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Ann Thorac Surg 2004;77:1353-1358
© 2004 The Society of Thoracic Surgeons
a Departments of Cardiothoracic Surgery and Cardiology, Our Lady's Hospital for Sick Children, Crumlin, Dublin, Ireland
* Address reprint requests to Dr Wood, Professor Eoin O'Malley National Centre for Cardiothoracic Surgery, Mater Misericordiae Hospital, Eccles Street, Dublin 7, Ireland
e-mail: freddie{at}woodcts.iol.ie
Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.
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Abstract |
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METHODS: From January 1, 1986, to June 30, 2002, a consecutive series of 181 patients less than 1 year of age (range 1 to 300 days, median 13.5 days) were referred for CoA repair. Neonates accounted for 135 patients, and hypoplastic arch (less than 1 mm/kg plus 1) was present in 107 infants. Coarctation of aorta was simple (group 1) in 71 patients; complicated by ventricular septal defect (group 2) in 62; and complicated by complex congenital heart disease (group 3) in 48. All patients were assessed by right arm/left leg Dynamap pressures and routine follow-up was performed by the cardiologists. Follow-up was complete in all patients (range 6 months to 16 years, median 7.5 years).
RESULTS: The overall hospital/30-day mortality was 0.5% (group 1 = 0, group 2 = 0, group 3 = 1 [2.0%]). Complications other than recoarctation occurred in 5 patients (2.7%). Late mortality occurred in 15 (11 at intracardiac repair). Recoarctation, ie, a gradient of more than 20 mm Hg, occurred in 4 patients (2.2%). All 4 patients were noted to have a gradient of more than 10 mm Hg (right arm/left leg) postoperatively and as such had residual coarctation. All 4 were successfully treated by balloon aortoplasty.
CONCLUSIONS: Extended arch aortoplasty in association with ductal and coarctation excision provides excellent coarctation repair with a low incidence of recoarctation. Recoarctation occurred only in proximal aortic arch hypoplasia or low birth weight. Balloon aortoplasty easily and effectively relieved the recoarctation in all cases.
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Introduction |
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Aortic arch hypoplasia is a common finding in neonates with aortic coarctation—its prevalence can be as high as 70% [1, 2]—and is associated with increased risk of recurrent arch obstruction [3]. Debate persists regarding whether the surgical technique used should address this problem as well as the actual coarctation [2, 4, 5, 6]. Subclavian flap aortoplasty with its many modifications, resection, and end-to-end anastomosis and extended arch aortoplasty (EAA) have been tried and each method has their advocates. Recently, end-to-side anastomosis has been described by Rajasinghe and associates and Younoszai and colleagues and intermediate follow-up has shown promising results [5, 7]. However, recoarctation is a persistent problem with a reported incidence of 10% to 50% [2, 4, 8, 9]. Residual ductal tissue, aortic arch tubular hypoplasia, suture type, suture line tension, type of operation, and diameter of completed initial repair have all been implicated as causes of recoarctation [8–14].
To address all these issues and exclude operator variability, one of us (A.E.W.) has used wide coarctation and ductal excision combined with EAA (incision in the concavity of the aortic arch proximal to the origin of the left common carotid artery) as first described by Zannini [15] and later by others [4, 16, 17] on all infants and neonates referred to him for CoA repair since January 1, 1986, and this experience is reported herein.
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Material and methods |
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The patients were divided into three groups depending on whether the coarctation was present in isolation (71 infants, group 1) or in association with ventricular septal defect (62 infants, group 2) or complex cardiac defects (48 infants, group 3). Table 1 summarizes the cardiac defects among the last group of patients. The transverse aortic arch was considered hypoplastic if the diameter was less than 1 mm/kg plus 1 [18], and was present in 107 patients (59%).
