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Eur J Cardiothorac Surg 2007;32:202-208. doi:10.1016/j.ejcts.2007.04.022
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Clinical results of staged repair with complete unifocalization for pulmonary atresia with ventricular septal defect and major aortopulmonary collateral arteries

Nobuyuki Ishibashi*, Toshiharu Shin’oka, Masakuni Ishiyama, Takahiko Sakamoto, Hiromi Kurosawa

Department of Cardiovascular Surgery, Heart Institute of Japan, Tokyo Women's Medical University, Tokyo, Japan

Received 5 September 2006; received in revised form 10 April 2007; accepted 12 April 2007.

* Corresponding author. Address: Department of Cardiovascular Surgery, Children's National Medical Center, 111 Michigan Avenue, NW, Washington, DC 20010-2970, United States. Tel.: + 1 202 884 2593; fax: +1 202 884 5572. (Email: nishibas{at}cnmc.org).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 Appendix A
 Appendix B
 References
 
Objective: Our treatment strategy for pulmonary atresia with ventricular septal defect (VSD) and major aortopulmonary collateral arteries is a staged repair that comprises the first complete unifocalization (UF) with ‘unification’ of intrapulmonary arteries and then the definitive repair. The purpose of this study is to evaluate the outcome of our staged repair strategy with complete UF and to determine the results of our current management strategy. Methods: From 1982 to 2004, 113 consecutive patients were treated with staged repair at our institute. We evaluated the risk of definitive repair failure or death in the 3 years after definitive repair using logistic regression. Furthermore, we compared the early group (patients who underwent UF before December 1995) and the late group (patients who underwent UF after January 1996). Results: The mean follow-up interval was 8.8 years (0.8 months to 23.3 years), and Kaplan–Meier-estimated overall survival rates after first UF were 80.9, 73.8, and 69.9% at 5, 10, and 15 years, respectively. Survival in patients with an absent central pulmonary artery (PA) was significantly lower than in those with a central PA (p < 0.05), and the factor that was significantly associated with definitive repair failure or death in the 3 years after definitive repair was central PA morphology (p < 0.05). Higher mean PA pressure after UF was detected in patients with hypoplastic central PA, compared with those without hypoplastic PA (30.9 mmHg vs 23.3 mmHg, p < 0.05). In the late group, age (in years) at first UF (3.9 vs 8.4, p < 0.01), second UF (4.3 vs 9.2, p < 0.01), and definitive repair (5.8 vs 9.1, p < 0.01) was significantly younger than in early group, and the survival rate after first UF in the late group was 96.2 and 91.3% at 3 and 7 years, respectively. Systolic right ventricular pressure and the pressure ratio between the right and the left ventricles after definitive repair in the late group were significantly lower than in the early group (53.6 mmHg vs 75.0 mmHg, p < 0.01; 61.7% vs 75.9%, p < 0.05). Conclusions: Hypoplastic central PA was a significant risk factor in this disease. The overall survival was improved by our current management strategy. Improved RV pressure after definitive repair appears to affect the long-term outcome.

Key Words: Major aortopulmonary collateral arteries • Unifocalization • Staged repair • Surgery


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 Appendix A
 Appendix B
 References
 
The surgical strategy for pulmonary atresia with ventricular septal defect (VSD) and major aortopulmonary collateral arteries (MAPCAs) is still controversial. While sufficient results using the staged approach have been reported [1–3], the benefits of midline primary repair have also recently been reported [4–8]. Furthermore, it has recently been reported that unifocalization (UF) does not bring any long-term benefit in terms of late survival [9].

Our management for these patients is staged repair: (1) first complete UF with ‘unification’ of intrapulmonary arteries and (2) second-stage establishment of right ventricle (RV)–pulmonary artery (PA) continuity and VSD closure [10]. Since 1982, this staged repair procedure has been performed with several modifications introduced at later dates. The purpose of this study is to evaluate the outcome of our staged repair with complete UF and to determine the results of our current management strategy which was modified in the middle of 1990s.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 5. Conclusions
 Appendix A
 Appendix B
 References
 
2.1 Study population
Between April 1982 and June 2006, staged repair with complete UF was performed in 113 patients with pulmonary atresia with VSD and MAPCAs at the Heart Institute of Japan, Tokyo Women's Medical University.

