Eur J Cardiothorac Surg 2005;28:736-741
© 2005 Elsevier Science NL
Repair of persistent truncus arteriosus with interrupted aortic arch 
Tomas Tlaskal
*
,
Bohumil Hucin,
Vladimir Kucera,
Pavel Vojtovic,
Roman Gebauer,
Vaclav Chaloupecky,
Jan Skovranek
Kardiocentrum, University Hospital Motol, V Uvalu 84, 150 06 Prague 5, Czech Republic
Received 17 May 2005;
received in revised form 19 July 2005;
accepted 11 August 2005.
* Corresponding author. Tel.:+420 224432900; fax:+420 224432920. (Email: tomas.tlaskal{at}lfmotol.cuni.cz).
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Abstract
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Objective: The aim of our study was to analyse experience with repair of truncus arteriosus with interrupted aortic arch. Methods: Between 1993 and 2004, eight consecutive patients underwent repair of truncus arteriosus with interrupted aortic arch. The median age was 6.5 days (range 1–85 days) and median weight was 3.2 kg (range 2.6–4.8 kg). Five patients had type A and 3 patients had type B aortic arch interruption. The repair was performed in deep hypothermia with circulatory arrest in 4 patients and isolated selective low-flow perfusion of the head and the heart in the last 4 patients. The repair consisted in aortic arch reconstruction by direct anastomosis between descending and ascending aorta, closure of ventricular septal defect and reconstruction of the right ventricular to pulmonary artery continuity using a valved conduit. Results: One (12.5%) patient died from sepsis and hepato-renal failure 18 days after surgery. Seven (87.5%) patients were followed up for 2.0–11.7 years (median 2.6 years). No patient died after the discharge from hospital. In 4 patients 1–3 reinterventions were required 0.6–10.0 years after repair. Reoperations were performed for conduit obstruction in 2 patients, aortic regurgitation in 2 patients, right pulmonary artery stenosis in 2 patients and airway obstruction in 1 patient. In 2 patients concommitant aortic valve and conduit replacement was required. Balloon angioplasty for aortic arch obstruction was necessary in 1 patient, and for bilateral pulmonary branch stenosis in 1 patient. Five (28.6%) surviving patients are in NYHA class I and 2 (71.4%) patients are in NYHA class II. Conclusions: Primary repair of persistent truncus arteriosus with interrupted aortic arch can be done with low mortality and good mid-term results. Aortic arch reconstruction in isolated low-flow perfusion of the head and the heart influences favourably the postoperative recovery. The main postoperative problems are associated with conduit obstruction and aortic insufficiency.
Key Words: Congenital heart disease • Persistent truncus arteriosus • Interrupted aortic arch • Surgery • Mid-term results • Isolated perfusion of the head • Neonates
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1. Introduction
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Repair of persistent truncus arteriosus (PTA) can be performed with a low mortality rate [1]. Presence of severe truncal valve insufficiency, coronary artery anomalies and interruption of the aortic arch (IAA) were determined as the main risk factors for death after repair of this lesion [2]. Combination of PTA with IAA represents a rare and complex critical heart disease where the repair should be performed during the neonatal period because the circulation is dependent on patency of ductus arteriosus (PDA). The repair of PTA with IAA was first reported in 1971 by Gomes and McGoon [3], and successful repairs of PTA and IAA have been subsequently presented as case reports [4–9]. Most often, the surgical repair involved a period of circulatory arrest for aortic arch reconstruction. Due to the complex nature of this lesion, early and long term results of the primary repair of PTA with IAA depend on heart and aortic arch anatomy, clinical condition, method of perfusion and all the details of both the surgical repair and the postoperative care. The optimal timing of surgery and methods of perfusion, heart and brain protection, aortic arch repair, truncal valve repair as well as the right ventricular to pulmonary artery continuity reconstruction continue to be the most challenging issues.
