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Right arrow Congenital - cyanotic

Eur J Cardiothorac Surg 2001;20:221-227
© 2001 Elsevier Science NL

Truncus arteriosus repair: outcomes, risk factors, reoperation and management

John W. Brown, Mark Ruzmetov, Yuji Okada, Palaniswamy Vijay, Mark W. Turrentine

Section of Cardiothoracic Surgery, Indiana University Medical Center, 545 Barnhill Drive, EH 215, Indianapolis, IN, 46202-5123 USA

Received 9 October 2000; received in revised form 17 April 2001; accepted 18 May 2001.

Corresponding author. Tel.: +1-317-274-7150; fax: +1-317-274-2940
e-mail: jobrown{at}iupui.edu


   Abstract
Top
 Abstract
1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
Objectives: Truncus arteriosus (TA) continues to be associated with significant morbidity and mortality, but there have been clinically significant improvements with early repair. Methods: Sixty patients underwent physiological correction of TA between November 1978 and January 2000. The average age was 76 days (range, 3 days–20 months). Associated cardiac anomalies were frequently encountered, the most common being severe truncal valve regurgitation (n=7), interrupted aortic arch (n=6), coronary artery anomalies (n=6), non-confluent pulmonary arteries (n=4), and total anomalous pulmonary venous return (n=1). Truncal valve replacement was performed initially or subsequently in seven patients with severe regurgitation (mechanical prostheses in six patients and a cryopreserved aortic homograft in one patient). Right ventricle–pulmonary artery continuity was established with an aortic (n=16) or pulmonary homograft (n=32) in 48 patients, a Dacron polyester porcine valved conduit in five, a non-valved polytetrafluoroethylene (PTFE) tube in three, direct anastomosis to the right ventricle with anterior patch arterioplasty in three, and a bovine jugular venous valve conduit in one patient. Results: There were ten hospital deaths (17%; 70% confidence limit, 7–25%). Multivariate and univariate analyses demonstrated a relationship between hospital mortality and associated cardiac anomalies. In the 43 patients without these associated cardiac anomalies, the early survival was 91% (group I). In the 17 patients with one or more of these risk factors, the survival was 71% (group II, P=0.002). There was one late death. Twenty-three patients (46%) required reoperation for right ventricular outflow tract (RVOT) obstruction at a mean follow-up time of 59.1 months. In 23 patients, the RVOT reconstruction was performed with a PTFE monocusp, and six patients had of a variety of replacement conduits inserted. Postoperatively, there were 34 (68%) patients in New York Heart Association functional class I and 16 (32%) in class II. Twenty-eight surviving patients are reported as doing well without any medication. The freedom of reoperation in the 39 hospital survivors (group I) without risk factors was 64% at 7 years; and 36% at 10 years in the 11 patients (group II) surviving with risk factors. Conclusions: Associated cardiac anomalies were risk factors for death after the repair of TA. In the absence of these associated lesions, TA can be repaired with an excellent surgical outcome in the neonatal and early infancy period.

Key Words: Congenital valve disease • Children • Truncus arteriosus communis • Truncal valve


   1. Introduction
Top
 Abstract
 1. Introduction
2. Patients and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
Truncus arteriosus (TA) is an uncommon congenital cardiac malformation presenting for less than 3% of all congenital heart malformations [1–3]. The features of TA include a single great artery arising from the base of the heart, that supplies systemic, coronary and pulmonary blood flow, together with a ventricular septal defect (VSD). The two main classification systems used to describe the anatomy of TA are those of Collett and Edwards (1949) [4] and Van Praagh (1965) [5]. Without surgical treatment, 80% of patients die within the first year of life, many during early infancy [1,2,6]. The results of physiological repair have improved over the years, but pulmonary hypertensive episodes in the immediate postoperative course are major risk factors.

