethylene terephthalate fiber (Dacron) -pledgetted horizontal mattress sutures. At the anterosuperior half of the VSD margin, the stitches were placed through the VSD itself and on the right ventricular side of the VSD crest, as suggested by de Leval and colleagues [12].
The exact attachment of the mitral anterior papillary muscle was identified in the midportion of the anterior free wall by digital manipulation from inside, and a left ventriculotomy was created in the apex to serve as the inflow of the extracardiac conduit. The pulmonary trunk was opened, and the hypoplastic pulmonary valve was either left open or a primary suture-closure was done. A nonvalved Dacron woven fabric graft conduit (Cooley Veri-Soft Vascular Graft; Meadox Medicals, Inc, Oakland, NJ) with a diameter of between 18 and 22 mm was tailored and placed between the left ventricular apex and the pulmonary artery (Fig 1). An interrupted pledgetted mattress suture technique was used for the proximal anastomosis, and an equine pericardial cuff was placed to reinforce the distal anastomosis. The conduit was placed between the right atrium and lateral pericardium, and was separate from the sternum along its entire course. A permanent pacemaker lead was placed in 2 patients for potential future use, but no generators were connected.
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All the data were obtained from retrospective review of patients' hospital and clinical records preoperatively and postoperatively. The ventricular wall motions and the atrioventricular valve competence were assessed from serial echocardiography and the cineangiograms. Late follow-up cardiac catheterization was performed in all patients, with 4 patients catheterized in the 10th follow-up year and 1 patient (patient no. 3) catheterized in the third year. Data are presented as range and mean with standard deviation.
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Results |
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All patients were generally complaint-free during the follow-up period. However, 1 patient (No. 4) had a minor cerebral infarction in the left middle cerebral arterial region in the second year. Another patient (No.3) who was complaint-free showed moderately depressed right ventricular wall motion with moderate tricuspid regurgitation, and therefore underwent a tricuspid valve replacement within 1.8 years of the primary repair. Thereafter, this patient's course was uneventful, but he died suddenly in the 10th follow-up year.
The latest available chest roentgenogram showed that cardiothoracic ratio remained within the normal range (47.7% to 55.1%; mean, 49.8% ± 3.5%). On the latest echocardiographic evaluation the right ventricular wall motion was assessed as normal in 3 patients, mildly depressed in 1 patient, and moderately depressed in 1 patient. Tricuspid valve regurgitation was moderate in 2 patients, and mild or trivial in 2 patients (1 tricuspid valve was replaced). Of note, left ventricular wall motion was not depressed, and mitral valve regurgitation did not develop in any of the patients. No significant deterioration of the ventricular wall motion and atrioventricular valve regurgitation was observed in the follow-up period. At follow-up catheterization, the right ventricular end-diastolic pressure ranged from 4 to 11 mm Hg, with a mean of 6.8 ± 3.1 mm Hg, and the left ventricular end-diastolic pressure ranged from 3 to 10 mm Hg, with a mean of 6.5 ± 2.9 mm Hg. The peak systolic pressure gradient across the extracardiac conduit ranged from 14 to 29 mm Hg, with a mean of 21.2 ± 5.6 mm Hg, and angiography revealed the conduit diameter to be 91% ± 6% of the original conduit diameter (Fig 2). The conduit flow was nonturbulent, and pulmonary regurgitation flow was minimal in all patients. There were no patients with increased end-diastolic or end-systolic volume in the right or left ventricle that exceeded 150% of normal value for age. Other than patient 3, no reoperations were required for any reason such as conduit restenosis, tricuspid or mitral valve regurgitation, or residual VSD. Three patients (Nos. 1, 4, and 5) underwent exercise performance examinations, which showed 100% functional aerobic capacity, with a maximum oxygen uptake of from 35.8 to 52.6 mL · kg-1 · min-1.
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Comment |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Left ventriculotomy done at the apex for an apico-aortic valved conduit has been used to relieve aortic stenosis in hearts with normal atrioventricular and ventriculoarterial alignment. Successful clinical results after such apicostomy [15] substantiate the advantage of a minimally sacrificed ventricular function that this approach offers. However, one can argue that the functional impact of an apicostomy in the CCTGA-VSD-POTO heart may be different from relatively normal heart.
