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Ann Thorac Surg 2005;79:2077-2082
© 2005 The Society of Thoracic Surgeons

Original article: Cardiovascular

Repair of Truncus Arteriosus and Aortic Arch Interruption: Outcome Analysis

Takashi Miyamoto, MD, Nicodème Sinzobahamvya, MD*, Daiva Kumpikaite, MD, Boulos Asfour, MD, Joachim Photiadis, MD, Anne Marie Brecher, MD, Andreas E. Urban, MD

Department of Paediatric Cardiothoracic Surgery, German Paediatric Heart Centre, Deutsches Kinderherzzentrum, Sankt Augustin, Germany

Accepted for publication November 17, 2004.

* Address reprint requests to Dr Sinzobahamvya, Deutsches Kinderherzzentrum Sankt Augustin, Arnold-Janssen-Strasse 29, 53757 Sankt Augustin, Germany (E-mail: sinzo.md{at}dkhz.de).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Comment
 Acknowledgments
 References
 
BACKGROUND: The excellent results for repair of truncus arteriosus reported in some centers have not applied to patients with associated interrupted aortic arch. This work aims at understanding the discrepancy of results in our own experience.

PATIENTS AND METHODS: Ten patients among 83 consecutive children with truncus arteriosus repaired from 1987 to September 2004 who had aortic arch interruption were analyzed, with particular emphasis on clinical presentation and outcome. The comprehensive Aristotle complexity score was calculated for each patient. The Kaplan-Meier method was used to estimate survivals.

RESULTS: Preoperative mechanical ventilation was necessary in 5 of the 10 patients; 2 of them were moribund. Associated major lesions were as follows: severe (n = 2) and moderate (n = 4) truncal valve regurgitation, coronary artery anomalies (n = 3) and Di-George’s syndrome (n = 4). The comprehensive Aristotle score was at least 20 in 6 patients. There were 5 operative deaths (5 of 10); early mortality was 50% (95% confidence limits: 19% to 81%). These deaths occurred in patients with Aristotle score of 20 or greater (5 of 6 = 83%). All 4 patients who had no moderate or severe truncal valve regurgitation survived the intervention. Survival was a low 37.5% ± 16.1% from 1 year on compared with a high 95.5% ± 2.5% for the 73 patients without aortic arch interruption.

CONCLUSIONS: This study confirms the predictive value of the Aristotle score, hospital mortality being significantly correlated with the highest Aristotle score (p = 0.024). To improve outcome in these high-risk patients, preoperative management should be optimized, repair should not be delayed, and regurgitant truncal valve should be repaired or replaced.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Comment
 Acknowledgments
 References
 
Despite improved results for repair of truncus arteriosus, overall mortality rates continue to be higher than for neonatal correction of many congenital heart diseases. In 1987, we started a program of early primary repair using valved homografts to reconstruct the right ventricular outflow which brought excellent results [1, 2]. Postoperative survival approached 100% in all patients except those with associated interruption of the aortic arch. The difference in outcome persisted over time. This work aims at understanding reasons for the discrepancy between the overall unusually successful results for repair of truncus arteriosus and the unsatisfactory outcomes for patients with associated interrupted aortic arch.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Comment
 Acknowledgments
 References
 
Preoperative and perioperative data were collected on retrospective review of patients’ records, with particular emphasis on age, weight, and clinical presentation before repair, associated anomalies, data of cardiopulmonary bypass, type of valved allograft conduit used, type of aortic arch reconstruction, associated procedures, and early and late outcome. The comprehensive Aristotle complexity score [3] was thereafter evaluated to estimate the operative risk. The Kaplan-Meier method was used to calculate actuarial survival for these patients and for comparison (the log-rank test) with patients without aortic arch interruption. For discussion, this study is compared with reports about truncus arteriosus repair published in the last 10 years that include at least 50 patients and clearly mention early mortality in the cases with associated interrupted aortic arch. Means ± standard deviation and percentages with 95% confidence limits (CL) are given.

Patients
Between June 1987 and September 2004, 83 consecutive children with truncus arteriosus underwent repair with homograft reconstruction of the right ventricular outflow tract. According to the Van Praagh classification [4], it was a common arterial trunk type A1 in 48 cases, type A2 in 23, type A3 in 2, and type A4 with associated interrupted aortic arch in 10 patients. These last patients constitute the material for this study. This group included 8 girls and 2 boys.

