HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Boulos Asfour Ehrenfried Schindler Andreas E. Urban Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sinzobahamvya, N. Articles by Urban, A. E. Search for Related Content PubMed PubMed Citation Articles by Sinzobahamvya, N. Articles by Urban, A. E. Related Collections Congenital - cyanotic

Eur J Cardiothorac Surg 2007;31:873-878. doi:10.1016/j.ejcts.2007.02.004
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Right ventricular outflow tract obstruction after arterial switch operation for the Taussig–Bing heart

^a Department of Pediatric Thoracic and Cardiovascular Surgery, Congenital Cardiac Center ("Deutsches Kinderherzzentrum"), Sankt Augustin, Germany
^b Department of Anesthesiology and Critical Care Medicine, Congenital Cardiac Center ("Deutsches Kinderherzzentrum"), Sankt Augustin, Germany

Received 6 September 2006; received in revised form 26 January 2007; accepted 2 February 2007.

^_* Corresponding author. Address: Deutsches Kinderherzzentrum, Asklepios Klinik, Arnold-Janssen-Strasse 29, 53757 Sankt Augustin, Germany. Tel.: +49 2241 249601; fax: +49 2241 249602. (Email: n.sinzobahamvya{at}asklepios.com).

	Abstract

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

 
Objective: Incidence of right ventricular outflow tract obstruction (RVOTO) may be suspected to be higher after arterial switch operation (ASO) for Taussig–Bing heart than after ASO for transposition of the great arteries (TGA), as Taussig–Bing anomaly is frequently associated with aortic arch obstruction and subvalvular aortic stenosis. We evaluated the risk to develop RVOTO after ASO for Taussig–Bing heart. Methods: The 34 Taussig–Bing cases who underwent ASO from 1984 to 2005 were reviewed. RVOTO was defined as peak echo-gradient 30 mmHg across right ventricular outflow tract. Kaplan–Meier method was used to estimate time-related events. Results: Subaortic stenosis was resected in 25 patients, 20 of whom (80%: 20/25) were discharged from hospital free from RVOTO. There was one early death: 2.9% mortality. Three patients died late. Actuarial survival was 85.1% ± 7.0% from 54 month onwards. Eleven survivors (36.7%: 11/30) experienced postoperative RVOTO. Obstruction was seen in 82% (9/11) of cases at subvalvular and/or valvular level. Surgery (n = 4) or percutaneous intervention (n = 2) was required in six patients. Patients discharged from hospital with RVOTO (n = 8) were more likely to undergo reintervention for RVOTO (p = 0.026). Freedom from reintervention for RVOTO decreased rapidly in the first two years to 86.5 ± 6.3%, slowly thereafter (80.4 ± 8.4% at year 7) and stabilized at 70.3 ± 11.9% from year 11 on. Risk for RVOTO occurrence was 23.5 ± 7.3% early after repair and progressively increased to level out at 53.6 ± 11% at year 11. Patients who underwent subaortic resection were more likely (p = 0.023) to be free from RVOTO occurrence or development. In the period under review, for patients who underwent ASO for simple (n = 355) and complex (n = 92) TGA, reoperation rate for neopulmonary stenosis was 0.3% (1/355) and 5.4% (5/92), respectively, to be compared to 11.8% (4/34) RVOTO rate of reoperation for Taussig–Bing heart in this study. Conclusions: Postoperative right-sided obstruction occurs more frequently after ASO repair of Taussig–Bing heart than after TGA arterial switching, leading to higher reintervention rate. Resection of the commonly associated subaortic stenosis often prevents RVOTO development.

Key Words: Taussig–Bing heart • Arterial switch operation • Pulmonary stenosis

	1. Introduction

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

 
The success story of the arterial switch operation (ASO) used for correction of transposition of the great arteries (TGA) is still dimmed by complications, the most frequent one being right ventricular outflow tract obstruction (RVOTO) [1–4]. Commonly reported anatomic factors in occurrence of neopulmonary stenosis are associated aortic arch obstruction, side-by-side position of the great arteries, coronary artery anomalies and preoperative presence of organic subaortic RVOTO [1,5–7]. As these features are often seen in Taussig–Bing anomaly, RVOTO incidence might be expected to be higher after ASO for this lesion.

This study was conducted to evaluate the risk for patients with Taussig–Bing heart to develop right-sided outflow obstruction after arterial switch procedure.