In all patients of this series, mitral valve function was well maintained. Currently, a conventional repair is often indicated for patients with a preexisting abnormal mitral valve [16, 17] inasmuch as this represents a contraindication for an anatomic repair approach. In such circumstances, a left ventriculotomy on the apex rather than in the anterior free wall may be of particular benefit, because it should not lead to a deterioration of the preexisting abnormal mitral valve function, which could be potentially fatal. With regard to development of tricuspid valve regurgitation, our outcome is essentially parallel to previous reports after conventional repair [1–3]. Because tricuspid valve regurgitation is closely interlinked with right ventricular dysfunction and complete heart block [18, 19], an aggressive approach for tricuspid valve regurgitation or the prophylactic placement of a permanent pacemaker may play a beneficial role in dealing with the concern about long-term right ventricular function.
Despite these potential advantages of our approach, we were initially concerned about the fate of the conduit. By necessity, the conduit is longer and more winding than others, and intuitively one can suppose that the conduit may be short-lived owing to the proliferation of pseudointima rather than being outgrown, because the conduit size ranged from 18 to 22 mm and therefore was probably large enough to last into adulthood. Our surgical experience with nonvalved Dacron conduit repair in more conventional outflow tract positions is composed of 20 procedures, of which 6 conduits were replaced between 8 and 12.5 years after the operation, and is at least similar to one with this anomaly. The encouraging long-term result of the conduit in this series may warrant reconsideration of the surgical intuition on which the current clinical approach is based.
Several new surgical options have been advocated since the patients in this series were operated on, and patient selection for this operation at this moment is debatable. Anatomic repair is the procedure of choice in cases without unfavorable circumstances as discussed earlier. Even in conventional repair, a patch reconstruction of pulmonary outflow tract reconstruction is an attractive option if the anatomy of the pulmonary valve annulus and left circumflex coronary artery is suitable for it. The indication of conventional conduit repair may be therefore limited in highly selected patients.
In conclusion, the reportedly poor early and late outcomes that occur after the conventional repair of CCTGA-VSD-POTO with placement of an extracardiac conduit between the left ventricle and the pulmonary artery may be partially neutralized by relocating the inflow position to the apex. This encouraging outcome may warrant the continuation of conventional conduit repair with our modification in selected patients rather than attempting to perform an anatomic repair or a modified Fontan procedure.
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Acknowledgments |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Discussion |
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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Ryo, there are several things that strike me before one even gets to the anatomic substrate of congenitally corrected transposition. Long-term patency and durability of crimped Dacron conduits between a subpulmonary ventricle and pulmonary arteries with only 9% reduction in the luminal diameter is quite atypical, and I do not know whether it is related to patient age or to some other factor that you might comment on.
Second, of course, of interest is the 100% aerobic capacity and the excellent exercise performance of patients with a nonvalved conduit between the subpulmonary ventricle and the pulmonary arteries at this long-term follow-up. I wonder if there are other instances where you and your colleagues by choice use nonvalved conduits between the subpulmonary ventricle and pulmonary arteries.
And finally, with this very nice cohort from 1985 to 1990, are you continuing to do this operation or would similar patients in the current era be managed by an atrial inversion and a Rastelli type conduit repair?
DR AEBA: Thank you, Dr Jacobs.
Actually, in terms of the first question, I do not have any good explanations regarding why our patients had such good pressure gradient between the left ventricle and the pulmonary artery. However, all conduit are separated from the sternum or any bone structures along its entire course, which is unusual for the other anomalies.
DR JACOBS: No turbulence from compression to create a nidus.
DR AEBA: I think so. The completely round shape of the conduit's cross-section may be good.
DR JACOBS: The second question was just about the general utility of nonvalved subpulmonary conduits.
DR AEBA: With regard to the second question it was 10 years ago or even more when these patients were operated on. At that time in my country no homograft was available whatsoever. So our policy was we did not put any valves in a conduit unless it was absolutely necessary, but in the current era we have much greater availability of more sophisticated and new-generation valves, so I would put the valves in the conduit for selected patients.
DR JACOBS: Many of these patients might have required earlier reoperations if a homograft valve had been incorporated into the Dacron conduit.