The first successful surgical repair of TA was performed by McGoon, Rastelli and Ongley [7] in 1967. They used an aortic homograft including the aortic valve to establish continuity from the right ventricle (RV) to the pulmonary artery (PA). Since then, various means of reconstruction have been developed, and controversies remain concerning which method is the best to use and at what age surgery should optimally be performed. The main long-term management issues relate to conduit stenosis and truncal valve incompetence and stenosis. The necessary reoperations to address these complications are associated with further risk of mortality and morbidity. Risk factors and outcomes related to this anomaly have been incompletely defined. The purpose of this report was to study whether the type of surgical procedure used to reconstruct the RV–PA tract has influenced the early outcome of the surgical repair, and to carefully examine risk factors for adverse long-term outcomes after the repair of TA at a single institution.


   2. Patients and methods
Top
 Abstract
 1. Introduction
 2. Patients and methods
3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
2.1. Study patients
Between November 1978 and January 2000, 64 patients with the diagnosis of TA were seen at James W. Riley Hospital for Children of the Indiana University. One 2-month-old infant with TA and hypoplastic left heart underwent repair with heart transplantation and three patients who underwent repair after pulmonary artery banding were excluded from the review. The remaining 60 patients with primary repair in infancy form the basis of this report.

There were 22 male and 38 female infants. The mean age at the time of surgery was 76 days, with a range of 3 days–20 months. In 82% (49/60), the operation was done in the first 100 days of life.

All patients were in cardiac failure and four had required previous ventilatory support. Patients with interrupted aortic arch (IAA) received an infusion of Prostaglandin E1. Echocardiography was performed in all patients, and cardiac catheterization was performed routinely through 1991 and selectively since 1991 in our patients with suspected complex morphological features or unusual physiological lesions.

According to the classification of Collett and Edwards [4], 23 patients had type I TA, 29 had type II, the remaining four patients had a mixture between those two anatomic types, and four had type III.

Associated cardiac lesions are listed in Table 1. Seventeen patients had one or more major associated lesions. The most common cardiac conditions consisted of IAA in six patients, coronary artery anomalies in six, non-confluent pulmonary arteries in four, and a supracardiac type of total anomalous pulmonary venous return in one patient. Truncal valve regurgitation was absent or trivial in 22 patients, mild to moderate in 16, and severe in the remaining seven patients. Peak instantaneous truncal valve systolic gradients were present by Doppler examination in seven patients, ranging from 20 to 69 mmHg (mean, 40 mmHg). The number of truncal valve leaflets was variable: 45 patients had three leaflets, nine had four leaflets, and six had two leaflets. Either the complete or the partial form of DiGeorge's syndrome was present in six patients (10%).


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  		Table 1. Associated congenital cardiovascular anomaliesa

 
Before total correction of the TA, three patients had repair of type B IAA through a left thoracotomy using a left carotid swing-down, one patient had end-to-end repair of coarctation aorta with ligation of patent ductus arteriosus, and one patient had repair of a supracardiac type of total anomalous pulmonary venous return.

2.2. Surgical techniques
Operative repair was performed using bicaval cannulation with full-flow cardiopulmonary bypass at systemic temperatures of 20°C. The pulmonary arteries were snared at the onset of bypass, and cold potassium crystalloid cardioplegia (4°C) was delivered through the truncal vessel after placement of the cross-clamp. Cross-clamp times ranged from 40 to 100 min (mean time, 73±28 min). The pulmonary arteries were excised from the truncal vessel after the bifurcation and exposed through a short, horizontal anterior incision. This allowed accurate removal of the pulmonary bifurcation without injury to the truncal valve or left coronary artery. The resultant defect was closed primarily or with a patch of homograft tissue or prosthetic material. In two cases with type II TA, a Lecompte maneuver [8] was performed to bring the pulmonary bifurcation in front of the aorta.

Right ventricle–pulmonary artery continuity was established (Table 2) with an aortic (n=16) or pulmonary cryopreserved homograft (n=32; CryoLife, Inc., Kennesaw, GA) in 48 patients (range, 8–12 mm), a valved heterograft conduit (woven Dacron graft containing a glutaraldehyde-preserved porcine valve from Medtronics, Inc., Minneapolis, MN) in five patients (range, 12–14 mm), a non-valved polytetrafluoroethylene (PTFE) tube (W.L. Gore & Associates, Inc., Naperville, IL) in three patients (range, 10–13 mm), and a bovine jugular venous valve conduit (VenPro, Inc., Irvine, CA) in one patient (12 mm). In three cases, direct anastomosis to the right ventricle was used according to the technique described by Barbero-Marcial and associates [9].