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2. Patients and methods
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2.1 Patients
Between May 1993 and December 2004 eight consecutive patients with PTA and IAA were examined and corrected at Kardiocentrum, University Hospital Motol, Prague. The diagnosis was set by ECHO. All patients with PTA and IAA were examined for DiGeorge syndrome, but this diagnosis was not confirmed. In one patient, Jacobs syndrome (partial deletion of 11q chromosome) was diagnosed. Five (62.5%) patients had type A and 3 (37.5%) patients had type B IAA. In 3 patients with IAA type A a thin and long fibrous continuity without a lumen was found between the two parts of the aortic arch. There was present arteria lusoria dextra in two of the 3 patients with the type B anomalous right subclavian artery arising from the distal part of the aortic arch as the last branch. PTA was very large in 2 patients, 2 other patients had aneurysmatic dilatation of PDA and the distal part of the aortic arch. The truncal valve was usually thick and dysplastic. It was tricuspid in 5 and quadricuspid in 3 patients. Signs of truncal valve regurgitation were preoperatively found in 5 patients. The regurgitation was mild in 2 patients and moderate in 3 patients. VSD was infundibular and nonrestrictive in all patients. In 7 patients VSD was subarterial and in 1 patient it was perimembranous. The two oldest patients (85 and 26 days old), in whom presence of IAA was diagnosed later after birth, had PDA patent without administration of prostaglandins. In the remaining 6 patients infusion with prostaglandins was introduced as soon as IAA was diagnosed. One patient had preoperatively signs of infection and hepato-renal failure after closure of PDA. He required antibiotics, mechanical ventilation and peritoneal dialysis. In all patients the surgery was indicated after stabilization of hemodynamics, correction of metabolic disorders and treatment of complications. The median age at operation was 6.5 days (range 1–85 days), 6 patients were 10 days old or younger. The median weight was 3.2 kg (range 2.6–4.8 kg).
2.2 Surgery
All the surgeries in patients with PTA and IAA were performed by one surgeon (TT). The repair was performed through the midline sternotomy approach in deep hypothermia. Cardioplegic heart protection was performed using St Thomas crystalloid solution, which was administered repeatedly every 30 min in a doses of 30 ml/kg. For aortic arch reconstruction, in the first 4 patients deep hypothermic circulatory arrest at 17 °C was used. In the subsequent group of 4 patients continuous low-flow isolated selective perfusion of the head and the heart with a perfusate temperature of 20 °C was preferred. Two arterial cannulae were inserted: the first cannula into the right brachiocefalic trunk and the second one into PTA just superior to the truncal valve. Both arterial cannulae were connected using a Y-connector. Two venous cannulae were inserted transatrially. After the institution of cardiopulmonary bypass, both pulmonary branches were snared and a vent was inserted into the left atrium so as to prevent left ventricular distension. The repair consisted in aortic arch reconstruction, closure of VSD and reconstruction of the right ventricular-to-pulmonary artery continuity. For aortic arch reconstruction, wide dissection and mobilisation of PTA, main aortic branches, PDA and descending aorta was performed. After cooling the circulatory arrest was introduced and both arterial cannulae were withdrawn. In the second group of 4 patients the perfusion flow was decreased to 20 percent of the full calculated blood flow at 20 °C, the brachiocefalic trunk was centrally closed with a turniquet, the left carotid and the left subclavian arteries were snared, the descending aorta was closed with a Cooley clamp, and PDA was ligated and transsected. PTA was cross-clamped close to the truncal arterial cannula. Continuous flow to the head and to the coronary arteries was maintained and reconstruction of the aortic arch was done on a beating heart. In no patient signs of severe left ventricular dilatation or signs of myocardial ischemia were observed clinically or on ECG. In all patients with the type B IAA the left subclavian artery and, in 2 patients with abberrant right subclavian artery, both subclavian arteries had to be ligated and transsected so as to improve mobilisation of the descending aorta. A direct anastomosis with the ascending aorta was performed using a fine polypropylene monofilament (Prolene 7/0). After completion of the aortic anastomosis the suture-line was treated using a biological glue (Tissucol). The aorta was filled and deaerated. The Cooley clamp from the descending aorta and turniquets from the head vessels were released. The cannula from PTA was then withdrawn and the aortic clamp was repositioned higher, just below the aortic anastomosis. Cold St Thomas cardioplegic solution was administered into the aortic root. Pulmonary arteries were excised. The trunk was transsected in one patient with a more complex anatomy of the truncal valve and coronary arteries so as to make excision of pulmonary arteries safer, decrease the risk of damage to the valve and coronary arteries and make aortic reconstruction more appropriate. Foramen ovale was sutured and VSD was closed with a patch. The cross-clamp was released and the right ventricular-to-pulmonary artery continuity was established using a valved conduit on a beating heart (Table 1
). Because of lack of small pulmonary homografts which were preferred, in 3 recently operated patients a bileaflet conduit was tailored from an adult sized pulmonary homograft (20–25 mm in diameter) by excision of one cusp of the valve. In two patients in whom homograft was used the right ventricular outflow tract was enlarged with a glutaraldehyde treated pericardial patch. In all patients the sternum was left open. Survivors were followed up and examined regularly by ECHO.
