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Ann Thorac Surg 2001;71:1530-1536
© 2001 The Society of Thoracic Surgeons
a Division of Cardio-Thoracic Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, Georgia, USA
b The Sibley Heart Center Children’s Healthcare of Atlanta at Egleston, Division of Pediatric Cardiology, Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia, USA
* Address reprint requests to Dr Kanter, Division of Cardiothoracic Surgery, Emory University School of Medicine, 1365 Clifton Rd, Atlanta, GA 30322 (Email: kkanter{at}emory.org).
Presented at the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.
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Abstract |
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Methods. Since 1988, 46 of 162 infants less than 3 months undergoing coarctation repair had hypoplastic arch enlargement with reverse subclavian flap aortoplasty. Median age was 11 days; mean weight was 3.2 kg. Thirty-seven patients (80%) had associated cardiac defects including single or multiple ventricular septal defects (14 infants), transposition of the great arteries (7), aortic or mitral stenosis (5), and complete atrioventricular septal defect (5 infants). Twenty-eight patients had pulmonary artery banding; 2 had an arterial switch operation through a separate median sternotomy.
Results. There were two hospital deaths: one 4 months postoperatively in a patient requiring a Norwood procedure the next day for underestimated left ventricular hypoplasia; the other of sepsis more than 1 month postoperatively. On follow-up from 1 to 129 months (mean, 38 months), there were five recurrent obstructions: three at the coarctation site treated with balloon dilatation and two at the arch site. Twenty-six children had their heart defects corrected with 29 subsequent operations including an arterial switch operation for transposition of the great arteries/ventricular septal defect (3 infants), relief of aortic or mitral stenosis ± ventricular septal defect closure (5), multiple ventricular septal defect closure (3), a bidirectional Glenn (2), complete atrioventricular septal defect (2), and anomalous left coronary with ventricular septal defect repair (1 infant). Four children await debanding and ventricular septal defect closure or Glenn anastomosis. There have been two late deaths (overall survival, 91%).
Conclusions. Reverse subclavian flap aortoplasty is excellent for relief of arch hypoplasia and coarctation in infants with low recurrence rates and acceptable operative and intermediate survival.
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Introduction |
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsCommentDiscussionReferences |
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The distal left subclavian artery was now ligated at its first branching. The aortic isthmus was snared with a silicone elastomer tape between the left subclavian artery and the ductus arteriosus, thus allowing continued perfusion to the lower body through the patent ductus arteriosus (Fig 2). A clamp was carefully applied across the proximal transverse aorta between the innominate artery and the left carotid artery while insuring that the right radial (or axillary) arterial line trace was not dampened. Often, a pulse oximetry probe was placed on the right earlobe or cheek to monitor ongoing right common carotid artery perfusion. Although a C-shaped clamp could also encompass the proximal left carotid at the same time as the proximal arch, with experience we found that a separate vascular clamp or bulldog clamp on the left carotid artery improved exposure of the angle between the left lateral aspect of the proximal left carotid artery and the superior aspect of the adjoining hypoplastic transverse arch (Fig 2). With careful clamp placement, we were able to use this technique even in children with a bovine-type aortic arch (the left carotid artery arising from the proximal innominate artery rather than separately from the aortic arch). The left subclavian artery was now divided proximal to the previously placed ligature and opened on its right medial aspect. This incision was carried along the superior aspect of the hypoplastic transverse aorta and then continued up for 3 to 4 mm onto the lateral aspect of the proximal left carotid artery (dashed line in Fig 2).
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Other patients
During this same time period, 8 other infants aged 16 ± 18 days underwent isolated standard subclavian flap repair of aortic coarctations. In 7, at the time of operation, after the coarctation repair, an unacceptable gradient was measured across the transverse aorta and the previously unrecognized hypoplastic transverse aorta was enlarged with a patch of polytetrafluoroethylene or pericardium at the same operation. An eighth patient who had an arterial switch procedure through a separate median sternotomy during the same anesthetic as his standard subclavian flap coarctation repair developed evidence of arch obstruction. He required reoperation to enlarge his hypoplastic transverse aortic arch at 80 days of age.
Follow-up and restenosis
After hospital discharge, all survivors were followed with routine cardiology appointments including upper and lower extremity blood pressure determinations and periodic echocardiograms. Cardiac catheterization was performed if there was a suspicion of recurrent arch obstruction or coarctation (defined as a gradient of 
20 mm Hg), in anticipation of surgical repair of other defects, or if the clinical situation could not be defined accurately by less invasive techniques.
Statistical methods
Values are shown as mean ± standard deviation. Actuarial survival was performed using a Kaplan-Meier analysis.