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  		Table 2. Conduit type and size

 
The type of right ventricular outflow tract (RVOT) reconstruction technique used has evolved with time. The Dacron valved conduits and direct anastomosis techniques were used in the early part of the study, whereas aortic, and recently, pulmonary homografts were the techniques used after 1987, and bovine jugular venous valve conduits were used selectively after 1999 (Fig. 1) .



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  		Fig. 1. Distribution of all RVOT reconstruction techniques between November 1978 and December 1999.

 
The pulmonary artery pressure was monitored occasionally in the postoperative course. Some patients had placement of a pulmonary artery catheter through the right ventricle during the operation if they were felt to be at high risk for a pulmonary hypertensive crises. Pulmonary hypertensive crises were prevented by deep sedation and with drugs, including Prostaglandin E1, Thorazine, Minipres, and more recently, nitric oxide.

Additional procedures performed before TA repair included repair of IAA (n=3), closure of a patent foramen ovale or secundum atrial septal defect (n=10), pulmonary arterioplasty (n=3), ligation of the left superior vena cava (n=2), and De Vega tricuspid valve annuloplasty (n=1).

2.3. Operative findings and procedures
Seven patients (12%) underwent replacement of the truncal valve for severe valvular insufficiency. The truncal valve was replaced with a mechanical prosthesis in six patients (St. Jude Medical in four cases, Carbomedics in two cases) and with a cryopreserved aortic homograft in one newborn patient. In three children, a concomitant Nicks's aortic annular enlargement was performed.

IAA was repaired in six patients (10%). Their ages ranged from 3 to 60 days. The arch was interrupted between the left carotid and left subclavian arteries (type B) in three cases, and interruption distal to the left subclavian artery (type A) in three cases. Aortic arch repair was completed before TA repair by an extended end-to-end anastomosis in three cases, and carotid artery swing-down in the remaining three neonates were done via a left thoracotomy.

In four patients (7%), whose ages ranged from 8 to 26 days, one or more pulmonary arteries were discontinuous. In two patients, the right pulmonary artery arose from the usual position on the ascending aorta and the left pulmonary artery arose from a normally positioned ductus arteriosus. In the other two patients, the right pulmonary artery arose from the right side of the ascending aorta and the left pulmonary artery arose from a normally positioned ductus arteriosus.

Coronary artery anomalies exhibited a different pattern and were present in six patients (10%). Their ages ranged from 7 days to 8 months. There were four single coronary arteries, and two cases of a high origin of the left coronary artery.

2.4. Statistical analysis
Preoperative and perioperative data were collected from retrospective medical records. Results classified as ‘early’ are those that occurred before hospital discharge or within 30 days of surgery if the patient was discharged from the hospital before this duration. Specific software SPSS for Windows version 10 (SPSS, Inc., Chicago, IL) was used for data analysis. The Kaplan–Meier product limit method and Cox proportional hazards regression methods were used for survival analysis and analysis of freedom from reoperation (all reoperations, conduit reoperations, and truncal valve reoperations). Multiple regression analysis was performed as conditional backward stepwise proportional hazards regression. Continuous data were presented as means±SD.


   3. Results
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
4. Discussion
 Appendix A. Conference...
 References
 
3.1. Early results
There were ten hospital deaths (17%; 95% confidence limits, 7–25%). Hospital deaths have been attributed to the following causes: severe myocardial failure in four cases, uncontrollable pulmonary hypertensive crises in three cases, intracranial hemorrhage in two cases, and bacterial pneumonia in one patient.

