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Ann Thorac Surg 2001;72:391-395
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Neonatal repair of truncus arteriosus: continuing improvement in outcomes

^a Divisions of Cardiothoracic Surgery and Pediatric Cardiology, University of California, San Francisco, San Francisco, California, USA

Accepted for publication April 27, 2001.

Address reprint requests to Dr Thompson, University of California, San Francisco, 505 Parnassus Ave, M593, San Francisco, CA 94143-0118

	Abstract

Top Abstract Introduction Material and methods Results Comment References

 
Background. Repair of truncus arteriosus in the neonatal and early infant periods has become standard practice at many centers. We reviewed our recent experience with repair of truncus arteriosus in neonates, with a focus on early and intermediate outcomes.

Methods. From July 1992 to December 1999, 65 patients 1 month of age or less underwent primary complete repair of truncus arteriosus. Median age was 10 days, and median weight was 3.2 kg. Major associated anomalies included moderate or severe truncal valve regurgitation in 15 patients (23%), interrupted aortic arch in 8 (12%), coronary artery abnormalities in 12 (18%), and nonconfluence of the pulmonary arteries in 3 (5%). Median durations of cardiopulmonary bypass and cardioplegic arrest were 172 minutes and 90 minutes, respectively. Circulatory arrest was employed only in 7 patients undergoing concomitant repair of interrupted arch. Reconstruction of the right ventricular outflow tract was achieved with an aortic (n = 39) or pulmonary (n = 26) allograft valved conduit (median diameter, 12 mm). Replacement (n = 6) or repair (n = 5) of a regurgitant truncal valve was performed in 11 patients, and interrupted arch was repaired in 8.

Results. There were three early deaths (5%). Early reoperations included reexploration for bleeding in 3 patients, emergent replacement of a pulmonary outflow conduit that failed acutely in 1 patient, and placement of a permanent pacemaker in 1. Mechanical circulatory support was required in 1 patient. During the median follow-up of 32 months, there were two deaths. The Kaplan-Meier estimate of survival was 92% at 1 year and beyond. The only demographic, diagnostic, or operative factors significantly associated with poorer survival over time were operative weight of 2.5 kg or less (p = 0.01) and truncal valve replacement (p = 0.009). Actuarial freedom from conduit replacement among early survivors was 57% at 3 years.

Conclusions. Repair of truncus arteriosus in the neonatal period can be performed routinely with excellent survival, even in patients with major associated abnormalities.

	Introduction

Top Abstract Introduction Material and methods Results Comment References

 
Since McGoon and colleagues [1] first described repair of truncus arteriosus more than 30 years ago, major advances have been made in the management of this lesion, transforming it from a condition that was fatal early in life in greater than 50% of patients to one in which neonatal repair is increasingly common and increasingly successful [2–14]. The trend toward early repair in infancy began at our institution in the mid-1970s and early 1980s [3], and over the past decade, several series comprised largely of neonates and young infants have been published, with progressively promising results [5–8, 11, 13]. Even since the seminal 1993 reports of Bove and associates [6] and Hanley and co-authors [5], there has been a continuing improvement in outcomes after neonatal repair, as demonstrated by several recent articles [8, 13]. Since July 1992, our policy has been to perform primary complete repair at the time of presentation. In this report, we describe our experience with repair of truncus arteriosus in 65 consecutive neonates.

	Material and methods

Top Abstract Introduction Material and methods Results Comment References

 
Between July 1992 and December 1999, 65 patients underwent primary complete repair of truncus arteriosus at the age of 1 month or less (neonates) by surgeons in the University of California, San Francisco, Division of Pediatric Cardiac Surgery (procedures performed at University of California, San Francisco, Medical Center, Children’s Hospital of the East Bay, and Valley Children’s Hospital). This represents all but 2 of the patients undergoing primary repair of common arterial trunk at our institution during this period. Early in our experience, 2 patients who were referred late underwent primary repair at approximately 4 months of age, and 2 additional patients underwent complete repair at 5 and 6 years of age after prior palliation. These 4 patients are not included in this study. No patient underwent a palliative procedure during the period of this study, and no patient died at our institution while awaiting surgical intervention.