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Results |
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Restenosis
The 44 survivors have been followed a mean of 38 months (range, 1 month to 10.8 years). There have been five recurrent obstructions (defined as a gradient 20 mm Hg by arm/leg pressures, echocardiogram, or cardiac catheterization) ranging from 2.6 to 7.2 months postoperatively (mean, 4.9 months). Three were stenoses occurring at the site of end-to-end anastomosis; all three were successfully managed with percutaneous balloon dilatation. There were two recurrent arch obstructions. One was successfully balloon dilated 6 months postoperatively. The other child had a 30 mm Hg gradient across the proximal aortic arch between the innominate artery and left carotid artery at catheterization 1 month postoperatively. This required pericardial patch enlargement using profound hypothermia and circulatory arrest 4 months postoperatively. Interestingly, at operation, a mildly obstructive bar of fibrous tissue was excised from the lumen of the aorta at the most proximal site of the reverse subclavian flap. Presumably, this tissue was caused by inadvertently catching the back wall of the aorta when constructing the most proximal portion of the reverse subclavian flap anastomosis stressing the importance of clear exposure of the angle between the left carotid artery and the hypoplastic transverse aortic arch during this anastomosis. Actuarial freedom from recoarctation in this series was 86% ± 14% after 7 months since there have been no episodes of recoarctation recognized after this time.
Subsequent operations
There have been 29 subsequent operations in 27 children (Table 2). None of the 9 children with isolated coarctation with arch hypoplasia have required further surgical intervention. Of the 14 patients in the group with only an associated VSD, 9 of the 10 with pulmonary artery banding have had the band removed with VSD closure (including 3 with multiple VSDs) 7.4 ± 9.0 months after the original operation (range, 1 to 30 months). One patient still awaits pulmonary artery debanding and VSD closure.
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Three of the 6 patients in the group with univentricular heart disease have had subsequent operations including the infant who had a first-stage Norwood procedure the day after his arch/coarctation repair (Table 2). The other 3 patients are awaiting a bidirectional Glenn anastomosis in preparation for an eventual Fontan procedure.
Late survival
There have been two late deaths 3 and 4 months after arch/coarctation repair, both in patients with severe systemic ventricular hypertrophy. One was in an infant with severe left ventricular outflow tract obstruction due to accessory mitral valve tissue. She suffered a cardiac arrest on induction of anesthesia for mitral valve replacement and could never be weaned from cardiopulmonary bypass postoperatively despite 10 days of support with extracorporeal membrane oxygenation. The other child with unbalanced complete atrioventricular septal defect, hypoplastic left ventricle, and a restrictive ventricular communication died 9 days after a bidirectional Glenn anastomosis and modified Damus-Stansel-Kaye procedure due to clotting of his Glenn anastomosis, probably related to marginally low cardiac output. Overall survival in this entire series of 46 infants was, therefore, 91% on follow-up of 36 ± 35 months (range, 1 month to 10.8 years).
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Comment |
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There are some who contend that it is unnecessary to repair the hypoplastic arch as it will grow with time [11, 12]. Careful reading of these reports, however, reveals possible flaws in the analysis of the data presented. Siewers and colleagues [11] described 33 of 102 (32%) infants with coarctation with associated arch hypoplasia that was not addressed surgically at the time of coarctation repair. At a mean interval of 39 ± 29 months postoperatively, evaluation of the transverse arch showed good growth. However, only 18 of the original 33 patients underwent reevaluation by imaging (presumably the remainder had no arm/leg pressure gradients). There were 3 early and 12 late deaths, although they state that "there was no evidence that the arch hypoplasia itself in any way contributed to the late deaths."
Another article commonly cited as evidence for growth of the hypoplastic transverse aorta after coarctation repair is by Myers and colleagues [12]. Careful reading of this article reveals that they believe a priori that "tubular hypoplasia of the aortic arch proximal to the left subclavian artery require[s] augmentation . . .; therefore, these patients [were] not included in [that] series."
On the other hand, there is reasonable evidence that the hypoplastic aortic arch should be repaired at the time of coarctation repair. Early reports show that the presence of arch hypoplasia is an independent risk factor for early mortality after coarctation repair with all 5 patients with arch hypoplasia in the series by Herrmann and associates [13] and 3 of 4 patients with arch hypoplasia in the series by Baudet and Al-Qudah [14] dying early after coarctation repair. Qu and colleagues [15] reported that of 23 infants younger than 6 months undergoing coarctation repair, 5 of the 6 infants with arch hypoplasia (defined as distal arch outer diameter < 3.9 mm) required arch augmentation. Our own experience is in agreement with these findings. During the same time period of this study, we encountered 8 infants with coarctation who initially underwent only standard subclavian flap repair. They then required augmentation of the aortic arch during this same operation (7 patients) or during a second operation 3 months later (1 patient).