2.2 Patient demographics
The patient demographics at primary diagnosis are summarized in Table 1 . The definition of a central PA was one that was located at the anterior of the trachea in the pulmonary hilum and the cranial portion of the left atrium in the pericardial cavity. From 1993, a genetic test with the consent of the family was performed for almost all patients with tetralogy of Fallot and PA with VSD in our institute, and 29 patients (25.7%, 29/113) were diagnosed as having microdeletion of chromosome 22q11.2. Out of seven patients with the coronary anomaly, five patients were diagnosed as having a single coronary artery and two patients as having a fistula between the coronary artery and the central PA.


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  		Table 1 Patient's demographics (n = 113)
 
2.3 First-stage repair: complete unifocalization
First-stage repair, complete UF, is aimed at remodeling the pulmonary arterial structures and converting a multifocal pulmonary blood supply to a unifocal supply. To achieve this purpose of complete UF, ‘unification’ of intrapulmonary arteries is necessary for patients with stenosis of the intrapulmonary arteries [10]. This first-stage repair is performed separately on the right and left lung using the standard technique involving a posterolateral thoracotomy.

For patients with a central PA, MAPCAs are anastomosed to the central PA in the hilum of lung. If pulmonary flow is insufficient, a Blalock–Taussig shunt is performed for the growth of the central PA and intrapulmonary arteries (Fig. 1A).


Figure 1
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  		Fig. 1. Surgical technique and angiography after final UF. (A) For patients with a central PA, the hilar pulmonary arteries that connect with MAPCAs are anastomosed to the central PA. For patients with localized or segmental pulmonary arterial stenosis, the reconstruction of localized or segmental pulmonary arterial stenosis is performed. (B) For patients with an absent or vestigial central PA, a large MAPCA or unified MAPCA is translocated to the anterior position of the trachea (arrow) and the shunt is proximally anastomosed.

 
For patients with absent or vestigial central PA, MAPCAs are translocated to the anterior potion of the trachea and then reconstruction of central PA is performed using a large MAPCA or unified MAPCA (Fig. 1B). If sufficient reconstruction cannot be performed using MAPCAs, autologous pericardium is used. Reconstruction with the equine pericardium [10] or prosthetic graft [11] has not been performed in recent years because of the poor long-term outcomes.

For the indication of surgery, it is necessary to evaluate whether MAPCAs sufficiently connect to central pulmonary arterial circulation and whether MAPCAs have arborization anomaly [12] and localized or segmental pulmonary arterial stenosis [13] by direct injection of MAPCAs or retrograde filling after pulmonary vein wedge injection. Surgical ligation or catheterized embolization is indicated to MAPCAs with sufficient connection to central pulmonary circulation. On the other hand, UF is indicated to MAPCAs with insufficient connection to central pulmonary circulation. Complete UF with reconstruction of intrapulmonary stenosis is indicated to MAPCAs with arborization anomaly or localized and segmental pulmonary stenosis (Fig. 1A)

Regarding optimal timing of surgery, UF in the late era is indicated as soon as possible to induce the adequate growth of the pulmonary arteries and vasculature. Rapid UF also provides a sufficient surgical field to access the intrapulmonary arteries, and UF at more than 1 year of age has no benefits. However, reconstruction of central PA and intrapulmonary stenosis for neonate with small MAPCAs, especially less than 2 mm in the size, is difficult. The optimal timing is ultimately decided by the size of reconstructed MAPCAs. The operative data in the UF are summarized in Table 2 .