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3. Results
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3.1 Early results
One (12.5%) patient died from sepsis and hepato-renal failure 18 days after surgery. It was a 6 days old neonate with IAA type A who had a quadricuspid truncal valve with a mild regurgitation in whom a 12 mm Hancock conduit (Medtronic) was used. The sternotomy was closed 4 days after surgery. After chest closure, signs of congestion with general edema persisted. Repeated respiratory tract infections were observed and the patient required prolonged mechanical ventilation, antibiotics administration and central venous access. However, the child died on the 18th postoperative day from sepsis. Seven (87.5%) patients survived. All patients needed inotropic support with dopamine, dobutamine and/or epinephrine in combination with sodium nitroprusside or milrinone. The chest was secondarily closed after median 1.5 days. In 3 patients the postoperative course was complicated by an infection, and in 1 patient by arrythmia, stridor and wound dehiscence. Pulmonary hypertension, however, did not represent any special concern in this series and no hypertensive crises were observed. Surgical results in patients operated using circulatory arrest (Group I) and using selective head and heart perfusion (Group II) are compared in Table 2
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3.2 Mid-term results
Four (57.1%) out of 7 survivors required reinterventions, which were performed 0.6–10.0 years after the repair (Table 3
). In one of them 3 reoperations were required 0.6, 5.5 and 10.0 years after the original surgery. Reoperations were performed for conduit obstruction in 2 (28.6%) patients, aortic regurgitation in 2 (28.6%) patients, right pulmonary artery stenosis in 2 (28.6%) patients and airway obstruction in 1 (14.3%) patient. In 2 (28.6%) patients a concommitant aortic valve replacement and conduit replacement was required. Balloon angioplasty for aortic arch obstruction was necessary in 1 (14.3%) patient, and for bilateral pulmonary branch stenosis in 1 (14.3%) patient. Seven (87.5%) survivors were followed up for 2.0–11.7 years (median 2.6 years, mean 5.7 ± 4.0 years) and regularly examined by ECHO. Five (71.4%) surviving patients were in NYHA class I and 2 (28.6%) patients were in NYHA class II. On ECHO pulmonary stenosis with a peak gradient of more than 30 mmHg in 2 (28.6%) patients and mild to moderate stenosis of both pulmonary branches was found in 2 (28.6%) patients. Balloon angioplasty was successfully performed in one of them 9 months after surgery. Grade 2 or 3 aortic insufficiency were found in 3 (42.9%) patients who had had aortic insufficiency preoperatively. Peak gradient across the aortic valve of 20 and 34 mmHg, respectively, was found in 2 (28.6%) patients. On last examination no gradient across the aortic arch was found in any patient clinically but a gradient of 30 mmHg was found in 1 patient and a gradient of 20 mmHg was found in another patients by ECHO.
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4. Discussion
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Experience with repair of PTA with IAA is limited and there is great variance in surgical results expressed by surgical mortality between individual centers. Some successful repairs of this lesion were published as case reports [4–9] but only few papers reporting larger series of operated patients with PTA and IAA have been found in the literature [1,2,10–14]. Our early and mid-term results are comparable with results recently reported from other centers (Table 4
). Brown presented a series of 60 patients with PTA operated on during 1978–2000 [10]. Six (10%) patients had IAA and in 3 of them reconstruction of the aortic arch using the left carotid artery was performed before the repair of PTA. Three (50%) patients with PTA and IAA died. In the series of 46 patients with PTA analysed by Bove, 5 (10%) patients had IAA [13]. All these patients except one were younger than 8 days and all had type B IAA. One (20%) patient in this series died. Sano analysed experience with repair of 7 patients with PTA and IAA operated at a median age of 8 days [14]. Six patients had type B and 1 had type A IAA. There were no early or late deaths in this series. In the most recent study from the Boston Children's Hospital, Jahangiri presented a series of 50 infants with PTA [1]. Nine (18%) patients had IAA and the median age was 17 days. In 5 patients it was possible to perform direct anastomosis of the descending and the ascending aorta but in 3 patients it was required to reconstruct aortic arch using a pericardial or a homograft patch. No patient in this series died during a median follow up of 13 months.