Further evidence that the hypoplastic arch does not always grow after coarctation repair is demonstrated by DeLeon and colleagues [16] who reported 6 patients requiring repair of arch hypoplasia late after successful coarctation repair. Even more compelling is the report by Poirier and associates [17] in which 27 patients with previous coarctation repair required subsequent surgical enlargement of a hypoplastic aortic arch. Finally, Machii and Becker [18] examined autopsy specimens of hypoplastic aortic arches and found fewer α-actin-positive cells that could indicate a diminished growth potential.
Other than these anatomic reasons for repairing the hypoplastic arch at time of coarctation repair, there are convincing physiologic reasons succinctly enumerated by Vouhé and colleagues [10]. They argued that any residual arch gradient, even slight, would be poorly tolerated in an infant with preoperatively depressed ventricular function. Second, if there were coexisting left ventricular outflow tract obstruction, an incremental increase in left ventricular work caused by an unrepaired aortic arch would be detrimental. Finally, in patients who undergo concomitant pulmonary artery banding, any unrelieved arch gradient would effectively result in biventricular obstruction.
Once one decides it is important to repair the hypoplastic aortic arch at the time of coarctation repair, there are a variety of available surgical techniques. These include the use of a left carotid artery flap [2, 4], resection with extended end-to-end anastomosis [3, 19, 20], repair through a midline sternotomy [8], and use of the left subclavian artery as a free flap [5].
In this series, we have used the left subclavian artery as a viable autologous flap to augment the hypoplastic aortic arch followed by coarctation resection with end-to-end anastomosis (Figs 2 to 4). Tiraboschi and colleagues [6] first described the use of a reverse subclavian flap for repair of an unusual coarctation located between the left carotid and left subclavian arteries which was also described later by Hart and Waldhausen [21]. Amato and associates [7] depicted a side-to-side anastomosis between the left carotid and left subclavian arteries augmenting the hypoplastic aortic arch without transecting the subclavian artery distally. The coarctation was resected with end-to-end anastomosis during the same clamp period. Interestingly, Amato and coworkers [22] later reported a 30% early recoarctation rate with this technique.
The modifications we have made with our technique for reverse subclavian flap aortoplasty are important. First, the arch is repaired during a clamp application separate from that used for the coarctation repair (Fig 2). This allows continued perfusion to the lower half of the body through the patent ductus arteriosus. Thus, not only are the spinal cord, kidneys, and viscera protected, but also the amount of cardiac afterload is dramatically reduced as compared to placing a clamp on the proximal aorta between the innominate artery and the left carotid artery at the same time the patent ductus arteriosus is ligated. Second, our technique should minimize the period of left carotid artery clamping as it remains open during the second stage of the repair when the coarctation is resected with end-to-end anastomosis (Fig 4). Although this consideration may be theoretical, there are reports of neurologic complications with extended end-to-end repair of coarctation [23], which often is associated with longer carotid occlusion times than described with our technique. Finally, we stress the importance of dividing the left subclavian artery distally. This not only increases the amount of tissue available for arch augmentation, but also allows a tension-free anastomosis (Fig 3) as opposed to the Amato technique with its relatively high recurrence rate [22].
The operative survival in our series of 96% and the intermediate survival of 91% in a fairly heterogeneous group of patients is comparable to or better than survival reported with other techniques for repair of hypoplastic aortic arch with coarctation in infancy [8, 10, 23]. Also our actuarial freedom from restenosis rate of 86% past 7 months up to 10.8 years is respectable compared with other published reports [10, 22, 23]. On reflection, we believe that all three restenoses at the coarctation repair site almost certainly were due to inadequate resection of ductal tissue and thus were technical errors. One of the two arch obstructions was actually not a restenosis but rather uncorrected hypoplasia of the proximal aorta between the innominate artery and the left carotid artery, which of course is not addressed with this surgical technique.
Finally, of late there has been interest in simultaneous correction of underlying heart defects at the time of repair of the hypoplastic aortic arch and coarctation arguing that the one-stage approach affords superior results [8]. Thirty-seven of the 46 patients in this series (80%) had additional heart lesions other than the aortic abnormalities. Yet only 2 patients in this series had simultaneous correction of the heart defects (both had an arterial switch procedure through a separate sternotomy). One of these patients accounted for one of the two hospital deaths (Candida sepsis 5 weeks postoperatively). On the other hand, 27 of our patients went on to a staged surgical repair with reasonable results. It could be argued that the only two deaths in these patients would not likely have been avoided by a one-stage approach.