	2. Patients and methods

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

 
2.1 Definitions
Definition of Taussig–Bing malformation encompassed all sorts of double outlet right ventricle (DORV) lesions with subpulmonary ventricular septal defect (VSD) and without pulmonary stenosis, the aorta arising entirely and the pulmonary trunk at least 50% from right ventricle, that were amenable to ASO.

Postoperative RVOTO was defined as a peak echo-Doppler gradient at least 30 mmHg across the right ventricular outflow tract (RVOT). Level of stenosis was classified as subvalvular (right ventricular infundibulum), valvular (neopulmonary valve: leaflets or annulus) or supravalvular (reconstructed pulmonary trunk or right and left pulmonary artery).

Reintervention for RVOTO included any postoperative surgical or percutaneous interventional procedure to address any right-sided outflow obstruction.

2.2 Patients
All consecutive 34 patients who underwent ASO for Taussig–Bing anomaly from 1984 until the end of December 2005 were reviewed. These included 27 patients reported in a previous publication [8].

Median age at ASO was 34 days (range 8–154 days) for patients who underwent primary complete repair (n = 27). It was 66 days (range 14–291 days) for those with two-stage correction (n = 7). Fifteen patients were neonates. Mean comprehensive Aristotle score was 16.8 ± 1.6, range 15–21 for primary repair cases and 18.1 ± 1.3, range 16–20 for the other patients. The main clinical and surgical characteristics of these patients are shown in Table 1 . Subvalvular aortic stenosis (primitive RVOTO) caused by conal muscle was preoperatively present in 28 patients, but was recognized only in 24 of them at the time of surgery. In an additional case, it was discovered perioperatively (overall 25 patients with operatively recognized RVOTO). Obstruction of aortic arch was common (n = 23), and the repair was staged in seven patients. The usual coronary artery pattern with left coronary artery (LCA) arising from Sinus 1 and right coronary artery (RCA) arising from Sinus 2 was found in only 32% (11/34) of cases.

2.4 Follow-up and evaluation of right ventricular outflow tract
To assess follow-up, all available clinical and surgical records, echocardiographic and postoperative catheterization data were collected. A thorough transthoracic echo-Doppler examination was realized before discharge from hospital. Particularly, the peak pressure gradient (calculated using the simplified Bernoulli equation: gradient = 4V ², where V is the peak instantaneous transvalvular or transvascular Doppler velocity) was recorded. Afterwards, patient was usually reviewed by the referring cardiologist at interval 1, 3 and 6 months and at least once yearly thereafter, and we were informed about outcome. Assessment for this study took place from April to June 2006 by contacting attending physicians. The study put emphasis on variables related to right ventricular outflow tract. Our policy is to consider reintervention if peak echo-Doppler gradient through RVOT is 50 mmHg.

2.5 Statistical analysis
Kaplan–Meier curves for actuarial survival, freedom from reintervention for RVOTO and for RVOTO occurrence were calculated using the Graph Pad Prism (San Diego, CA, USA). The following parameters served as end points: time of death, first surgical or percutaneous reintervention to manage RVOTO, first demonstration of a peak echo-Doppler gradient at least 30 mmHg across RVOT. The probabilities are given as percentages (%) ± standard error of the mean (S.E.M.). Univariate analysis with Fisher's exact test was used to compare variables. The level of statistical significance was set at a p-value of less than 0.05. Medians and means are given with range and standard deviation.

	3. Results

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

 
3.1 Survival and functional status
There was one hospital death in a neonate who was reoperated upon on the ninth postoperative day because of residual aortic arch obstruction. He died 2 months later from multi-organ failure. Three patients died late. The first patient succumbed to septicemia unrelated to cardiac surgery after 8 months. The second late death was sudden, after 36 months, presumably from cardiac arrhythmia. Rhythm disturbances had already complicated postoperative course. LAD arose from Sinus 2 and peak echo-Doppler gradient through the neopulmonary valve was 50 mmHg at the day of discharge from hospital. The cause of the third late death (54 months) was attributed to an acute coronary insufficiency and myocardial infarction. The patient had a single coronary artery system, which previously came off Sinus 2.