At Kardiocentrum, University Hospital Motol in Prague a total of 46 patients with PTA were operated on between 1993 and 2004 with 6 (13.0%) early deaths. All 8 (17.4%) patients with PTA and IAA, who were seen at Kardiocentrum during this period were indicated for surgery. It is true, however, that compared to other series our group of patients with PTA and IAA was somewhat different. There was a much higher prevalence of the type A IAA (62.5%) and only 3 (37.5%) patients had type B though in some series type B was present in 80–100% of operated patients with PTA and IAA [11–14]. Two of the 3 patients with type B had right subclavian artery arising from the distal part of the aortic arch. DiGeorge syndrome was not proved in any our patient though two patients had a hypoplastic thymus. According to Van Mierop about 68% of patients with IAA and about 33% patients with PTA have DiGeorge syndrome [15]. Low incidence of this syndrome in our series could be explained by the fact that it is typically associated with the type B.
Good results reached at our center were certainly determined by several factors. In Czech Republic the care for patients with congenital heart diseases is centralized into one center. Very often the correct diagnosis is set up prenatally or early after birth. The neonate is transferred immediately to our center. The surgical mortality in the whole spectrum of heart diseases has decreased substantially in course of the last 15 years and has remained at the level of 1% since 1999. The repair of PTA and IAA was always performed after a short period of stabilization and after treatment of all complications. All the surgeries in patients with PTA and IAA were performed by one surgeon. In all patients a strict protocol of preoperative management, surgical approach, perfusion, heart protection and postoperative care was applied with a routinely delayed chest closure. Localisation of a homograft bank in the hospital represents also an advantage. Isolated perfusion of the head and the heart improved the postoperative recovery. However, it is necessary to say also that we had an opportunity to learn from the experience of other surgeons and to apply some of their recommendations.
The deliterious effect of circulatory arrest on brain is well known and many authors recommend avoiding circulatory arrest whenever possible. Isolated continuous low flow perfusion of the head for the period of aortic arch reconstruction was recommended by several groups [16–18]. In 4 patients in our series the method of a concommitant isolated cerebral and myocardial perfusion was applied. This approach enabled us to exclude an appropriate segment of the ascending aorta for the direct end to side anastomosis between descending and ascending aorta without circulatory arrest and on a beating heart. This led to a shortening of the time of aortic-cross clamping. We compared the group of patients in whom the method of deep hypothermic circulatory arrest was used with the group where isolated cerebral and myocardial perfusion was used (Table 2). In the group of isolated perfusion the aortic cross-clamping time was shorter, which resulted in less congestion, less signs of low cardiac output and postperfusion lung problems. In this group the postoperative course was rather smooth with a shorter period of open chest, artificial ventilation, ICU stay, hospital stay, and less occurance of postoperative complications and need for reintervention. We did not observe any differences as far as the occurance of neurological complications or signs of myocardial injury is concerned. Our observations, though they did not reach statistical significance, have supported the theory that isolated perfusion of the brain and the heart is advantageous compared to the hypothermic circulatory arrest. So far, we have not used this method for treatment of other diseases but a similar method was already described by others for one stage repair of coarctation of the aorta and VSD [19].
Until present it is not clear, which is the best method of aortic arch reconstruction in patients with PTA and IAA, however, in the majority of patients direct anastomosis of descending and ascending aorta can be performed [1]. It is true that in some patients with type B IAA, especially in presence of aberrant right subclavian artery, and when the ascending aorta is extremely narrow and shifted more to the right, reconstruction may be difficult. The distance between descending and ascending aorta may be as long as 2–3 cm. Under these settings, it is usually necessary to transsect one or both subclavian arteries and mobilise aorta as much as possible. It is crucial, however, to construct the aortic anastomosis without tension so as to prevent anastomotic stenosis on one hand and tracheo-bronchial compression on the other hand. The risk of complications related to aortic arch stenosis is increased when the ascending aorta is short and the root of the truncus excessively dilated preoperatively as it was the case in our 85 days old infant in whom the root dilatation caused the left bronchus and the right pulmonary artery compression [20]. A similar case of the left bronchus compression by the truncal root was described by Sano [13]. Under these morphological conditions plasty of the aortic root and alternative methods of aortic arch reconstruction should be considered. The use of the left subclavian artery with an enlargement using a homograft patch seems to be the most suitable alternative approach [2]. This method is useful especially in the type B IAA. The left subclavian artery is transsected and anastomosed to the ascending aorta. Aortic arch is enlarged with a patch cut from a pulmonary homograft as in Norwood operation for hypoplastic left heart syndrome. Anterior translocation of the pulmonary bifurcation is considered to be an efficient method to prevent tracheobronchial compression [21] but sometimes this maneuver could probably increase the risk of stenosis or compression of the right pulmonary artery between the dilated truncus and the thoracic wall. In some patients with type A IAA it would be possible to do reconstruction in a similar way as in coarctation repair. However, in patients with PTA and type A IAA no isthmus is present and aortic arch reconstruction would require to perform the anastomosis between the base of a narrow left subclavian artery and a large descending aorta. As the aortic arch is almost always short and narrow the risk of restenosis might be higher than after anastomosis between ascending and descending aorta.