In summary, we have presented a series of 46 infants with coarctation of the aorta and associated arch hypoplasia treated with reverse subclavian flap aortoplasty and resection of the coarctation with end-to-end anastomosis. This technique is technically simple and effective with low operative and intermediate mortality and good freedom from restenosis. Good relief of the arch obstruction allows later correction of heart defects with acceptable results.
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Discussion |
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DR KANTER: Certainly if they had a hypoplastic ascending aorta, then we would use the Norwood technique. The key point was the measurement of the arch between the innominate artery and the carotid artery. If that was less than 60% of the ascending aorta, then we would go ahead with Norwood palliation rather than this technique.
DR CHRISTOPHER J. KNOTT-CRAIG (Oklahoma City, OK): I enjoyed the presentation very much, and I was interested to note the heart catheterization visualizing the aorta in the one patient that you presented. Is this something that you do frequently? And if not, can you give us some idea about when you would encourage your cardiologist to catheterize an infant with coarctation?
DR KANTER: No. As I said, this series started in 1988 and it dates back from then. Certainly during the past 8 or 10 years it has been terribly uncommon for us to take these children to the operating room with catheterization. We almost always go by echocardiogram alone.
DR JOSEPH J. AMATO (Chicago, IL): Doctor Kanter, I congratulate you and your group on an excellent presentation and the wonderful results that you have achieved. I rise to tell you that I have encountered in my experience with repair of coarctation over 16 methods to repair coarctation of the aorta. This comes from the realization that there is a spectrum of entities that require tailoring the operation to the anatomy that the surgeon finds. Although the reverse subclavian flap for repair of the hypoplastic transverse aorta as you described is a highly effective method, it does sacrifice the function of the subclavian artery. I would propose that another method of repairing the hypoplastic arch is to use the extended end-to-end anastomosis as Zannini described in 1985 and Elliott further modified in 1987 using a radical extended end-to-end repair, which actually saves the subclavian artery as it lies over the anastomosis. Again, I congratulate you on your presentation.
DR CARL L. BACKER (Chicago, IL): I also congratulate you, Kirk, very nice results. I think that this technique is something everyone should have in their armamentarium for that unusual patient that you can run into. This is another "trick" we can have up our sleeves.
I rise mostly to remind and defend the technique of resection with extended end-to-end anastomosis. We presented our results with that that technique at this meeting 2 years ago. For the patient with a hypoplastic arch, much like you showed, I think that that technique is useful. It is interesting that if you look at the series from Great Ormond Street (London) and Marie Lannelongue (Paris) (Leipzig, Germany), and then the series that Joe mentioned from Italy, there is probably over a thousand neonates from Europe that have been treated with the resection and extended end-to-end anastomosis, of whom probably 30 to 40% have a hypoplastic arch with really excellent results. When I reviewed that for our manuscript, the recurrence rate was about 5% to 10% with a similar low mortality to yours. And I think that in my mind this is becoming, at least at our institution, the procedure of choice. And it is a successful operation for the patient with a hypoplastic arch.
I would also remind everyone that when you take the subclavian artery, although the risk is small, there is a risk of hand ischemia. And I was recently shown a case where the surgeon had required amputation of the arm following a subclavian flap.
The other thing is that some of these patients—
DR JACOBS: The surgeon or the patient?
DR BACKER: Both!
I remember when we did subclavian flaps routinely, a lot of times the baby’s arm would be quite cool and pale after this surgery, and I would be a little nervous, as a young attending. I wonder if you have seen any problems with hands being cool after this operation?
Again, great results and I congratulate you on a nice presentation.
DR KANTER: We certainly do see that the hands early on are cool and can sometimes be congested, but we have not had any difficulties with using the subclavian.
I am not proposing that this method is to supplant the extended resection with end-to-end anastomosis, but an alternative to it. I don’t want this audience to believe that technique is not without its problems as well. In one large series there was a definite but small incidence of neurologic problems associated with it. The clamp times of the left carotid are clearly longer than with the technique that I have shown here. Although this difference may not be statistically different, all the reported series had longer clamp times than we found.
Finally, if there is a technical error in that very proximal, most difficult part of the anastomosis, underneath the proximal aortic arch, then you have converted the patient to a much more difficult problem of proximal arch stenosis, which has to be dealt with from the front on bypass.
DR KOZO ISHINO (Okayama, Japan): In terms of ischemic time during arch repair through median sternotomy, we perfuse the innominate artery or subclavian artery during arch repair, placing a cross-clamp between the innominate artery and left carotid artery, so that we can perform the arch repair with heart beating and brain perfusion as well. We have never encountered any neurological problem even in patients with hypoplastic aortic arch.
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