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Results |
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Late results
Late death occurred in 15 infants (8.3%): 3 in group 2 (4.8%) and 12 in group 3 (25%). These deaths occurred 2 to 60 months after CoA repair. Eleven deaths occurred at intracardiac repair (1 in group 2 and 10 in group 3). Four deaths occurred due to sepsis, 3 due to congestive cardiac failure, 2 due to multiple organ failure, 1 infant could not be weaned off cardiopulmonary bypass after a Damus-Kay-Stansel procedure, and 1 died while waiting for repair of an intracardiac defect. Postmortem examinations were conducted for all deaths. All surviving children other than those with recoarctation were normotensive.
Recoarctation
Residual or recurrent coarctation was defined as the presence of a resting peak pressure exceeding 20 mm Hg across the repaired area [4, 6, 11]. Recoarctation occurred in 4 patients (2.2%), who underwent initial operation at 3, 12, 14, and 20 days of life and weighing 3.8, 1.5, 2.0, and 0.85 kg at operation, respectively. Three of the patients had proximal tubular hypoplasia. The diagnosis of recoarctation was made by noninvasive blood pressure measurements and confirmed by Doppler echocardiography and cardiac catheterization within 6 to 12 months of surgery. All 4 patients had an arm-leg pressure gradient of 10 mm Hg or more immediately after the initial operation, and as such this condition constituted residual coarctation. The recoarctation occurred at the most proximal site of the anastomosis in the aortic arch (Fig 2A).
All patients were treated successfully by a single balloon aortoplasty (Fig 2B) at a median time of 7 months postoperatively. Postmortem examinations were conducted for all deaths (both hospital and late); the coarctation repair site was deemed satisfactory in all.
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Comment |
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The other important feature of neonatal coarctation is its association with tubular hypoplasia of the aortic arch, which may be present in as much as 70% of patients (59% in this series). Twenty-five to 30 years ago, aortic arch hypoplasia was an independent risk factor for early mortality after CoA repair [19, 20]. Poirier and colleagues [21] reported a significant number of patients with previous coarctation repair requiring later enlargement of a hypoplastic aortic arch. This condition was first identified by Amato [22] in 1977 and further defined in 1991 [23]. Recently, McElhinney and associates [3] reported further evidence to support tubular hypoplasia of the aortic arch as a risk factor for recoarctation. Some of the techniques used in repair of CoA fail to address this problem. Simple end-to-end anastomosis with ductal and coarctation excision will deal with the primary obstruction but will not alter tubular hypoplasia of the aortic arch, although Brouwer and associates [13] demonstrated growth in the hypoplastic arch with this technique. Subclavian flap aortoplasty also fails to address this issue; however, different modifications of this technique have been devised to reconstruct the distal transverse aortic arch.
Recoarctation defined as peak arm/leg gradient of more than 20 mm Hg at rest in this series is reported to occur from 12.5% to 50% [2, 4, 6, 11]. Subclavian flap repair, while simple and expeditious, devascularizes the left arm, which can result in either limb shortening [24] or exercise intolerance [25]. The reported recoarctation rate with this repair varies from 10% to 18% [10, 11]. On-lay patch using prosthetic material, while again easily applied, fails to grow and has a high incidence of recurrence [10], which logically should reach 100% by 15 years. Simple end-to-end anastomosis has also proved to result in a high incidence of recoarctation [8].
Extended arch aortoplasty [2, 4, 16, 17] has the advantage of wide ductal and coarctation excision combined with a long oblique circumferential suture line to augment the transverse aortic arch, a technique which when used in the neonatal arterial switch operation for transposition of great arteries has proven to grow adequately. The technique of end-to-side aortic anastomosis (ESAA) of descending aorta to proximal aortic arch also addresses transverse tubular hypoplasia [5, 7]. We emphasize the long oblique suture line of the EAA versus ESAA and simple end-to-end anastomosis. The ESAA results in a circular suture line with a smaller diameter and hence cross-sectional area, while EAA has an elliptical suture line and a similar growth rate that results in a significantly larger cross-sectional area. It will be interesting to see if the recoarctation rate differs between the two techniques. Both EAA in this series and ESAA result in no recoarctation when used for isthmus CoA or associated distal tubular hypoplasia [5, 7].