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  		Table 2 Operative data (n = 113)
 
2.4 Definitive repair
The surgical indication for definitive repair should be on the basis of pulmonary resistance after complete UF, because the postoperative pressure ratio between RV and left ventricle (LV) is correlated with the risk of surgical death and the long-term outcome [14], and the number of centrally connected pulmonary arterial segments has been shown to be highly and inversely correlated with pulmonary pressure and resistance in the late period following surgical repair [15]. Our current indications for definitive repair are less than 0.7 of estimated postoperative RV/LV systolic pressure ratio and less than 8.0 wood unit m2 of pulmonary resistance after UF. In case intraoperative RV/LV pressure ratio of more than 1.0 is detected after weaning from cardiopulmonary bypass, cardiopulmonary bypass is re-instituted and fenestration of VSD patch is made [16,17].

We have described our approach to RV–PA continuity at definitive repair in a previous report [18]. Our current surgical policy is direct anastomosis, when possible, between the PA and the RV by bridging the distal end of the PA and the ventriculotomy and covering the anterior aspect of the outflow tract with an autologous pericardial patch with an ePTFE monocusp valve. When a direct anastomosis is impossible, an autologous pericardial conduit with an ePTFE bicusp or tricusp valve is placed between the PA and the RV. In the early era, a handmade tricuspid valve conduit, made of equine pericardium preserved in glutaraldehyde (Xenomedica, Baxter, IL), was used. The operative data in the definitive repair are summarized in Table 2.

2.5 Data analysis
Perioperative and follow-up data were collected retrospectively by review of hospital records and operative records. Cross-sectional follow-up was performed in August 2006. Cardiac catheterization was performed after final UF and after definitive repair.

The median interval from final UF and from definitive repair at catheterization was 7.8 and 4.2 months, respectively. The size of the PA was assessed based on the PA index [19]. According to central PA morphology, the patients were divided into three groups: (1) patients with central PA (83 patients), (2) patients with vestigial central PA (13 patients), and (3) patients with absent central PA (17 patients). A vestigial central PA was defined as one that was less than 2 mm in the first angiogram. Survival and hemodynamic data were compared between these groups.

We examined clinical and hemodynamic variables using univariate and multivariate analysis to identify risk factors that affected the risk of definitive repair failure and early death within 3 years after definitive repair. The variables and univariate analysis are listed in Appendix B.

Our current management of UF, which indicates rapid surgical intervention and involves use of autologous tissue, was initiated in the middle of 1990s to ensure sufficient growth of pulmonary vasculature. For our analysis, we divided the patients into two groups: (1) early group (79 patients who underwent first UF before December 1995) and (2) late group (34 patients who underwent first UF after January 1996). Survival and hemodynamic data were compared between these groups.

2.6 Statistical analysis
Data are presented as median and standard deviation. The estimated actuarial survival was determined by the Kaplan–Meier product-limit method, and significance was assessed by the log rank test. Continuous variables were compared using the unpaired Student's t-test. The clinical and hemodynamic variables were analyzed using logistic regression analysis, and the factors that affected definitive repair failure and early death within 3 years after definitive repair were identified using multivariate logistic analysis. Variables were retained in the multivariate analysis if their p-value was less than 0.05. The odds ratio and the corresponding 95% confidence intervals for each statistically significant variable were calculated based on the estimated coefficients obtained from the logistic model. Statistical analysis was performed using the StatView 5.0 software package (SAS Institute Inc., Cary, NC).


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 5. Conclusions
 Appendix A
 Appendix B
 References
 
3.1 Survival
A mean follow-up period from first UF was 8.8 years (range, 0.8 months to 23.3 years). Ninety-one patients (80.5%) were subjected to definitive repair and five patients (4.4%) were followed as candidates for definitive repair (waiting on definitive repair: three patients; waiting for next UF: two patients). Six patients (5.3%) died before definitive repair was carried out, and early and late death after UF each occurred in three patients. Six patients (5.3%) dropped out as candidates, and five patients (4.4%) were followed at other institutes after UF.

