Eur J Cardiothorac Surg 2007;31:242-248. doi:10.1016/j.ejcts.2006.10.035
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved
One-stage total repair of aortic arch anomaly using regional perfusion
Hong-Gook Limb,
Woong-Han Kima,*,
Woo-Sung Janga,
Cheong Lima,
Jae Gun Kwaka,
Cheul Leeb,
Seong Wook Hwangb,
Chang-Ha Leeb
a Department of Thoracic and Cardiovascular Surgery, Clinical Research Institute, Seoul National University Children's Hospital, College of Medicine, Seoul National University, Seoul, Republic of Korea
b Department of Thoracic and Cardiovascular Surgery, Sejong General Hospital, Sejong Heart Institute, Bucheon, Republic of Korea
Received 2 September 2006;
received in revised form 18 October 2006;
accepted 23 October 2006.
* Corresponding author. Address: Department of Thoracic & Cardiovascular Surgery, Seoul National University, College of Medicine, Seoul National University Children's Hospital, 28 Yongon-Dong, Jongno-Gu, Seoul 110-744, Republic of Korea. Tel.: +82 2 2072 3637; fax: +82 2 3672 3637. (Email: woonghan{at}snu.ac.kr).
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Abstract
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Objective: Primary repair of aortic arch obstructions and associated cardiac anomalies is a surgical challenge in neonates and infants. Deep hypothermic circulatory arrest prolongs myocardial ischemia and might induce cerebral and myocardial dysfunction. Methods: From March 2000 to December 2005, 69 neonates or infants with aortic arch anomaly underwent one-stage biventricular repair with continuous cerebral perfusion in the presence of a nonworking beating heart using the dual perfusion technique on the innominate artery and aortic root. Preoperative diagnoses of arch anomaly comprised aortic coarctation (n
= 54) or an interrupted aortic arch (n
= 15). Combined anomalies were ventricular septal defect (n
= 52), anomalous origin of the right pulmonary artery from ascending aorta (n
= 3), hypoplastic left heart syndrome (n
= 2), truncus arteriosus (n
= 2), atrioventricular septal defect (n
= 2), double outlet right ventricle (n
= 1), total anomalous pulmonary venous return (n
= 1), partial anomalous pulmonary venous return (n
= 1), and aortic stenosis (n
= 1). Results: The mean regional perfusion time was 27.8 ± 9.8 min. There was no operative mortality. Postoperative low cardiac output was present in four patients (5.8%). A neurologic complication was noted in one patient (1.5%) who developed transient chorea, but recovered completely. During 32.8 ± 17.5 months of follow-up, one late death (1.5%) occurred. There was neither reoperation associated with arch anomaly nor recoarctation except in one patient. One patient developed left main bronchial compression necessitating aortopexy. Conclusions: One-stage total arch repair using our regional perfusion technique is an excellent method that may minimize neurologic and myocardial complications without mortality. Our surgical strategy for arch anomaly has a low rate of residual and recurrent coarctation when performed in neonates and infants.
Key Words: CHD, great vessel anomalies • Aortic arch • Coarctation • CPB, circulatory arrest • Neurocognitive deficits
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1. Introduction
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Primary repair of aortic arch obstructions and associated cardiac anomalies is a surgical challenge in neonates and infants. Deep hypothermic circulatory arrest, which was used as perfusion strategy for aortic arch repair, prolongs myocardial ischemia and might induce cerebral dysfunction. To eliminate these potential side effects, we [1] introduced a combined perfusion technique using dual arterial cannulas; one was placed into the innominate artery and the other into the aortic root. By snaring the innominate artery and crossclamping the ascending aorta, we performed an extended aortic arch anastomosis with continuous cerebral perfusion and a nonworking beating heart in neonates and infants.
The purpose of this study was to evaluate the outcomes of our surgical strategy for arch anomaly using our regional perfusion techniques in neonates and infants.
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2. Materials and methods
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2.1 Patient profiles
From March 2000 to December 2005, 69 neonates or infants with aortic arch anomaly underwent one-stage biventricular repair at less than 1 year of age through extended resection and end-to-side or end-to-end anastomosis with continuous cerebral perfusion and a nonworking beating heart by the dual perfusion technique on the innominate artery and aortic root as previously described [1].