There were five deaths (5/17; 29%) in patients with associated morphological lesions. Three deaths occurred in six patients with IAA. Two of the patients underwent aortic arch reconstruction as part of the initial repair. Two of those deaths occurred in patients with severe truncal valve insufficiency (two of seven patients with this lesion). For both of these deaths, truncal valve replacement was performed as a planned part of the primary repair. One death occurred in a patient with a coronary anomaly (1/6; 17%). This death was associated with IAA.

There were five perioperative deaths in the 43 patients (12%) without associated complex lesions, such as truncal valve insufficiency, IAA, and coronary anomalies. Four of these deaths occurred in patients who underwent repair before 1991, and one after 1991. Three of these patients had postoperative mean pulmonary artery pressures greater than 60% of the systemic pressure and they had pulmonary hypertensive episodes, which may have contributed to the outcome. One of the patients had bacterial pneumonia. The other patient, who underwent repair after 1991, had intracranial hemorrhage in the early postoperative period.

3.2. Follow-up
Patients were followed-up to a median of 9.4 years (range, from 3 months to 20 years). No patient was lost to follow-up. The actuarial survival was 82% at 4 months (Fig. 2) . There was no additional mortality after the 4th postoperative month. Postoperatively, there were 34 patients (69%) in New York Heart Association (NYHA) functional class I and 15 (31%) in class II. Twenty-eight surviving patients are doing well without any medication. The patients with mechanical prostheses are on a regimen of warfarin sodium, aiming to maintain the INR between 2.5 and 3.5. Absent to mild truncal valve insufficiency is present in 30 patients, and this is moderate in three patients. The mean Doppler gradient across the conduit in the RVOT is 24±16 mmHg (range, 2–79 mmHg; median, 20 mmHg).



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  		Fig. 2. Actuarial patient survival after TA repair, including operative mortality.

 
3.3. Late results
There was one late death in a 30-day-old 3.5-kg infant, whose multiple congenital anomalies, including TA, hydrocephalus and agenesis of a corpus callosum, had been repaired with a 12 mm cryopreserved pulmonary homograft. The patient tolerated that procedure well, but had difficulty in being weaned from the ventilator and eventually required a tracheostomy. A few days before the demise (4 months after repair), the patient developed fever and was seen in the emergency room on the day of death with septic shock, diagnosed and identified later as necrotizing fasciatis.

3.4. Risk factor analysis
Hospital mortality was studied for the following possible risk factors: age, age of less than 1 month, weight, preoperative ventilatory support, IAA, presence of truncal valve regurgitation, coronary artery anomaly, RVOT techniques, postoperative pulmonary valve regurgitation, cross-clamp time, and hospital mortality from 1978 to 1991 versus that from 1992 to 1999.

The significant risk factors for hospital mortality according to univariate analysis are listed in Table 3. Multivariate analysis by logistic regression shows that, of seven factors deemed significant on univariate analysis, only two independent significant risk factors remain associated: IAA (P<0.001), and hospital mortality from 1978 to 1991 versus that from 1992 to 1999 (P=0.002).


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  		Table 3. Risk factors for hospital deathsa,b

 
In the 43 patients without risk factors, the hospital survival was 91%. In the 17 patients with one or more of these risk factors, the survival was 65%.

3.5. Reoperations
3.5.1. All reoperations
During the follow-up period, among 50 hospital survivors, 23 patients required, on average, 46 reinterventions (Table 4). In some cases, multiple procedures were performed at the time of reoperation (e.g. closure of a residual VSD and conduit replacement).


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  		Table 4. Reoperationsa,b

 
3.5.2. Conduit reoperations
A total of 30 conduit-related reoperations were performed in 23 patients for RVOT stenosis (while two patients had two reoperations and another two had three reoperations). None of the patients died during reoperation. The actuarial freedom from reoperation at 7 years was 64% in the 39 survivors without risk factors; and 36% at 10 years in the 11 patients surviving with risk factors. Assessed according to the different techniques used for RVOT reconstruction (Fig. 3) , the freedom from reoperation was as follows: 20% for the Dacron valved conduits, 100% for the non-valved PTFE tube, 50% for the direct anastomoses, 45% for the aortic homograft (P=0.05), 57% for the pulmonary homograft (P=0.02), and 100% for the single patient with a bovine jugular venous valve conduit.