The causes of early deaths after UF were shunt occlusion, gastrointestinal bleeding, and paralytic ileus. The causes of late deaths were infective endocarditis, pulmonary hemorrhage, and sudden death. One patient, who had complicated shunt occlusion, was diagnosed as having a coagulation anomaly with positive anti-p1 antigen. Reasons why definitive repair was not indicated were hypoplastic PA in five patients and severe pulmonary arteriovenous fistula in one. In two of five patients with hypoplastic PA, one patient complicated ventricular dysfunction and the other complicated brain abscess.

Of 91 patients who underwent definitive repair, mean follow-up period after the operation was 7.6 years (range, from 0 to 19.7 years), 20 patients died. Early and late deaths after definitive repair occurred in 5 and 15 patients, respectively. The causes of early death were acute pulmonary hypertension and heart failure in one patient, congestive heart failure in two, and infection in two. The causes of late death were congestive heart failure in five patients, infection or infective endocarditis in five, sudden death in two, gastrointestinal bleeding in one, right heart failure after re-operation in one, and tracheal bleeding after re-operation in one.

Kaplan–Meier-estimated overall survival ratios after first UF were 80.9, 73.8, 69.9, and 69.9% at 5, 10, 15, and 20 years, respectively (Fig. 2A). There was a statistically significant difference (log rank test; p = 0.045) in the survival ratio between the three groups depending on central PA morphology (Fig. 2B), and Kaplan–Meier-estimated survival ratios in patients with central PA were 84.5, 79.1, and 75.8% at 5, 10, and 15 years, respectively. In patients with vestigial central PA, the survival ratios were 82.1, 61.5, and 61.5% at 5, 10, and 15 years, respectively. In patients with absent central PA, the survival ratios were 63.5, 55.6, and 47.6% at 5, 10, and 15 years, respectively.


Figure 2
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  		Fig. 2. Kaplan–Meier estimated survival ratio. (A) Survival ratio after first UF in overall 113 patients. (B) Survival ratio after first UF in the three groups depending on central PA morphology. (C) Survival ratio after definitive repair in 91 patients who underwent definitive repair. (D) Survival ratio after definitive repair in patients who underwent definitive repair with complete VSD closure and with fenestrated VSD closure.

 
Of 91 patients who underwent definitive repair, Kaplan–Meier-estimated survival ratios after definitive repair were 81.2, 73.9, and 71.4% at 5, 10, and 15 years, respectively (Fig. 2C). Fifteen patients died within 3 years after definitive repair.

3.1.1 Risk factor analysis
Long-term outcome in patients who survived past 3 years after the definitive repair was excellent. Therefore, we identified the risk factors that affected definitive repair failure or death within 3 years after definitive repair. The results of univariate analysis are shown in Appendix B. In multivariate analysis, the presence of central PA was the only significant positive factor (Table 3 ).


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  		Table 3 Multivariate logistic regression
 
3.2 Comparison between patients with central PA and hypoplastic PA
On catheterization after UF, mean PA pressure in patients with hypoplastic central PA (vestigial and absent central PA) was significantly higher than that in patients with central PA (30.9 mmHg vs 23.3 mmHg, p = 0.024), and pulmonary resistance in patients with hypoplastic central PA was higher than that in patients with central PA (5.0 wood unit m2 vs 3.2 wood unit m2, p = 0.064) (Fig. 3 ). PA index, aortic saturation, and RV pressure were not statistically different between these groups. On catheterization after the definitive repair, systolic RV pressure in patients with hypoplastic PA was significantly higher than that in patients with central PA (84.1 mmHg vs 64.9 mmHg, p = 0.011); however, the RV/LV pressure ratio was not statistically different (70.5% vs 80.6%, p = 0.203).


Figure 3
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  		Fig. 3. Catheter data after UF in patients with central PA and with hypoplastic central PA (absent or vestigial central PA). (A) Mean PA pressure. (B) Pulmonary resistance. CPA: central PA.