All patients were diagnosed by cross-sectional and Doppler echocardiography. In 3 patients, preoperative cardiac catheterization was performed to confirm or better characterize the diagnosis (n = 2) or to evaluate ventricular function (n = 1).

The median age at operation was 10 days (range, 2 to 30 days); 18 patients (28%) were 1 week old or younger. The median weight was 3.2 kg (range, 2.1 to 4.3 kg); 24 patients (37%) weighed less than 3 kg and 9 (14%) less than or equal to 2.5 kg. Sixty percent of patients (n = 39) were male. In all but 3 patients, the pulmonary arteries arose from the common trunk either as a single artery that divided at or soon after its origin or as separate left and right branches from the posterior, posterolateral, or lateral aspect of the trunk. In 3 patients, the origin of one branch pulmonary artery was from the common trunk, and the other arose from the underside of the aortic arch (nonconfluent pulmonary arteries). Moderate (n = 10) or severe (n = 5) regurgitation of the truncal valve was present in 15 patients (23%). In 8 patients (12%), there was associated interruption of the aortic arch with a widely patent arterial duct providing flow to the descending aorta. In all instances, the interruption was between the left common carotid artery and the left subclavian artery. In 4 patients, there was both an interrupted arch and moderate truncal valve regurgitation. Anomalies of the coronary arteries were present in 12 patients (18%): a single coronary artery in 5; origin of the left anterior descending branch from the right coronary artery in 4; a high and posterior origin of the left coronary artery just proximal to the pulmonary artery in 2; and a separate origin of the right coronary artery from the left coronary sinus in 1. In 3 of these patients, both moderate truncal valve regurgitation and an interrupted arch were present as well.

Operative procedures
Right ventricular outflow tract reconstruction was performed with either an aortic (n = 39) or pulmonary (n = 26) allograft valved conduit. The type of conduit used was generally determined on the basis of size availability. The median conduit diameter was 12 mm (range, 9 to 15 mm). After separation of the pulmonary arteries from the common trunk, the right ventricular infundibulum was incised, and the ventricular septal defect was closed with a patch of glutaraldehyde-fixed autologous pericardium, using an interrupted suture technique. The defect in the wall of the aorta was repaired either primarily or with a patch of allograft tissue. The distal end of the conduit was then sewn to the pulmonary artery defect, with extension of allograft tissue from the conduit into one or both branch pulmonary arteries, as necessary, to alleviate proximal branch pulmonary artery stenosis. The proximal end of the valved conduit was sewn to the infundibulotomy, usually with a hood of prosthetic material, or the anterior mitral valve leaflet from an aortic allograft, used to complete the anastomosis proximally.

Additional procedures, such as truncal valve replacements, repair, or correction of interrupted aortic arch, were performed as necessary prior to reconstructing the right ventricular outflow tract. In 11 patients with severe or moderate truncal valve regurgitation, the truncal valve was replaced with either an aortic allograft root (n = 5) or a mechanical valve (n = 1) or repaired with techniques of annuloplasty, commissural suspension, resection of a minor leaflet followed by reapproximation of the contiguous leaflets and annular plication, or a combination of these (n = 5). Since 1996, only 1 patient has undergone truncal valve replacement, and this was performed with a 15-mm mechanical prosthesis after enlargement of the truncal root.