DR AEBA: Yes. But if you compare it with 10 years ago, we have a much better valved conduit.
DR JACOBS: And what would be your current approach to these patients?
DR AEBA: It depends on the conditions of the associated lesions as discussed in the slides. If I would have a patient with preexisting mitral problems, or preexisting supraventricular tachyarrhythmia, and so forth, I wouldn’t do the anatomic repair, which means an atrial baffle plus a left-sided right ventricle-to-pulmonary artery repair. So it depends on the other conditions.
DR ALEX PALACIOS (Mexico City, Mexico): What do you think about the technique of enlarging the outflow tract through the atrioventricular (AV) groove, close to the AV groove, only with a patch, and have you had any experience with this technique?
DR AEBA: I am sorry, I did not understand your point.
DR PALACIOS: The technique of enlarging the outflow tract only by cutting through the AV groove, close to the AV groove, and enlarging it with a patch that was described just a few months.
DR JACOBS: Direct assault on the subpulmonary obstruction through the AV groove, which is a new alternative to extracardiac conduit repair.
DR AEBA: In selected patients we can do that, but I think a significant number of the patients cannot undergo this kind of a newer technique, for example, a narrow region for the ventricular outflow tract. So in such cases we still need these kinds of operations.
DR TOM R. KARL (San Francisco, CA): I thought that was a fantastic presentation. You know, it seems the more we discuss this disease, the less we understand it, and one would not have predicted that the results with this approach would be so good. So I wonder, is the good late hemodynamic result of a nonvalved conduit partly because it is attached to a left rather than a right ventricle, or is it because of the extreme length of the conduit that naturally limits some of the insufficiency, or do you have other explanations?
Second, could you say again exactly how you decide on the best site for the ventriculotomy and the proxima attachment of the conduit, which seems to be the key point in your technique.
DR AEBA: Thank you.
I would like to answer the second question first. Before I determine the ventriculotomy site, I use digital manipulation. We should identify the attachment of the mitral anterior papillary muscle and then we can avoid the ventriculotomy site far away from the attachment of the papillary muscle. Eventually we incise the real apex in the left ventricle, where I believe it is quite unusual for the attachment of the papillary muscle or other dangerous structure.
The first question is related to the.
DR JACOBS: The first question was related to the excellent performance of the nonvalved conduit, and Dr Karl speculated whether the length had some effect on limiting regurgitation.
DR AEBA: Initially we thought that this type of conduit may be short-lived, which is kind of surgical intuition. Surprisingly enough, our data did not support my surgical intuition. So our point is, in terms of the longevity of the extracardiac conduit, the longevity might have nothing to do with its length or curvature.
DR JACOBS: Ryo, does the left ventricular apical attachment of the conduit involve any stent or sewing ring, or is it simply a running anastomosis to the epicardium?
DR AEBA: Actually no particular device. Just pledgeted horizontal mattress sutures were placed.
DR PEDRO J. DEL NIDO (Boston, MA): One of the things I found quite remarkable about your presentation is that in the end, you still have a systemic right ventricle, and what was most impressive, is the finding that the patients that you did exercise testing on had normal exercise capacity. I found this quite surprising, and one would not predict it. Could the findings of exercise testing be age related, because if you evaluate 15- or 20-year-old patients who had a Mustard procedure, they have reasonably well-preserved exercise capacity. If you look at 25- to 30-year-old patients who have had just a Mustard, they have markedly diminished exercise capacity. So could your findings simply be that at the time you study them, they are still relatively young?
DR AEBA: Yes, that is a good point, Dr Del Nido. It will be our greatest concern, you know, maybe only after 20 or 30 years later. Even in the isolated congenitally corrected transposition with no ventricular septal defect or no pulmonary stenosis, its natural history is similar to the patient after the Mustard repair. However, anatomic repair has also the different kinds of long-term problems, and ventriculo- arterioplasty may be often associated with need for a bidirectional Glenn shunt which causes the chronic pulmonary arteriovenous fistula. So I think it compares different kinds of long-term problems.
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TopAbstractIntroductionPatients and methodsResultsCommentAcknowledgmentsDiscussionReferences |
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