Selection of the most suitable conduit for the right ventricular-to-pulmonary artery continuity reconstruction represents a challenging issue in neonates with PTA. A fresh frozen pulmonary homograft is considered to be the best type of valved conduit with a prolonged durability [22]. Pulmonary homografts usually remain pliable for a long time. In some of them, however, there may develop the stenosis at the site of the periferal anastomosis or stenosis of the pulmonary branches with subsequent conduit dilatation and pulmonary insufficiency [23]. The lack of small pulmonary homografts and less favourable mid-term experience after implantation of small aortic homografts forced us to use two specific conduits. Pulmonary bicuspid homograft tailored from an adult sized homograft represents an excellent alternative, though postoperatively mild pulmonary regurgitation is usually present. On mid-term follow up we have observed functioning bileaflet homograft valve with a mild to moderate regurgitation. In one of the patients, however, in whom stenosis at the site of the distal anastomosis and pulmonary branches developed, had the homograft dilated with grade 3 regurgitation. This type of conduit represents therefore our conduit of choice only in patients with PTA and good pulmonary branches. In situations, where the risk of pulmonary artery compression is critical, a stented 12 mm Hancock conduit with a porcine aortic valve is preferred. In neonates with very unfavourable anatomy of the truncal valve, small pulmonary arteries or in presence of severe cardiomegaly, small aortic homograft should be considered, especially with critical lack of space in the mediastinum.
In PTA with IAA truncal valve regurgitation is often present preoperatively. Presence of severe regurgitation requires that a special attention is paid to the risk of the left ventricular distension and a vent should be introduced. When the regurgitation is severe and the left ventricle distends it is possible to cannulate the ductus arteriosus as in hypoplastic left heart syndrome for perfusion of the lower part of the body. Valve repair should be probably performed in these patients at the time of PTA repair because otherwise regurgitation may progress with time. Different methods of truncal valve repair such as commisuroplasty, commisural resuspension and valve remodeling by suture or by resection of one leaflet, were described and applied on a limited number of patients [1,24]. Unfortunately, however, the truncal valve is very variable as far as the exact anatomy is concerned. Often it is quadricuspid and dysplastic with signs of combined truncal valve regurgitation and potential stenosis, which makes the plasty very difficult. In our series we observed grade 3 truncal valve regurgitation in 2 oldest patients and in both of them the valve was severely malformed and dysplastic. Regurgitation was clinically well tolerated and we therefore decided not to do the plasty. Today we would repair the valve but 10 years ago we considered this procedure to be time consuming and risky with unpredictable result. In one of our patients the progression of aortic regurgitation during follow up could be related to the development of aortic arch stenosis, which required balloon angioplasty. It is necessary to admit the fact that the problem of treatment of aortic insufficiency in patients with PTA remains an extremely important issue in many series with suboptimal long term results [25]. On the other hand excellent mid-term results of the tuncal valve repair have been reported from several centers where new methods of truncal valve remodeling were developed [1,24].
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5. Conclusions
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Primary repair of PTA with IAA can be done with low mortality and very good mid-term results. The method of selective low flow perfusion of the head and the heart permits avoiding the circulatory arrest and making the period of myocardial ischemia shorter. This method improved considerably the postoperative hemodynamics and influenced favourably the early results of the primary repair of PTA with IAA. The main long term problems after repair of this lesion are associated with conduit obstruction and progression of aortic insufficiency.
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Acknowledgments
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The study was supported by the research project VZ FNM No. MZO 00064203.
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Footnotes
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Presented at the joint 17th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 11th Annual Meeting of the European Society of Thoracic Surgeons, Vienna, Austria, October 12–15, 2003. 
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Top
Abstract
1. Introduction