Several different techniques were used to reconstruct the aortic arch in the 8 patients with arch interruption. All patients underwent reconstruction with a direct anastomosis (ie, no circumferential conduits were employed), but the approach that we believe allows optimal arch repair while minimizing the risk of bronchial or pulmonary artery obstruction involves wide mobilization of the arch branches and descending aorta, complete or subtotal transection of the common trunk proximal to the origin of the pulmonary arteries, and reconstruction of the underside of the arch with a triangular patch of aortic or pulmonary allograft tissue, similar to the technique employed for stage 1 palliation of hypoplastic left heart syndrome. This technique has been described and illustrated previously [5]. If necessary, the left subclavian artery can be sacrificed and its proximal aspect opened longitudinally to help reconstruct the superior aspect of the arch. This technique can be performed with or without the Lecompte procedure, which facilitates placement of the right ventricle–pulmonary artery conduit. A Lecompte maneuver was used in 2 of our patients. In most patients, a foramen ovale, if present, was left patent, or a small interatrial defect was created to allow for decompression of the right heart in the early postoperative period.

Repair was performed in all patients with the use of cardiopulmonary bypass and intermittent cold crystalloid cardioplegia delivered in an antegrade fashion. Bypass was performed with arterial cannulation of the aorta or innominate artery and bicaval venous cannulation in all patients. In very small infants, a left ventricular vent was used for venous cannulation if necessary. The median durations of cardiopulmonary bypass and cardioplegic arrest were 172 minutes (range, 128 to 526 minutes) and 90 minutes (range, 36 to 192 minutes), respectively. Circulatory arrest was used only in 7 of the 8 patients undergoing concomitant repair of interrupted arch (range, 15 to 55 minutes). In the remaining patient with interrupted arch, selective cerebral perfusion was maintained during the arch reconstruction by means of innominate artery cannulation. The sternum was frequently left open electively, with delayed sternal closure performed 2 to 3 days later [15].

Postoperative care
Inotropic support was initiated with a low-dose (3 to 5 µg · kg^-1 · min^-1) infusion of dopamine hydrochloride after the discontinuation of cardiopulmonary bypass, and weaning was done gradually over the first 24 to 48 hours. If additional inotropic support was indicated, the dopamine infusion was increased as high as 10 to 15 µg · kg^-1 · min^-1, after which an epinephrine infusion was started (0.03 to 0.05 µg · kg^-1 · min^-1) if necessary. An indwelling double- or triple-lumen catheter was placed in the right atrium before the patient left the operating room and was discontinued as indicated. A left atrial line was used only in patients with depressed left ventricular function or hemodynamic instability. Pulmonary artery catheters were not placed routinely, though on occasion a right atrial catheter was advanced antegrade into the pulmonary artery. Open sternotomy with delayed sternal closure was performed electively (ie, without a trial of sternal closure in the operating room) in patients with long bypass runs or in whom it was considered indicated for other reasons, such as respiratory insufficiency, ventricular dysfunction, persistent mediastinal bleeding, or mechanical circulatory support.

To minimize the likelihood of pulmonary hypertensive episodes, patients were kept warm and moderately hyperventilated, with a target systemic arterial pH of 7.5 to 7.55. Inhaled nitric oxide was available for the treatment of pulmonary hypertensive crises, though it was not required in any of the patients in this series. Patients were maintained on sedation with infusions of fentanyl and midazolam hydrochloride for the first 24 hours, or until extubation, unless clinical circumstances demanded more prolonged sedation. Neuromuscular blockade was used only in patients who were in unstable condition or in whom it was indicated for other reasons.

Data analysis
Preoperative and perioperative data were collected on retrospective review of patient records. Cross-sectional follow-up was carried out by means of physician or patient contact or both and was completed by May 2000. The primary outcome measure was early survival. Secondary outcomes of interest included early morbidity, intermediate survival, and intermediate morbidity. Results classified as "early" are those that occurred prior to hospital discharge or within 30 days of operation if the patient was discharged before this duration.

Independent variables analyzed for correlation with outcome measures included demographic, diagnostic, and operative factors. Demographic variables included age, weight, sex, and date of repair. Diagnostic variables included presence of associated anomalies such as interrupted aortic arch, moderate or severe truncal valve regurgitation, abnormal coronary artery anatomy, and discontinuous pulmonary arteries. Operative variables included duration of cardiopulmonary bypass, duration of cardioplegic arrest (see Table 1), type of allograft conduit used (aortic or pulmonary), size of conduit used, and additional procedures such as repair of interrupted arch, truncal valve repair, or truncal valve replacement.