Table 1 summarizes the clinical presentation. Median age at operation was 17 days (range, 3 to 31) and median weight 3 kg (range, 1.7 to 3.7 kg). All patients received prostaglandin E1 therapy to keep the ductus arteriosus patent. Five (50%; 5 of 10) presented in severe heart failure requiring ventilation and inotrope therapy before operation. Two had been referred to our unit after more than 2 weeks of mechanical ventilation. Patient 1 (see Table 1) who had severe renal insufficiency and patient 8 who had closing ductus arteriosus that did not respond to prostaglandine infusion were moribund. In patient 6, necrotizing enterocolitis with colon necrosis and perforation dictated bowel resection and colostomy. According to the classification of Celoria and Patton [5], 9 patients had type B aortic arch interruption and the remainder, type A.


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  		Table 1. Truncus Arteriosus With Interrupted Aortic Arch (IAA): Clinical Presentation
 
Surgical Technique
Except for the first patient of this series who had reconstruction of type B interrupted aortic arch through a left thoracotomy 2 weeks before truncus repair, all the other 9 children underwent one-stage complete repair. The technique used in our unit for repair of truncus arteriosus and to prevent pulmonary hypertensive crises has been described in previous reports [1, 2]. It is to be noted that we routinely used irradiated packed cells for bypass priming and for any transfusion. After median sternotomy, the proximal aortic arch and its branches were dissected before the opening of the pericardium. Cardiopulmonary bypass was started with double arterial cannula (ascending aorta and ductus) and a single venous cannula. The patient was cooled down to 15° to 18°C nasopharyngeal temperature (see Table 2). While excising the pulmonary arteries from the common trunk, care was taken to not injure the coronary arteries. The defect in the truncal wall was repaired with a patch to prevent obstruction of coronary blood flow (n = 6). In the other 4, the truncotomy was closed directly. The distal aortic arch and the descending aorta were extensively mobilized to allow, after resection of ductal tissue, reestablishment of aortic arch continuity without tension by direct aortic anastomosis. In case of arteria lusoria, a conduit was used to bridge the aortic interruption. Since 1997 (the last 5 cases), the reconstruction of the aortic arch was performed with the heart beating; coronary perfusion was maintained through a small cannula placed in the proximal ascending aorta. This cannula was later used for infusion of cardioplegic solution. In patient 7, aortic root application of blood had to be discontinued because of truncal valve regurgitation. In the last 2 patients, before aortic cross-clamping, the flexible aortic cannula was advanced from the ascending aorta into the innominate artery. Low-flow bypass maintained adequate cerebral perfusion and limited indirect circulation for the lower part of the body; at the same time, aortic root perfusion kept the heart beating during aortic arch repair.


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  		Table 2. Truncus Arteriosus With Interrupted Aortic Arch: Repair and Outcome
 
The ventricular septal defect was closed through right ventriculotomy with a patch using interrupted pledget-supported sutures, and the atrial septal defect was routinely closed during a brief period of circulatory arrest. The continuity between right ventricle and the pulmonary arteries was established with a valved homograft. Table 2 shows the type and size of the homografts used. The graft was connected to the ventriculotomy with help of a hood made either of pericardium (n = 6) or a polytetrafluoroethylene (PTFE) patch (n = 2), or a mitral leaflet from the aortic homograft donor (n = 2). Additional procedures included resection and pericardial patch enlargement of supravalvular aortic stenosis (patient 10), valvotomy for truncal valve stenosis (patient 4), resuspension of a traumatically torn truncal valve leaflet (patient 1), and the Lecompte maneuver (patient 6). The mean cross-clamp time was 109 ± 21 minutes (range, 84 to 148), and the mean circulatory arrest duration, 46 ± 22 minutes (range, 2 to 71). Modified ultrafiltration was used in the last 5 patients. Serum lactate levels have been measured during cardiopulmonary bypass since 1999.

The comprehensive Aristotle complexity score for each patient is given in Table 1. It reached 20 points in 6 patients and ranged from 16 to 17.5 in the others.

Outcome
The early postoperative course was uneventful in 2 patients (patients 2 and 4, Tables 1 and 2). It was complicated in patients 6, 9, and 10, but all 3 survived.