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  		Fig. 3. Actuarial freedom from reoperation according to right ventricle–pulmonary artery continuity.

 
At the time of the first conduit reoperation, the median pressure gradient from the right ventricle to the pulmonary artery was 49 mmHg (18–124 mmHg). Reintervention consisted of removal of the previous conduit and replacement with a pulmonary homograft in three cases, with an aortic homograft in one case, with a Medtronic freestyle aortic xenograft in one case, and with a bovine jugular venous valve conduit in one case. In 23 cases, the conduit was opened longitudinally and a Gore-Tex monocusp (0.1 mm thickness) was positioned and sewn into the RVOT. The homograft diameter was augmented with a generous patch of Gore-Tex (0.6 mm thickness; Table 4). In one patient, the conduit replacement included the resection of a pseudoaneurysm of the existing conduit.

3.5.3. Other reoperations
Sixteen patients underwent other reinterventional procedures, including closure of a small residual VSD in six patients, truncal valve replacement in three patients, closure of a secundum atrial septal defect in two patients, pulmonary artery patch angioplasty, and De Vega tricuspid valve annuloplasty in two patients.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
Appendix A. Conference...
 References
 
Timing of TA repair continues to be a point of discussion. Elective repair of TA without major associated cardiac anomalies during the first 3 months of life is advocated by some surgeons [10,11]; others prefer primary neonatal correction [12–14]. In our series, only 11 of 60 patients (18%) were operated on after 3 months of age because of late referral. Delaying the operation beyond 100 days increases the risk of pulmonary hypertensive crises [12,13]. The presence of major associated anomalies, such as IAA [15], severe truncal valve insufficiency [16,17], anomalies coronary arteries [13,18], and non-confluent pulmonary arteries [12], mandates surgical intervention regardless of age or weight [11,12].

The presence of IAA has been previously reported to increase mortality. Pearl et al. [19] reported that the presence of IAA increased early mortality with TA repair (2/3; 67% patients with IAA died in early postoperative period). Williams et al. [6] and Lacour-Gayet et al. [11] reported that associated cardiac defects were not associated with increased mortality. Sano et al. [15] reported zero mortality of their series in seven patients with TA and IAA. This is in contrast with our results. We agree with Hanley et al. [13] who found that IAA was a considerable risk factor for mortality after TA repair.

Repair of the truncal valve is an option that has been employed increasingly and successfully in recent years, both at the time of initial repair and at reoperation [16–18]. Truncal valve insufficiency is more complicated to deal with. A mild to moderate regurgitation is usually well tolerated postoperatively after reduction of the volume overload [10,20]. The decision to replace the truncal valve is often influenced by the desire not to further complicate an already complicated procedure. Truncal valve replacement can be accomplished with a low risk and should be performed when severe regurgitation is present. Studies have reported good results with the aortic allograft in truncal valve replacement [12,21], but we have been disappointed with allografts in children, primarily with their intermediate-term function. McElhinney et al. [18] reported that severe allograft insufficiency developed less than a year after operation in two of their three early survivors with allograft truncal valve replacement and the other survivor died suddenly 2 months after operation. We prefer to use an oversized mechanical valve along with annular enlargement.

The presence of non-confluent pulmonary arteries can add considerable risk to the operative procedure and can necessitate individual technical modification depending on the specific anatomy. It is perhaps even more important in this group of patients to operate early in life because delay may increase the risk of development of pulmonary vascular disease [20]. If the right or left pulmonary arteries are extensively mobilized, a direct anastomosis between them and the right ventricle–pulmonary artery conduit can generally be constructed, even when one or both intrapericardial branches are absent [12,22].

Recognition of the proximal coronary arterial anatomy is essential and anomalies must be regarded as a risk factor [20,22]. A high incidence of coronary ostial and arterial abnormalities are well described [23,24]. There is the potential risk of distortion of the coronary ostia or proximal coronary segments during the removal of pulmonary arteries from the trunk reconstruction. Closure of the trunk with a patch after removal of the pulmonary arteries can prevent coronary artery distortion when coronary anomalies are present.