	Results

Top Abstract Introduction Material and methods Results Comment References

 
Early outcomes
There were three early deaths (5%). All 3 patients underwent operation in 1996 or before, and 2 weighed less than 2.5 kg at the time of repair. Associated anomalies in the patients who died included interruption of the aortic arch in 2, moderate truncal valve regurgitation in 1, a single coronary artery in 1, and DiGeorge syndrome in 2. One patient died after the development of sepsis and multiple-organ failure, and the other 2 died of cardiopulmonary failure. One of the latter was supported for 7 days on extracorporeal membrane oxygenation but could not be weaned successfully. Postoperative mechanical circulatory support was not required in any other patient. By univariable analysis, none of the demographic, diagnostic, or operative variables analyzed were found to correlate with early mortality. The only independent variables to approach significance were interrupted aortic arch (p = 0.07) and operative weight of 2.5 kg or less (p = 0.09).

Early reoperations, aside from delayed sternal closure, were performed in 5 patients: 3 for exploration and control of mediastinal bleeding, 1 for emergent replacement of a right ventricle–pulmonary artery conduit 5 days after repair because of free regurgitation and consequent heart failure, and 1 for placement of a permanent pacemaker for complete heart block (this patient was on extracorporeal membrane oxygenation and subsequently died). As discussed in a previous report, we [15] frequently elect to perform delayed sternal closure in patients undergoing complex neonatal operations, including those with truncus arteriosus, usually without a trial of sternal closure in the operating room. There were no sternal wound infections in this patient cohort. Two patients had a postoperative seizure that was detected clinically, with no subsequent electroencephalographic evidence of seizure activity, and no further clinical seizure episodes. Two patients had pulmonary hypertensive crises, and 1 sustained a cardiac arrest requiring open cardiac massage. Inhaled nitric oxide was not used in any patient. The median duration of postoperative mechanical ventilation was 3 days (range, 1 to 15 days), and the median postoperative hospital stay was 14 days (range, 8 to 34 days).

Intermediate outcomes
Cross-sectional follow-up was available for all patients at a median of 32 months after repair (range, 6 to 92 months). During the follow-up period, there were two late deaths, both of which occurred 8 months after complete truncus repair with allograft truncal valve replacement. One patient died suddenly at home of suspected asphyxia as a result of aspiration; the other died 2 months after repeat truncal valve replacement after the mechanical valve became lodged in the open position, leading to severe acute aortic regurgitation and left-sided heart failure. The Kaplan-Meier estimate of survival was 92% at 1 year and beyond (95% CI; 84% to 98%). Univariable Cox proportional hazards regression found weight of 2.5 kg or less at the time of operation and truncal valve replacement to be associated with poorer survival (Table 1). By multivariable Cox regression, both of these variables remained significant (both, p = 0.02).

During follow-up, 22 patients underwent reintervention for conduit replacement a median of 32 months after repair. The Kaplan-Meier estimate of freedom from conduit replacement was 91% at 1 year (95% CI; 84% to 98%) and 57% at 3 years (95% CI; 43% to 71%). Replacement of the truncal valve with a mechanical valve was performed 6 months postoperatively in a patient who had undergone replacement with an aortic allograft root at the time of truncus repair and 13 months postoperatively in another patient who had undergone allograft truncal root replacement as a neonate.

	Comment

Top Abstract Introduction Material and methods Results Comment References

 
As several centers have demonstrated in recent years, early primary repair of truncus arteriosus is becoming an increasingly successful approach to the management of this complex anomaly [5–8, 11, 13, 14]. Early survival has grown steadily better with advances in surgical and perioperative management over the past several decades and continues to do so. In particular, the prognosis seems to be improving most for patients with the more complex forms of truncus arteriosus, namely, those with associated interruption of the aortic arch, substantial truncal valve regurgitation, and coronary artery anomalies, as has been demonstrated in several recent series from Ann Arbor [6], Cleveland [8], and Boston [13]. Despite the many favorable reports that have emerged in recent years, however, it is premature to conclude that this is no longer a daunting lesion to manage. Other recent series [9, 11] have shown significant mortality, especially among patients with abnormalities of the truncal valve or aortic arch. Thus, additional data and analysis are necessary to understand better the optimal management of these patients and to further improve early and long-term outcomes.