There were 5 hospital deaths (5 of 10), resulting in an operative mortality of 50% (95% CL: 19% to 81%). Among the 6 patients with an Aristotle score of 20 or greater, there were 5 early deaths (Table 1). An Aristotle score of 20 or greater is a significant risk factor for mortality, even in this small series of 10 patients (p = 0.024, one-sided Fisher’s exact test).

The circumstances of these 5 early deaths and 1 late death are as follows (Table 2). Patient 1 had surgical correction in moribund state. Repair of torn truncal leaflet (presumably iatrogenic: at cardiac catheterization) did not succeed in improving the function of the regurgitant truncal valve. He died 4 hours after the operation in cardiogenic shock. The second operative death occurred in patient 3, whose operation had been delayed because of intracranial hemorrhage and convulsions. At correction, the truncal valve incompetence was not surgically addressed. After prolonged reperfusion, the patient could not be weaned from the extracorporeal circulation. Patient 5 had diminished perfusion of the left anterior descending coronary artery after repair related to its intramyocardial course. This was aggravated by right ventricular enlargement due to pulmonary hypertensive crises that did respond neither to medical therapy, nor to prolonged reperfusion time, causing irreversible failure of the right ventricle. Patient 7 experienced the occurrence of myocardial contracture ("stone heart") after infusion of cardioplegic solution that did not resolve after coronary reperfusion. Patient 8, who was moribund, died on the second postoperative day from multiorgan failure. Patient 4, one of the five early survivors, died after 4 months, after cardiac catheterization and dilatation of the obstructed aortic anastomosis in the catheterization laboratory.

Figure 1 depicts Kaplan-Meier actuarial survival for patients with interrupted aortic arch compared with those without this anomaly: a low 37.5% ± 15.8% survival for patients with truncus type A4 versus a high 95.5% ± 2.5% for those with truncus A1, A2, and A3, from 1 year on (p < 0.0001).



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  		Fig 1. Kaplan-Meier estimate of survival after repair of truncus arteriosus type A1, A2, and A3 (without interruption of the aortic arch; n = 73) and of truncus type A4 (with interrupted aortic arch; n = 10). The numbers indicate patients at risk at the time of estimate. Vertical bars represent standard error of the mean (SEM). The difference in survival between the two groups is highly significant: p less than 0.0001 (log-rank test).

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Comment
Acknowledgments
 References
 
Interruption of the aortic arch occurs in 15% of all cases of truncus arteriosus [11], which itself accounts for less than 3% of all cardiac defects. Thus, the number of type A4 truncus repaired in individual centers is small and does not allow a reliable statistical analysis of specific risk factors for this complex lesion.

The detrimental role of associated interrupted aortic arch on survival after surgical correction of truncus arteriosus is confirmed by most but not all recent large series (Table 3). The cumulative operative mortality in these series is 37.2% (28.36% to 46.7%; 42 of 113) in the presence of aortic arch interruption, and 20.3% (17.6% to 23.2%; 165 of 812) in its absence: a highly significant difference (p < 0.0001, {chi}2 test).


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  		Table 3. Repair of Truncus Arteriosus Communis (TAC): Operative Mortality in Recent Literature
 
In this study, 100% of the patients who died in the hospital had a comprehensive Aristotle score of 20 or more. This confirms the predictive value of the comprehensive Aristotle score. Recent data (under press) from the Aristotle committee have also observed that when the Aristotle score reaches 20/25, there is today almost no survival. The patients who did not survive were those with major morbidity factors and also truncal valve regurgitation, as clearly shown by the Aristotle scoring.

The operative mortality was particularly related to poor preoperative condition for the 2 moribund neonates; unrepaired severe truncal valve regurgitation, coronary artery anomaly, and an unexpected "stone heart," respectively, for the other 3 deaths. In the present era, physicians caring for neonates should be well aware of the vital importance of early referring of all newborns with truncus arteriosus. Repair should not be delayed, especially in case of associated aortic arch interruption, as prolonged therapy with prostaglandine carries its own risks, notably massive interstitial edema, respiratory insufficiency, and necrotizing enterocolitis. To improve outcome, preoperative management is crucial. This includes prostaglandin E1 infusion, minimizing the fraction of inspired oxygen, when necessary intubation and ventilation with positive pressure, and judicious use of volume and inotropic agents guided by measurement of serum lactate levels, to maintain adequate urinary output and to optimize the diastolic pressures. Thus, urgent repair can be undertaken in more favorable condition, which was not the case in the 2 moribund patients reported here.