Actuarial survival was 85.1 ± 7.0% at 54 months and remained constant thereafter (Fig. 1 ). Follow-up for the late 30 survivors is complete. Median time after ASO repair is 70 months, range 4–224 months. Ten patients underwent, after first hospital discharge, a total of 15 reinterventions to manage RVOTO (n = 6), aortic arch stenosis (n = 2), neoaortic valve regurgitation (n = 1) and complete atrio-ventricular block (n = 1). Twenty-two patients (73%: 22/30) were in functional NYHA class I and eight in class II. There was no case of significant (neo) pulmonary regurgitation. The (neo) aortic valve functioned normally or showed trivial or Grade 1 regurgitation in 26 cases. It was Grade 2 incompetent in two patients. Aortic valve was replaced by a mechanical valve in one patient and was planned to be repaired or replaced in the remaining patient with Grade 3 regurgitation.

View larger version (16K): [in this window] [in a new window]   Fig. 1. Kaplan–Meier estimate of survival of 34 patients after arterial switch operation (ASO) for Taussig–Bing heart. Vertical bars represent standard error of the mean (S.E.M.).

View larger version (17K): [in this window] [in a new window]   Fig. 2. Early and late mortality, reintervention for right ventricular outflow obstruction and levels of peak echo-Doppler gradients across right ventricular outflow tract at the time of discharge from hospital. The number of patients involved are schematically displayed.

Six patients had to undergo surgery (n = 4) or percutaneous intervention (n = 2). Table 2 details these patients lesions that were associated with Taussig–Bing anomaly, the type of procedure and outcome. Patient number 1 was reoperated twice because of recurrent RVOTO 25 months after ASO. The procedure consisted of transpulmonary resection of the hypertrophied infundibulum and removal of the previously implanted PTFE (polytetrafluoroethylene) conduit. A dilating stent was placed in the left pulmonary artery 50 months after initial operation. At recent follow-up, 3 years after the last intervention, echo-Doppler still exhibited supravalvular 98 mmHg gradient and thus, patient was scheduled for reintervention. It is to be noted that patients number 5 and 6 had left hospital after ASO repair with low RVOT gradients: 0 and 10 mmHg. Probability to undergo reintervention for neopulmonary stenosis was 50% (4/8) for patients discharged from hospital with RVOTO and 8.7% (2/23) for those leaving hospital without RVOTO: a significant difference of p = 0.026. Freedom from first reintervention for RVOTO (Fig. 3 ) decreased rapidly in the first 2 years to 86.5 ± 6.3%, slowly thereafter 80.4 ± 8.4% at year 7 and stabilized at 70.3 ± 11.9% from year 11 on.

View larger version (16K): [in this window] [in a new window]   Fig. 3. Kaplan–Meier estimate of freedom from reintervention for right ventricular outflow tract obstruction (RVOTO) for 34 patients after arterial switch operation (ASO) for Taussig–Bing heart. Vertical bars represent standard error of the mean (S.E.M.).

View larger version (23K): [in this window] [in a new window]   Fig. 4. Peak echo-Doppler gradients across right ventricular outflow tract in 28 late survivors and their evolution from time of discharge from hospital to last follow-up examination. Two late survivors whose discharge echo-Doppler results are missing were excluded. The horizontal bar at 30 mmHg delineates patients with (above) or without (below) right ventricular outflow tract obstruction (RVOTO).

View larger version (15K): [in this window] [in a new window]   Fig. 5. Risk of development or occurrence of right ventricular outflow tract obstruction (RVOTO) after arterial switch operation (ASO) for Taussig–Bing heart over time. The dashed lines indicate the standard error of the mean (S.E.M.).

	4. Discussion

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

 
Supravalvular neopulmonary artery stenosis is the most common complication and cause of reintervention after ASO for TGA, with a reported incidence varying from 1 to 42%, depending on obstruction criteria and length of follow-up [4], reoperation being observed up to 9–10 years after arterial switching [1,2]. Apart from the anatomic variables cited in Section 1, technical factors have been incriminated for RVOTO development: insufficient mobilization of the pulmonary arteries and inadequate size or form of the pericardial patch used to reconstruct the neopulmonary trunk. Some are controversial such as the Lecompte maneuver and the use of glutaraldehyde-treated pericardial patch. Whatever the cause, with experience, the reoperation rate for pulmonary stenosis in most series is reported to be decreasing in the last 10 years.