In conclusion, our experience encourages the repair of TA as early as possible in life. Small homografts or bovine jugular venous valved conduits are preferred for establishing right ventricular to pulmonary artery continuity. Aortic homografts are less preferred because of their high tendency for calcification and obstruction, and for the increased difficulty of revision or replacement. Small conduits do not necessarily predict early stenosis. Reoperation for conduit revision or replacement is straightforward provided that the pericardium has been closed with a Gore-Tex membrane. Preventing inadvertent cardiac entry during redo sternotomy can usually be accomplished without myocardial ischemia on a beating heart. RV–PA conduit replacement does not interfere with the satisfactory long-term results that can now be achieved with neonatal TA repair.


   Footnotes
 
Presented at the 14th Annual Meeting of the European Association for Cardio-thoracic Surgery, Frankfurt, Germany, October 7–11, 2000.


   Appendix A. Conference discussion
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
References
 
Dr G. Thiene (Padova, Italy): Have you had any problem with pulmonary hypertension in these young patients? In other words, were there pulmonary vascular disease cases with a postoperative fatal outcome?

Dr Brown: Obviously, there were three deaths associated with pulmonary hypertensive crisis, but this was mostly early in our experience when we were trying to wait until 3 or 4 months of age to do those repairs. In the last 8 or 10 years, we have tried to do the truncus repair in the first month or at least 6 weeks of life, and the incidence of pulmonary hypertensive crisis has essentially disappeared.


   References
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 

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  2. Di Donato R.M., Fyfe D.A., Puga F.J. Fifteen-year experience with surgical repair of truncus arteriosus. J Thorac Cardiovasc Surg 1985;89:414-422.[Abstract]
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  8. Lecompte Y., Neveux J.Y., Leka F. Reconstruction of the pulmonary outflow tract without prosthetic conduit. J Thorac Cardiovasc Surg 1982;84:722-733.
  9. Barbero-Marcial M., Riso A., Atik E., Jatene A. A technique for correction of truncus arteriosus types I and II without extracardiac conduits. J Thorac Cardiovasc Surg 1990;99:364-369.[Abstract]
  10. Brizard C.P., Cochrane A., Austin C., Nomura F., Karl T.R. Management strategy and long-term outcome for truncus arteriosus. Eur J Cardio-thorac Surg 1997;11:687-696.[Abstract]
  11. Lacour-Gayet F., Serraf A., Komiya T., Sousa-Uva M., Bruniaux J., Touchot A., Roux D., Neuville P., Planche C. Truncus arteriosus: influence of techniques of right ventricular outflow tract reconstruction. J Thorac Cardiovasc Surg 1996;111:849-856.[Abstract/Free Full Text]
  12. Bove E.L., Lupinetti F.M., Pridjian A.K., Beekman R.H., III, Callow L.B., Snider A.R., Rosenthal A. Results of a policy of primary repair of truncus arteriosus in the neonate. J Thorac Cardiovasc Surg 1993;105:1057-1066.[Abstract]
  13. Hanley F.L., Heinemann M.K., Jonas R.A., Mayer J.E., Jr, Cook N.R., Wessel D.L., Castaneda A.R. Repair of truncus arteriosus in the neonate. J Thorac Cardiovasc Surg 1993;105:1047-1056.[Abstract]
  14. Rajasinghe H.A., McElhinney D.B., Reddy V.M., Mora B.N., Hanley F.L. Long-term follow-up of truncus arteriosus repaired in infancy: a twenty-year experience. J Thorac Cardiovasc Surg 1997;113:869-879.[Abstract/Free Full Text]
  15. Sano S., Brawn W.J., Mee R.B.B. Repair of truncus arteriosus and interrupted aortic arch. J Card Surg 1990;5:157-162.[Medline]
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  20. Urban A.E., Sinzobahamvya N., Brecher A.M., Wetter J., Malorny S. Truncus arteriosus: ten-year experience with homograft repair in neonates and infants. Ann Thorac Surg 1998;66:S183-S188.
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