Preoperative diagnosis of arch anomaly consisted of coarctation of the aorta (CoA) in 54 patients and interruption of the aortic arch (IAA) in 15. Combined anomalies were ventricular septal defect (VSD) in 52 patients, anomalous origin of the right pulmonary artery from ascending aorta (AORPA) in 3, hypoplastic left heart syndrome (HLHS) in 2, truncus arteriosus in 2, atrioventricular septal defect (AVSD) in 2, double outlet right ventricle (DORV) in 1, total anomalous pulmonary venous return (TAPVR) in 1, partial anomalous pulmonary venous return (PAPVR) in 1, and aortic stenosis in 1. The study population was divided into patients with isolated CoA (group I), CoA with VSD (group II), IAA with VSD (group III), and arch anomaly combined with complex congenital heart defects, such as HLHS, truncus arteriosus, AORPA, AVSD, DORV, TAPVR, PAPVR, and aortic stenosis (group IV) (Table 1
). Patients were excluded if they were being considered for univentricular repair.
2.2 Surgical technique
After right radial arterial pressure monitoring, a standard midline sternotomy was made, and after full heparinization and purse-string sutures, a 6Fr (2.0 mm) or 8Fr (2.7 mm) arterial cannula (RMI®, Edwards Lifesciences LLC, Irvine, CA) was inserted directly through the innominate artery, and a standard bicaval cannulation was instituted. In cases of a ductal dependent descending aortic circulation, an 8Fr flexible arterial cannula (DLP®, Medtronic DLP, Grand Rapids, MI) was introduced at the proximal patent ductus arteriosus (PDA) and advanced into the descending aorta. These two arterial cannulas were then Y-connected and cardiopulmonary bypass was started. The PDA was snared immediately after the bypass. A left ventricular (LV) vent (10Fr, DLP®, Medtronic Inc., Minneapolis, MN) was then introduced through the right upper pulmonary vein or left atrial appendage, if appropriate. A pH-stat acid–base management strategy was used exclusively for cerebral protection. During cooling, distal pulmonary arteries up to the second branch level, arch vessels, and the descending aorta were extensively dissected and mobilized to relieve tension after anastomosis and avoid airway compression. An aortic root cannula (4Fr, DLP®, Medtronic Inc., Minneapolis, MN) was inserted and T-connected with the side hole of the innominate artery cannula. When the rectal temperature reached 28 °C, the proximal innominate artery, left common carotid artery, and left subclavian artery were snared down to initiate the regional cerebral perfusion. The ascending aorta was clamped just distal to the root cannula, and simultaneous myocardial perfusion was maintained using a T-connected infusion line. The descending aorta was also clamped as far as possible distally and gently elevated to produce a bloodless field and to reduce anastomotic tension. Mean blood pressure in the right radial artery was maintained at about 50–60 mmHg, and the flow rate was regulated at about 50–100 ml/(kg min). Mean hematocrit was maintained at around 30%. Extended aortic arch repair was performed using a native tissue-to-tissue technique [2]. All anastomoses were performed with 7-0 or 8-0 synthetic monofilament suture material. Currently at our institution, the choice of operation is predominantly determined by the anatomic characteristics of the coarctation segment and the aortic arch. If hypoplasia extends to the proximal arch, we prefer to perform extended resection with end-to-side anastomosis without prosthetic material to reduce the rates of residual and recurrent coarctation (Fig. 1
). When the hypoplasia is confined to the segment between the left common carotid artery and the left subclavian artery, extended end-to-end anastomosis is used. After the aortic arch repair is completed, arch vessel snares and the descending aortic clamp are removed after complete de-airing, and the flow rate is fully restored (150–200 ml/(kg min)). Myocardial perfusion is stopped and cardioplegia is applied for intracardiac repair. All operations are performed by a single surgeon (WH Kim).
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Fig. 1. Three-dimensional computed tomographic image shows coarctation of the aorta with arch hypoplasia in a 45-day-old boy (A), and reconstructed arch after extended end-to-side anastomosis was performed (B).
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2.3 Neurologic monitoring and follow-up
Our neurologic monitoring protocol included a perioperative neurologic examination, brain sonography, intraoperative cerebral oximetry, and a postoperative regular neurologic evaluation at the out-patient department of pediatric neurologist during follow-up. In patients with a neurologic abnormality, we checked electroencephalograms and performed brain single photon emission computed tomography (SPECT).