As for the Taussig–Bing lesion, little has been published about RVOTO complication after ASO correction. The multi-institutional study of Williams et al. [1] with a considerable number of patients does not include Taussig–Bing cases. The largest series from one institution with 79 Taussig–Bing patients [2] only reveals that the incidence of all reoperation was higher in complex TGA, without describing further details. The first study of RVOTO problem after ASO repair of these complex DORV lesions was published by Wetter et al. [8] from our Unit.

Peak echo-Doppler gradient 30 mmHg adopted in this study to define RVOTO could be challenged. The incidence of truly significant pulmonary stenosis may have been overestimated. Gradients 25–49 mmHg are commonly defined as mild stenosis. In the series of Ullmann et al. [4], 24.2% of cases had such postoperative gradients. Nevertheless, the authors claimed a low incidence of late supravalvular pulmonary stenosis after ASO for TGA. Like other investigators [3,10], we defined the threshold to be 30 mmHg, considering that such gradient is not insignificant, even if a good number would indicate an intervention at 40 mmHg. Indeed, on one hand, this study shows that patients discharged from hospital with gradient 30 mmHg are more likely to undergo reintervention for RVOTO than those leaving hospital with gradient under 30 mmHg (p = 0.026). It also indicates that RVOTO rarely develops in patients discharged from hospital with gradient under 30 mmHg. On the other hand, according to Krovetz and Goldbloom [11], normal systolic pressure in the right ventricle (RV) is 32.9 ± 14.7 mmHg. If a RVOT stenosis causes a peak echo gradient of at least 30 mmHg, corresponding systolic pressure in RV could be assumed to be at least 62.9 mmHg. As 50% of infants are reported to have 90 mmHg systolic systemic blood pressure on average [12], RV pressure may then be estimated to be at least 70% (62.9/90) of the systemic arterial pressure. This level of RV pressure, if it persists, can certainly be detrimental to RV function.

RVOTO evolved over time. Valvular and subvalvular obstruction appeared early and its occurrence approached 0% in later follow-up, which corresponds to higher reintervention rate in the first 2 years. This evolution was similar to the behavior of postoperative proximal pulmonary stenosis observed after ASO for TGA [1]. As shown in Fig. 4, half of pressure gradients subsided. But obstruction increased in all three children discharged from hospital with gradients above 40 mmHg. It is noteworthy that this group of patients keep requiring further management.

As described by Boyadjev et al. [5] and Akiba et al. [13], there is an anatomic substrate for subvalvular RVOTO after ASO TGA repair. In this series, the Taussig–Bing malformation was associated with stenosing subaortic conal muscle in at least 74% (25/34) of cases. Resection was effective in relieving this obstruction. Indeed, only 3 out of 25 patients (12%) with confirmed preoperative subaortic stenosis left hospital with RVOTO. Patients who underwent subaortic resection were more likely (p = 0.023) to be free from occurrence or development of RVOTO. Bulging myocardial tissue under the aortic valve must be identified and removed to avoid the problem of subpulmonary obstruction after arterial switching. Nevertheless, we cannot recommend infundibulotomy and transannular enlargement, considering that early survival does depend on a competent neopulmonary valve. Moreover, infundibulotomy could not be feasible in those patients with RCA crossing infundibulum, as seen in 29% (10/34) of our cohort.

In a great majority of cases (82%), postoperative RVOTO was located at subvalvular and valvular level. The supravalvular site is more affected after ASO for TGA [1–4]. It is therefore unlikely that technical factors in reconstruction of the neopulmonary trunk are involved in the genesis and development of this obstruction. Analysis of the usually evoked anatomic factors did not point at any specific lesion. It may be explained by a small number of patients or by the fact that most patients had combined associated malformations. Nevertheless, with a p of 0.07, two-stage repair should be accepted as a risk factor. This finding added to the fact that staged correction compounded with higher comprehensive Aristotle score constitutes additional argument to further recommend primary complete early repair of the Taussig–Bing lesion.

In five instances, position of the great arteries and coronary anomalies did not allow Lecompte maneuver and the pulmonary anostomosis had to be shifted to the right pulmonary artery not to compromise coronary circulation. All five patients survived but had postoperative RVOTO and three needed reintervention. Thus, abnormal coronary artery pattern played a role in RVOTO development. It is also clear that native aortic annulus was small: size ratio of pulmonary artery and aorta was 2:1 in 53% (18/34) of cases. Detachment of coronary buttons left limited tissue for later growth of the neopulmonary root. This might be the main explication of obstruction at the valvular region, which triggers increasing adaptive infundibular hypertrophy and subvalvular stenosis.