Despite increased surgical complexity, one-stage repair in the early neonatal period is mandatory [14], and has become the gold standard. Aortic arch repair with a beating heart, as first described by Sano and Mee [15], coupled with cerebral perfusion, as promoted by Tchervenkov and colleagues [16], was applied in the last patients. These techniques enable arch reconstruction without cessation of brain and myocardial perfusion. By avoiding or minimizing the duration of cardiac and total circulatory arrests, operative mortality and morbidity should improve. However, caution must be taken in case of truncal valve regurgitation: coronary perfusion may be not applicable. It had to be discontinued in patient 7.

A mild to moderate truncal valve regurgitation present in 40% to 50% of all truncus cases [10, 11] (although the grade of regurgitation is commonly underestimated due to the obligatory pulmonary "run-off") is usually well tolerated after repair of truncus arteriosus, because of volume overload reduction.

Nevertheless, moderate valve incompetence influences the outcome. It contributed to the death of 1 of 2 patients with truncus A4 who died in the series of Thompson and associates [7]. Grade III-IV regurgitant truncal valves, seen in 11% of cases [10, 11], should be repaired or replaced. Several authors have advocated techniques to repair incompetent truncal valve leaflets [9, 17–20]. In that way, Imamura and associates [19] managed to save two patients with combined truncus A4 and more than moderate truncal valve insufficiency. It is noteworthy that all 4 patients in our series, as well as the 9 neonates in the report of Jahingiri and associates [9] who had no moderate or severe truncal valve regurgitation, survived the intervention. As for the 10 patients who all survived in the series of Brizard and associates [12], in this publication concomitant presence or absence of truncal incompetence is not mentioned. From our experience and from the above-mentioned literature, one may therefore deduce that truncal valve regurgitation constitutes a specific incremental risk factor for hospital death after repair of truncus type A4.

The poor prognosis for patients with truncus arteriosus and interrupted aortic arch has been confirmed by the recent Congenital Heart Surgeons Society study with an overall survival of 39% at 1 year and 30% at 15 years [21]. Survivors face reinterventions not only to replace the implanted small homografts but also, in a good number, to relieve postoperative obstruction of the aortic arch. Debate still persists regarding the best method of aortic arch reconstruction to prevent this complication. In the study of Roussin and associates [22], the technique of pulmonary autograft patch augmentation resulted in the best outcome, but it can not be applied in case of truncus arteriosus as the pulmonary trunk is short or absent. These authors reported also that freedom from recurrent arch obstruction was higher after direct anastomosis technique than after homograft or pericardial patch aortoplasty, but other workers have different experience: for example, Tchervenkov and associates [23] report excellent results with pulmonary homograft patch aortoplasty. We used the direct anastomosis technique, except in the subset of patients with interrupted aortic arch type B and aberrant origin of the right subclavian artery from the descending thoracic aorta. In these patients, we prefer to use 8 to 10 mm conduit (PTFE or homograft) to bridge the aortic interruption, in order to preserve both subclavian arteries and to prevent obstruction of the left bronchus. Therefore, this prosthesis is expected to become too small and to require reoperation, after 10 to 12 years.

We conclude that despite increased surgical complexity, truncus arteriosus with aortic arch interruption can be repaired with a lower operative risk, provided that truncal valve is competent. Truncal valve regurgitation appears to constitute a specific incremental risk factor for hospital death after repair of truncus type A4. In this constellation, to enhance the chance of survival for these patients, preoperative management must be optimized and truncal valve regurgitation should be surgically addressed. The rapid deterioration of neonates with truncus arteriosus and interrupted aortic arch dictates early referral and early repair. This study confirms the predictive value of the newly introduced comprehensive Aristotle complexity score, a score of 20 or greater being significantly correlated with hospital death (p = 0.024).