Residual or recurrent coarctation was defined as a gradient of 20 mmHg or greater, either as determined by systolic blood pressure gradient determination on physical examination, or by echocardiography or by peak-to-peak systolic pressure gradient determination at catheterization [3]. The follow-up statuses of patients were determined by retrospective reviewing of hospital records or by telephone interviews.
2.4 Statistical analysis
Statistical analyses were performed using SPSS version 11.0 (SPSS, Inc., Chicago, IL). All results were expressed as medians and ranges or as mean ± SD. The significances of differences between four groups were assessed by analysis of variance or using Pearson's chi-square test. p-values of less than 0.05 were considered statistically significant.
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3. Results
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Median age at surgery was 26 days (range, 1–301); 54% of patients were 1 month old or less at the time of surgery and 83% were 2 months old or less. Median body weight and body surface area at surgery were 3.3 kg (range, 2.0–11.5) and 0.21 m2 (range, 0.16–0.5), respectively, and patients in group I had more body weight and body surface area than patients in groups II and III. In group I (n
= 10), early primary repair was performed by extended end-to-side anastomosis combined with closure of an atrial septal defect in three cases. In group II (n
= 36), early primary repair was performed by extended end-to-side anastomosis (n
= 29, 80.6%) or extended end-to-end anastomosis (n
= 7, 19.4%) combined with VSD patch closure. In group III (n
= 10), early primary repair was performed by extended end-to-side anastomosis (n
= 7, 70%) or extended end-to-end anastomosis (n
= 3, 30%) combined with VSD patch closure. In group IV (n
= 13), extended end-to-side anastomosis (n
= 10, 76.9%) or extended end-to-end anastomosis (n
= 3, 23.1%) was performed with associated procedures, which consisted of AORPA repair in three cases, the Norwood–Rastelli procedure in two, AVSD repair in two, the Rastelli procedure in two, DORV repair in one, TAPVR repair in one, the Warden procedure in one, and aortic valvotomy in one (Table 1).
Operative results are summarized in Table 2
. The median cardiopulmonary bypass time was 150 min (range, 74–338), and the median aortic cross-clamp time for the 61 patients who underwent intracardiac repairs was 46 min (range, 6–171). The median regional perfusion time of brain and myocardium was 25 min (range, 18–69). The patients with a combined complex intracardiac anomaly in group IV needed more cardiopulmonary bypass, aortic cross-clamp, and regional perfusion time than patients in the other groups. The patients in group I needed less cardiopulmonary bypass and aortic cross-clamp time than patients in the other groups. Temporary circulatory arrest was applied in four patients for closure of VSD in neonates with an exceptionally low body weight and a bilateral superior venae cava (n
= 2, 2.3 and 2.8 kg), and the transfer of arterial cannula from the innominate artery to the reconstructed main pulmonary artery during the Norwood procedure (n
= 1), and closure of an atrial septal defect (n
= 1). However, the arrest times were minimal (median 10 min, range, 2–18 min).
Postoperative results are summarized in Table 3
. There was no operative mortality. Complications consisted of a wound problem in six cases (8.7%), low cardiac output in four (5.8%), transient renal insufficiency in three (4.4%), and a transient neurologic problem in one (1.5%). No difference was observed between the four groups in terms of operative mortality or postoperative complications. Among four patients who developed postoperative low cardiac output syndrome, one in group II had extracorporeal membrane oxygenation (ECMO) support (severe biventricular hypertrophy and dysfunction preoperatively), and survived. Acute renal failure occurred in three patients in group II, but the patients recovered shortly after peritoneal dialysis. One infant with AORPA in group IV showed transient chorea during the postoperative period, but completely recovered after 11 months of follow-up. Fortunately, she had no abnormality on computed tomography scanning of the brain and by electroencephalography during the follow-up period. Median hospital stay was 18 days (range, 5–128 days), and at the time of discharge, no patient had a residual coarctation gradient by echocardiography.