Four recurrences of CoA were noted. All were among patients less than 30 days old, 2 who weighed 2.0 kg or less and 1 who weighed less than 1.0 kg. All 4 infants had an arm/leg gradient of 10 mm Hg postoperatively and as such had residual coarctation. Three had proximal arch hypoplasia. These findings support those of McElhinney and colleagues [3] that the risk of recoarctation is a function of aortic arch anatomy. In retrospect it may have been better to attempt the surgery for these patients through a median sternotomy using cardiopulmonary bypass utilizing the same technique of repair to advance to the inferior aspect of the ascending aorta.
Extended arch aortoplasty is now the procedure of choice for repair of neonatal and infant coarctation at our institution. All four recoarctations (2.2%) in this series were detected within 6 to 12 months of the repair and were treated successfully by balloon aortoplasty. We have not detected any other recurrences at a median follow-up of 90 months and a minimum follow-up of 6 months. Mortality was influenced only by complex intracardiac anomalies, particularly univentricular heart. The results of EAA in this series are compelling and we would advise it as the technique of choice to repair all forms of aortic coarctation presenting in the infant and neonatal period, especially in the presence of transverse aortic arch tubular hypoplasia.
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Discussion |
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Ten years ago we reported a similar enthusiasm for the extended end-to-end anastomosis technique. However, during the last decade the issues raised by surgical management of neonatal coarctation were somewhat different, particularly in three aspects.
First, surgical repair of isolated coarctation with absent or moderate arch hypoplasia is well controlled. As shown by Dr Wood's series and many other publications, the extended anastomosis is an excellent technique in which the rare recoarctation is successfully treated by balloon angioplasty. Other techniques respecting the left subclavian artery are also very safe, in particular the variant described by Joe Amato in the 1970s that realized a lateral anastomosis between the left carotid and the left subclavian arteries, creating a large distal arch.
Second, the optimal surgical treatment of the most severe form of transverse arch hypoplasia (either the diffuse tubular hypoplasia or the hypoplasia located on the proximal transverse arch) remains controversial. Although an extended anastomosis may offer a solution, this technique may be difficult because the anastomosis may be too long, creating an undue stretching on the transverse arch. The technique that brings the descending aorta on the proximal arch described years ago and recently published by the group of San Francisco offers a safer solution.
Finally, in the neonatal group, for more than two thirds of the patients, the major problem is the management of the associated lesion. The coarctation is, in fact, the tip of the iceberg. Inside the heart are severe lesions to treat, from malaligned ventricular septal defect to Taussig-Bing, to Shone complex and hypoplastic left heart. The introduction of cerebral perfusion through the brachiocephalic artery permits us to safely extend the indication of one-stage repair by sternotomy.
The real question nowadays may be to define the optimal technique of arch reconstruction through sternotomy. Whether the extended anastomosis is the most appropriate technique by sternotomy is questionable. The end-to-side technique seems preferable, treating the coarctation like an interrupted aortic arch. Patch enlargement aortoplasties are useful, particularly to control the aortopulmonary diameter mismatch in arterial switch surgery. Altogether, the extended anastomosis technique alone is probably not adapted to treat all anatomical lesions.
Freddie, I have two questions to ask you. It seems that your presentation excludes one-stage repair by sternotomy. Could you comment on that? Second, what do you think of the balloon angioplasty applied to native coarctation?
I want to thank the Association for the privilege of discussing this interesting paper.
DR CONSTANTINE MAVROUDIS (Chicago, IL): That was a lovely paper with almost unprecedented restenosis rates, being so low. The stellar results speak to the quality of the operation that was performed. I would like to explore the question of whether to ligate some of the intercostals arteries while performing this operation. I am glad that Dr Lacour-Gayet commented, because I recall that he and Dr Planche, in their nice study ligated at least three pairs of collateral or intercostal arteries in order to mobilize the descending aorta and perform an anastomosis that was without tension.
I noticed, Freddie, that your approach to this situation was not to ligate these arteries. The incidence of paraplegia in the Lacour-Gayet-Planche group was very low, zero if I recall correctly, and it was zero in your group as well. What led you to preserve these arteries? Of course the dilemma is to preserve collateral flow while preserving the arteries and to prevent tension on the anastomosis by ligating these vessels. So would you comment, please, about taking those intercostal arteries, and if you are fearful of ligating them, tell us why, and what is the nature of your proposal?