In the present series, we demonstrated an early mortality rate of 5% in an unselected, consecutive population of patients undergoing repair of truncus arteriosus in the neonatal period over the past 7 years. There were two additional deaths during follow-up, for an overall actuarial survival of 92% at 1 year postoperatively and beyond. All five deaths occurred during the first half of our reported experience (1996 or before). The only factors associated with poorer survival over time were an operative weight of 2.5 kg or less and truncal valve replacement, though the number of deaths was small and the CIs for these risk factors were wide. Three of the patients who died had a low weight and had major truncal valve regurgitation (n = 2), interrupted aortic arch (n = 2), or both of the latter. Thus, although surgical weight of 2.5 kg or less was identified as a significant risk factor for poorer survival, all of the patients who had a low weight and did not survive also had complex associated anomalies, which confounds the aforementioned analysis. It is notable that these associated conditions per se were not risk factors for poor outcome. In a series from Boston [5] published in 1993, all three of these complicating factors were associated with an increased risk of perioperative death. In the more recent experience of that group [13], however, these features were no longer significant predictors of early mortality, and as the authors discuss, this finding suggests that growing experience with the surgical and perioperative management of patients with such complicated anatomy has effectively improved their outcome. Our experience and the experiences of others [6, 8] seem to support this contention as well.

Despite the progressive improvement in outcomes, especially among patients with complex truncus arteriosus, there is continuing debate about the optimal approach to management. For patients with truncus arteriosus and important associated lesions, such as moderate to severe truncal valve regurgitation or interrupted aortic arch, most surgeons would agree that early primary repair is generally the preferred approach. In the case of straightforward truncus arteriosus, however, there are surgeons who often or sometimes elect to wait until the patient is several months of age to perform a definitive repair, frequently with excellent results [7, 8, 16]. Although repair at less than 30 days of age was associated with poor outcome in some earlier series, it is not clear whether there is a substantial difference in outcome after repair at the time of neonatal presentation versus delayed correction at 2 to 3 months of age in patients whose condition is not complicated. To be sure, there are potential benefits to operating on a larger patient, but there are also potentially important drawbacks to delayed repair. We prefer to perform primary complete repair at the time of presentation in virtually all patients with truncus arteriosus and have experienced very encouraging results with this approach.

An issue of particular importance in the subset of patients with major truncal valve regurgitation is the management of the truncal valve. For many years, truncal valve regurgitation was the most important factor contributing to early death in patients with truncus arteriosus, whether they underwent early repair or not [17]. As we have discussed previously, replacement of the truncal valve with a mechanical prosthesis was of only minimal benefit in improving survival [17]. Replacement with an aortic allograft root, although effective in some patients, is equally problematic, as patients almost inevitably have development of allograft failure and frequently experience major morbidity as a result of recurrent aortic regurgitation, reoperation, or both. In the present series, truncal valve replacement, which was performed in only 1 patient after 1995, was a risk factor for poorer survival over time. In recent years, we [17] and others [8, 13, 18] have advocated truncal valve repair as an arguably superior alternative to replacement. Of the 5 patients who underwent truncal valve repair in this series, 2 were included in previous reports [17, 19]. Three others who underwent repair of the truncal valve earlier in our institutional experience (before 1992) are not included in this report. Of these 8 patients, only 2 (neither included in the present series) have required replacement of the truncal valve, and in both cases, this was at least 10 years after the initial repair. Thus, the limited available data suggest that truncal valve repair is effective and durable, and our current recommendation is that this should be the first option in essentially all neonates with major truncal valve regurgitation.

	References

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