 
3.3 Survival in patients who underwent definitive repair with fenestrated VSD closure
In 11 patients with preoperative pulmonary hypertension or higher intraoperative RV pressure than LV pressure, definitive repair with fenestrated VSD closure was indicated. Kaplan–Meier-estimated survival from definitive repair in these patients was 38.2, 25.5, and 12.7% at 1, 5, and 10 years, respectively. There was a significant difference in the survival ratio in patients who underwent definitive repair with complete VSD closure and with fenestrated VSD closure (log rank; p < 0.0001) (Fig. 2D).

3.4 Comparison between the early series and the late series
The comparison between the early group and the late group according to the timing of surgery is summarized in Table 4 . There was no statistical difference in central PA morphology and other anomalies. In the late group, the age at each surgical intervention was significantly younger and the frequency of the use of equine pericardium significantly lower.


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  		Table 4 Comparison between the early group and the late group
 
The Kaplan–Meier-estimated survival ratios after first UF in the early group were 77.9, 70.4, and 66.7% at 5, 10, and 15 years, respectively, and in the late group were 96.2, 91.3, and 91.3% at 3, 5, and 7 years, respectively (Fig. 4A). The survival ratio in the late group was better than that in the early group (log rank; p = 0.063). Among 27 patients who underwent definitive repair in the late group, survival from the repair was 91.1% at 3, 5, and 7 years, respectively (Fig. 4B). Catheterization after definitive repair showed that RV pressure and the RV/LV pressure ratio in the late group were significantly lower than in the early group (Fig. 4C).


Figure 4
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  		Fig. 4. (A) Survival ratio after first UF in the early group and the late group. (B) Survival ratio after definitive repair in the late group. (C) Catheter data after the definitive repair in the early group and the late group. (Left) Systolic RV pressure. (Right) RV/LV pressure ratio.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
5. Conclusions
 Appendix A
 Appendix B
 References
 
Our study has disclosed five major findings: (1) Clinical outcomes were insufficient in patients with hypoplastic central PA, and hypoplastic central PA was a risk factor for death and failure within 3 years after definitive repair on multivariate analysis. (2) Mean PA pressure and pulmonary resistance after final UF were higher in patients with hypoplastic central PA. (3) Clinical outcomes of definitive repair with fenestrated VSD closure were poor. (4) In the late group, each surgical intervention was rapidly performed, and UF was performed using autologous tissue. As a consequence, the clinical outcomes in the late group were improved. (5) RV pressure after definitive repair in the late group was significantly lower than in the early group.

Griselli and colleagues reported that central PA morphology was the only factor that influenced actuarial survival after definitive repair, regardless of the surgical strategy [20]. In our study, clinical outcomes of patients with hypoplastic central PA were significantly worse and the morphology of the central PA was the only significant factor for death and failure within 3 years after definitive repair. In addition, PA pressure and pulmonary resistance after UF were higher in these patients. Our results may show congenitally hypoplasia of the pulmonary vasculature in patients with hypoplastic PA.

Definitive repair with fenestrated VSD closure was indicated for patients with pre-operative or intraoperative pulmonary hypertension. However, the outcome was significantly worse. The main cause of death was RV failure, which suggested that the indication of this procedure was much more severe than that estimated by us.

Based on the results in the early era, we have performed rapid staged surgical intervention and complete UF using autologous tissue since the middle of 1990s. The purpose of this strategy was to induce the growth of PA and pulmonary vasculature and to reduce PA pressure before definitive repair. As a consequence, the clinical outcomes in the late group was better than that in the early group, and the RV pressure after definitive repair in the late group was significantly reduced. Improved RV pressure in the late group appears to affect sufficient long-term outcome.