Follow-up data were available on 68 patients (98.6%) for a mean duration of 32.8 ± 17.5 months (range, 7.2–65.4 months). There was one late death of a 20-day-old neonate weighing 2.9 kg who had HLHS with aortic atresia, severe long segmental arch hypoplasia, and large VSD. She was discharged uneventfully 38 days after one-stage biventricular repair that consisted of a modified Norwood procedure and Rastelli operation. About 7 months after the first operation, she went into cardiac arrest during catheterization for evaluation of right ventricular outflow tract obstruction, and was supported with ECMO. She underwent right ventricular outflow tract reconstruction 7 days later, but expired due to acute respiratory distress syndrome on the sixth postoperative day. No reoperation was required in association with arch anomaly during follow-up. Recurrent aortic arch obstruction occurred in one patient. He was an 8-day-old neonate who had HLHS with aortic atresia, diminutive ascending aorta, severe arch and isthmic hypoplasia, and large VSD. Five months after the Norwood–Rastelli procedure, recoarctation developed and balloon dilatation was performed. One patient developed left main bronchial compression necessitating a thoracotomy with aortopexy of the descending aorta (Fig. 2
). Three patients in group II underwent reoperation for subaortic stenosis or aortic stenosis, which developed during follow-up after arch repair, and two patients in group IV for change of right ventricular outflow tract conduit after the Norwood–Rastelli procedure. At last follow-ups, subaortic stenosis was noted in three patients and aortic stenosis in three. All patients were asymptomatic and all except eight patients did not require antihypertensive medication at their last follow-up visit. One patient who needed ECMO assist for low cardiac output syndrome just after operation and one patient who had residual aortic stenosis were taking angiotensin-converting enzyme (ACE) inhibitor and ß-blocker for LV dysfunction, and six ACE inhibitors for aortic stenosis, subaortic stenosis, LV dysfunction or mild cardiomegaly. No difference was observed between the four groups in terms of late mortality or postoperative morbidity during follow-up.
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Fig. 2. A female neonate whose left main bronchus was compressed after aortic coarctation repair and the Warden procedure for partial anomalous pulmonary venous return at 10 days old: (A) she had tracheal bronchus, (B) aortopexy was performed 1 year after operation, and the left main bronchial compression was relieved (C).
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4. Discussion
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We used simultaneous cerebral perfusion combined with myocardial perfusion during the repair of aortic arch anomalies, and this needed a somewhat higher flow rate of 50–100 ml/(kg min) in order to maintain a perfusion pressure of 50–60 mmHg, since the cerebral blood flow is related to pressure rather than rate [4]. In our series, early postoperative neurologic complications occurred in one patient (1.5%), which is lower than the reported rates (4–25%) in total circulatory arrest groups [5], and fortunately this female patient recovered completely. She was presumed to have experienced a preoperative hypoxic insult and had poor collaterals. There was no evidence of cerebral hyperperfusion syndrome in our study populations since the risk of cerebral edema could be reduced using careful monitoring of right radial artery pressure. However, long-term complications, such as neurodevelopmental abnormalities require further evaluation.
In neonates and some infants, low cardiac output can persist after coarctation repair due to preoperative LV dysfunction [6]. However, we used separate myocardial perfusion during aortic arch reconstruction, and hearts maintained an extremely slow, empty beating, and showed no signs of dilatation or functional derangement. Moreover, this technique reduced the myocardial ischemic time and enabled us to repair arch anomaly completely without being restricted by time. In our cohort, only four patients had postoperative low cardiac output syndrome, and these patients had preoperative severe ventricular hypertrophy and poor ventricular function requiring inotropics, sedation, and ventilator care. These results demonstrate that since the heart keeps beating during arch repair, this technique not only enables us to minimize low cardiac output syndrome but is also free of the mortality associated with low cardiac output syndrome. In addition to the use of regional perfusion, we believe that several factors, such as the pH-stat strategy used for acid–base management, high hematocrit, moderate hypothermia, improved surgical skills, and comprehensive perioperative intensive care contributed to our excellent results.
Numerous factors have been shown to increase the risk of recoarctation, including an age of less than 2–3 months, a low body weight, coarctation morphology (especially those with a hypoplastic aortic arch), silk suture material, and residual ductal tissue [7]. The risk of recoarctation appears to be high when simple end-to-end anastomosis and subclavian flap repair techniques are used [8], and the preferred technique for surgical repair in infants remains the subject of debate, particularly with respect to addressing aortic arch hypoplasia. Recently low recurrence rates have been reported for resection and extended end-to-end anastomosis or end-to-side anastomosis without prosthetic material [9–13]. In our cohort, follow-up data were available for 68 patients (100% of living patients), and only one patient underwent intervention for a recurrent arch gradient. Our review demonstrates that the surgical repair of aortic coarctation using resection and extended arch repair achieves excellent arch reconstruction and has a low rate of residual and recurrent coarctation even in neonates or infants, although it requires more extensive dissection and time.