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Comment
 Acknowledgments
References
 
We are very grateful to Prof François Lacour-Gayet, head of the Cardiac Surgery Department, Denver Childrens Hospital, Denver, Colorado, who helped us to calculate and to comment on the Aristotle comprehensive score.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Comment
 Acknowledgments
 References
 

  1. Sinzobahamvya N, Urban AE, Brecher AM, Arenz C, Wetter J. Réparation chirurgicale du tronc artériel commun à l’aide d’homogreffes Arch Mal Coeur 1994;87:673-678.
  2. Urban AE, Sinzobahamvya N, Brecher AM, Wetter J, Malorny S. Truncus arteriosusten-year experience with homograft repair in neonates and infants. Ann Thorac Surg 1998;66(suppl):S183-S186.
  3. Lacour-Gayet F, Clarke D, Jacobs J, et al. the Aristotle Committee The Aristotle scorea complexity-adjusted method to evaluate surgical results. Eur J Cardiothorac Surg 2004;25:911-924.[Abstract/Free Full Text]
  4. Van Praagh R, Van Praagh S. The anatomy of common aorticopulmonary trunk (truncus arteriosus communis) and its embryologic implicationsa study of 57 necropsy cases. Am J Cardiol 1965;16:41-50.
  5. Celoria GC, Patton RB. Congenital absence of the aortic arch Am Heart J 1959;58:407-413.[Medline]
  6. Brown JW, Ruzmetov M, Okada Y, Vijay P, Turrentine MW. Truncus arteriosus repairoutcomes, risk factors, reoperation and management. Eur J Cardiothorac Surg 2001;20:221-227.[Abstract/Free Full Text]
  7. Thompson LD, McElhinney DB, Reddy M, Petrossian E, Silverman NH, Hanley FL. Neonatal repair of truncus arteriosuscontinuing improvement in outcomes. Ann Thorac Surg 2001;72:391-395.[Abstract/Free Full Text]
  8. Danton MH, Barron DJ, Stumper O, et al. Repair of truncus arteriosusa considered approach to right ventricular outflow tract reconstruction. Eur J Cardiothorac Surg 2001;20:95-104.[Abstract/Free Full Text]
  9. Jahangiri M, Zurakowski D, Mayer JE, del Nido PJ, Jonas RA. Repair of the truncal valve and associated interrupted arch in neonates with truncus arteriosus J Thorac Cardiovasc Surg 2000;119:508-514.[Abstract/Free Full Text]
  10. Urban AE, Ebels T. Truncus arteriosusEuropean Congenital Heart Surgeons Club Study; 1998Paris meeting.
  11. Klewer SE, Behrendt DM, Atkins DL. Truncus arteriosusIn: Moller JH, editor. Perspectives in pediatric cardiology. surgery of congenital heart disease. Vol 6.. Armonk, NY: Futura Publishing; 1998. pp. 271-285Pediatric Cardiac Care Consortium 1984–1995.
  12. Brizard CP, Cochrane A, Austin C, Nomura F, Karl TR. Management strategy and long term outcome for truncus arteriosus Eur J Cardiothorac Surg 1997;11:687-696.[Abstract]
  13. Lacour-Gayet F, Serraf A, Komiya T, et al. Truncus arteriosus repairinfluence of techniques of right ventricular outflow tract reconstruction. J Thorac Cardiovasc Surg 1996;111:849-856.[Abstract/Free Full Text]
  14. Lacour-Gayet F, Serraf A, Galletti L, et al. Biventricular repair of conotruncal anomalies associated with aortic arch obstruction103 patients. Circulation 1997;96(Suppl 2):328-334.
  15. Sano S, Mee RBB. Isolated myocardial perfusion during arch repair Ann Thorac Surg 1990;49:970-972.[Abstract]
  16. Tchervenkov CI, Korkola SJ, Shum-Tim D. Surgical technique to avoid circulatory arrest and direct arch vessel cannulation during aortic arch reconstruction Eur J Cardiothorac Surg 2001;19:708-710.[Abstract/Free Full Text]
  17. Black MD, Adatia I, Freedom RM. Truncal valve repairinitial experience in neonates. Ann Thorac Surg 1998;65:1737-1740.[Abstract/Free Full Text]
  18. McElhinney DB, Reddy VM, Rajasinghe HA, Mora BN, Silverman NH, Hanley FL. Trends in the management of truncal valve insufficiency Ann Thorac Surg 1998;65:517-524.[Abstract/Free Full Text]
  19. Imamura M, Drummond-Webb JJ, Sarris GE, Mee RBB. Improving early and intermediate results of truncus arteriosus repaira new technique of truncal valve repair. Ann Thorac Surg 1999;67:1142-1146.[Abstract/Free Full Text]
  20. Mavroudis C, Backer CL. Surgical management of severe truncal insufficiencyexperience with truncal valve remodeling techniques. Ann Thorac Surg 2001;72:396-400.[Abstract/Free Full Text]
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