Recently, favorable results of midline primary repair have been reported [4–8]. We also performed this procedure in seven patients; however, in our strategy, midline primary repair was limited for patients with no intrapulmonary arterial stenosis and with sufficient central PA. We consider that posterolateral thoracotomy in the reconstruction of peripheral intrapulmonary stenosis allows better surgical field and better quality of anastomosis. Furthermore, stepwise improvement to pulmonary circulation by a staged approach may affect the outcomes in patients with hypoplastic central PA, which suggested insufficient growth of pulmonary vasculature [21]. In our late group, survival at 5 years after the first UF and at 4 years after the definitive repair were both 91%, and these outcomes of our staged repair were equivalent to or better than those achieved by the primary repair [4–8].

Compared with the results in other reports [4–8], age at each intervention is higher in our report although each intervention was performed as soon as possible. The reason is delayed referrals to our institute. Reddy and colleagues reported that severe stenosis has been documented angiographically in patients as young as 3–4 months old in vessels that showed normal caliber at neonatal angiography [4]. MAPCAs have the characteristics of muscular arteries until they penetrate the lung parenchyma where they assume characteristics that are more similar to that of pulmonary arteries. The segments that are muscular are particularly prone to the development of severe stenosis, which is often progressive [22]. In our series, it cannot be ruled out that the possibility of delayed referral is associated with an increase in patients with intrapulmonary arterial stenosis and a decrease in patients in whom primary repair is indicated.


   5. Conclusions
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
Appendix A
 Appendix B
 References
 
Hypoplastic central PA was a significant risk factor in this disease. The overall survival was improved by our current management strategy. Improved RV pressure after definitive repair appears to affect the long-term outcome.


   Appendix A
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 Appendix A
Appendix B
 References
 
Conference discussion

Dr W. Brawn (Birmingham, United Kingdom): My understanding is that you can do this operation in all patients. But clinically we see very cyanosed patients, patients who are balanced with saturations in the 80s, and those who are in heart failure.

My question really relates to these three groups. How can you manage all these three groups with the one strategy? For instance, do you need to use cardiopulmonary bypass to support some of these patients while you are doing this surgery, particularly in the very blue, the very cyanosed group? Do you always use thoracotomies or do you do it through the midline? So what is your support mechanism for the very blue patients, and what is your surgical approach through thoracotomies or through the midline?

Dr Ishibashi: Our indication for primary repair, a midline repair, was sufficient central PA and small number of multiples. There is no anomaly or intrapulmonary stenosis. And of 121 patients who underwent such staged approach at our institution, 7 patients was indicated primary repair with midline repair. And our basic surgical strategy for this disease was staged repair. And for patients with insufficient central PA or intrapulmonary stenosis is staged repair.

In our staged series, there are no patients with mechanical support due to low saturation. In our strategy, first UF is performed on smaller PA to prevent low saturation during operation.

Dr D. Metras (Marseilles, France): Considering the fact that the survival at 3 years and the pulmonary artery pressures were less good in the population where the true central pulmonary arteries were very hypoplastic, would you consider another strategy like, for example, rehabilitation of the pulmonary artery, the true pulmonary artery, by promoting forward flow instead of anastomosing all the collaterals?

Dr Ishibashi: For patients with absent central PA.

Dr Metras: I’m not talking of absence. I’m talking of very hypoplastic.

Dr Ishibashi: Very hypoplastic central PA. For very hypoplastic central PA, we use this staged approach, central PA reconstruction using MAPCA anastomosis.

Dr B. Maruszewski (Warsaw, Poland): What type of operations do you perform to promote growth of the central PAs? What surgical techniques do you use to promote growth of minute PAs?

Dr Ishibashi: For central PA hypoplastic, we perform the shunt proximally, reconstruction of central PA.

Dr Maruszewski: Blalock–Taussig shunt or central shunt or do you anastomose them to the aorta?

Dr Ishibashi: We always use BT shunt, not central shunt.


   Appendix B
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 Appendix A
 Appendix B
References
 
Variable and univariate logistic regression.


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   Footnotes
 
\#9734; Presented at the joint 20th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 14th Annual Meeting of the European Society of Thoracic Surgeons, Stockholm, Sweden, September 10–13, 2006.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 Appendix A
 Appendix B
 References
 

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