It was a very nice presentation. Thank you very much.
DR JOSEPH J. AMATO (Chicago, IL): I would like to congratulate the authors on an excellent paper and presentation. Although we reported the extended end-to-end anastomosis in 1977, other surgeons such as Mark Elliot and Zannini presented the extended and radical extended end repair. I would like to know what makes your repair different from those of Zannini and Elliot, because they have introduced a more radical extended type of end-to-end repair, which I believe depends on the extent of hypoplasia of the aorta.
I would like to make some comments and ask three questions. First, I do not believe that an end-to-end anastomosis, as we first reported, is necessary in all types of coarctation, especially the simple type coarctation. Will you explain the reason for performing this operation on all coarctations?
Second, you mentioned the fact that you did not use heparin. We consistently have used heparin in all of our patients. Whether you reverse it or not really makes no difference. What was the reason you did not use heparin?
I applaud you on the median time of coarctation repair, which was 15 minutes. What were the longer times and might you have considered giving heparin in those cases?
Finally, I would object to the concept that one size fits all. My belief is that each individual patient with coarctation should have an operation tailored to their type of coarctation. I am not certain that a simple coarctation really needs a radical end-to-end repair. However, you may prove me wrong as more results are gathered.
Thank you, again, on an excellent presentation.
DR CHARLES D. FRASER, JR (Houston, TX): I just wanted to follow up on the comments that Dr Lacour-Gayet made. We might take issue in Houston concerning the procedure of choice for patients other than those who have a completely normal aortic arch. As we reported here 2 years ago, our procedure of choice is now a one-stage complete repair from the front, and we are particularly emboldened because of the use of retrograde cerebral perfusion or regional cerebral perfusion.
Looking at the complex group of patients in whom there was significant mortality, based on your data now, Dr Wood, would you modify your approach for those patients to a more aggressive one-stage repair from the front?
DR WOOD: François, thank you for your comments. As I understand it, you have asked about one-stage repair for the more complex group 3 patients. It must be appreciated that I practice cardiothoracic surgery. By that I mean I practice in congenital heart surgery, adult cardiac surgery, thoracic surgery, and transplantation.
When I returned to Dublin in 1984 with my recently retired senior colleague, Maurice Neligan, who is a member of the Society, the two of us in fact had to provide a panoply of cardiothoracic services to the city of Dublin, one of which happened to be congenital heart disease. Since that time I have performed approximately 150 congenital heart operations a year out of a total yearly average of around 600 operations. As such, my views on one-stage repair back in 1986 were a little different than what they are today. I have to admit now, in 2003, that I would certainly consider one-stage repair for these more complex anomalies.
In relation to François' second question of balloon aortoplasty, I feel that this presentation and others that have been published recently should stand as a gold standard against which interventional cardiologists should compare their treatment of neonatal coarctation if they go on to use balloon aortoplasty.
Doctor Mavroudis, thank you for your comments. What put me off taking intercostal arteries was the published literature from the 1970s, and indeed early 1980s, that if you take three or more intercostal arteries in adolescents or, indeed, adults, you had a much higher incidence of paraplegia. As it happens, society in Ireland has become increasingly litigious and now has a litigious rate greater than that in the state of Florida. Throughout the whole period I never took intercostals because I considered it to be physiologically wrong to do so, and I have no reason to change my opinion or practice.
Doctor Amato, thank you for your comments. Indeed, it was your paper published in 1974 that stimulated me to consider this type of approach. This approach is no different from what was described by Zannini or Elliot and includes both extended arch aortoplasty and the radical extended aortoplasty to which you already alluded. It has never been my practice to use heparin, and during my time in the Hospital for Sick Children in Toronto, heparin was not used for coarctation repair.
Doctor Fraser, I do now consider that one-stage correction for complex group 3 type patients is probably the treatment of choice, but that is for the future.
Again, thank you for the honor of presenting our results to the Society.
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