The optimal age for repair of coarctation has yet to be resolved. Early correction as soon as possible tends to be recommended, since it reduces the risk of long-term hypertension and its associated cardiovascular risks [14]. However, repair in early infancy has been blamed for recoarctation [15]. Walhout et al. [16] analyzed aortic arch hypoplasia and an age of less than 1 month as independent factors of recurrence, whereas Pearl et al. [13] concluded that neonatal and infant coarctation repairs can be performed with very low risks of recoarctation and intervention. In Pandey et al.'s [17] analysis, although the recoarctation rate was found to be significantly higher in neonates than in older children, age did not emerge as a risk factor for recoarctation by multivariate analysis, because patients operated upon at a younger age fell into a morphologically poorer part of the spectrum, with borderline arches and complex anomalies. Thus, it could be that an adverse morphology of the coarctation segment rather than age per se affects recoarctation. In our opinion, it would be advisable to relieve coarctation at an early age to increase antegrade blood flow and stimulate the growth of these arches. Moreover, extended end-to-side anastomosis would be advisable to reduce the recoarctation rate, because it is clear that some patients will continue to remain at risk of recoarctation, based on the results of anatomic studies that show that the distal transverse arch and isthmus diameter in coarctation patients are significantly smaller than in normal patients [18], and despite good coarctation repair, obstruction is often seen due to growth failure of the transverse arch proximal to the site of repair, rather than ‘recoarctation’ at the site of repair [19]. We have tried to avoid recoarctation by excising all ductal tissue, minimizing tension at the anastomosis site (wide dissection of arch vessels and descending thoracic aorta and meticulous suture technique), minimizing purse-string effects of the anastomosis, using fine suture materials, correcting anatomic evaluations, applying proper surgical options, and modifying the techniques used [7,10]. Although we prefer to perform one-stage early correction with arch repair, our strategy for extended end-to-side anastomosis prevents recoarctation even in cases with an adverse morphology of the coarctation segment.
Airway compression can be almost avoided by extensive dissection of arch vessels, descending aorta, and left pulmonary artery, but if the airway is compressed by surrounding tissues after arch repair, position change and respiratory care can relieve or cure symptoms of airway obstruction. In our cohort, aortopexy was rarely necessary, except in a patient with tracheal bronchus.
Recurrent hypertension is commonly encountered despite successful coarctation repair. In general, the prevalence of hypertension is related to age at operation and to follow-up duration [14]. Late hypertension occurring in patients who have undergone repair as infants is usually associated with recoarctation [20], and recurrent hypertension should be prevented by early diagnosis and management in early childhood or in infancy. In our series, no patient had hypertension at the last follow-up because our patients had undergone arch repair at an early age, and no patient except one showed recoarctation. However, since the mean duration of follow-up was not so long (32.8 ± 17.5 months), the determination of whether our patients operated on in early age have a lower risk of hypertension in adulthood will require further long-term investigation. Although the present study is limited by the follow-up duration available thus far, intermediate term results are encouraging and support our current approach of using extended arch repair in patients with arch anomaly.
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5. Conclusions
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Our technique for extended aortic arch anastomosis with selective cerebral perfusion and a nonworking beating heart has been successfully utilized without mortality in 69 neonates and infants. One-stage total arch repair using our regional perfusion technique not only enables extended arch anastomosis without stopping brain and myocardial perfusion but also provides excellent neurologic and myocardial outcomes. Moreover, our surgical strategy for arch anomaly has a low rate of residual and recurrent coarctation when performed in neonates and infants.
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Acknowledgments
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This study was approved by the Institutional Review Board of Seoul National University College of Medicine/Seoul National University Hospital (H-0504-146-004).
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Footnotes
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\#9734; Presented at the joint 20th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 14th Annual Meeting of the European Society of Thoracic Surgeons, Stockholm, Sweden, September 10–13, 2006.
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Abstract
1. Introduction