We conclude that survival after ASO repair of the Taussig–Bing heart can be high despite concomitant major anomalies such as aortic arch obstruction, unusual coronary patterns and subaortic stenosis. In our experience, postoperative right-sided obstruction occurs or develops more frequently after arterial switching for Taussig–Bing heart than after ASO TGA correction, leading to higher reintervention rate. It rarely develops in patients discharged from hospital with gradient under 30 mmHg. It can be prevented by resection of subaortic stenosis in great majority of cases.

	Appendix A

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

 
Conference discussion

Dr B. Maruszewski (Warsaw, Poland): What technical precautions do you use during repair of Taussig–Bing anomaly nowadays to prevent recurrent or residual right ventricular outflow tract stenosis? And did you change your surgical technique over the years to minimize this percentage of recurrent stenosis?

Dr Sinzobahamvya: It is very important to resect the subaortic muscle that causes obstruction. You go either through the native aortic valve or transatrially. There is ventriculo-infundibular fold and the free anterior wall of right ventricle where you have really to be aggressive. In our series of 25 who had preoperative subvalvular aortic stenosis, only 3 of them had, at the time of discharge from hospital, gradient of 30 mmHg or more through right ventricular outflow tract.

But I must also say that even if you do it, even in patients who have no gradient at time of discharge from hospital, or gradient less than 30 mmHg, right-sided obstruction can develop, albeit less frequently. Because the native aortic annulus is very small. And whatever you do under the annulus, the annulus remains unchanged. We think this is the main reason for postoperative pulmonary stenosis. Sometimes it is better to accept some gradient than to be too aggressive and to have, after the operation, a free outflow tract but bad contractility and thus, to jeopardize early survival.

Dr D. Barron (Birmingham, United Kingdom): Can I ask, you had some patients who had a one-stage repair, some who had a two-stage repair. What criteria did you use to decide on a one- or two-stage repair? And did that have an effect on your incidence of right outflow tract obstruction?

Dr Sinzobahamvya: We favor one-stage repair. There are seven patients who underwent two-stage repair. Among these seven patients, three came from other units, two were operated upon in the year 1987. We decided to do two-stage repair in the remaining two patients, as these two neonates presented in functional NYHA class V, with a comprehensive Aristotle score, which would have been more than 20. We decided to first stabilize them. The aortic arch was first repaired and we went back 2 weeks later to do the intracardiac repair and arterial switching. But fundamentally, one should perform one-stage complete repair.

Patients who underwent two-stage repair have a tendency to have more frequently right-sided obstruction. We did do an analysis. The probability was 0.07. If we had more cases, the difference would become significantly different. But we are unlikely to have more cases, as we know that we have to go after one-stage repair.

Dr C. Kreutzer (Buenos Aires, Argentina): I think what we must emphasize here is that subaortic resection means resection of the infundibular septum, because this is actually a fundamental part of the complex. The anterior deviation of the infundibular septum is creating subaortic stenosis, and this is the anatomic substrate for the aortic arch obstructions usually seen in Taussig–Bing hearts. So there is a clear indication that in all patients with a Taussig–Bing, even though you are not performing Kawashima type of repair, you must resect the infundibular septum.

Dr Sinzobahamvya: I agree with you.

	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. Patients and methods 3. Results 4. Discussion Appendix A References

 

1. Williams WG, Quaegebeur JM, Kirklin JW, Blackstone EH. The Congenital Heart Surgeons Society. Outflow obstruction after the arterial switch operation: a multiinstitutional study. J Thorac Cardiovasc Surg 1997;114:975-990.[Abstract/Free Full Text]
2. Losay J, Touchot A, Serraf A, Litvinova A, Lambert V, Piot JD, Lacour-Gayet F, Capderou A, Planché C. Late outcome after arterial switch operation for transposition of the great arteries. Circulation 2001;104:121-126.
3. Gandhi SK, Pigula FA, Siewers RD. Successful late reintervention after the arterial switch procedure. Ann Thorac Surg 2002;73:88-95.[Abstract/Free Full Text]
4. Ullmann MV, Gorenflo M, Bolenz C, Sebening C, Goetze M, Arnold R, Ulmer HE, Hagl S. Late results after extended pulmonary artery reconstruction in the arterial switch operation. Ann Thorac Surg 2006;81:2259-2266.[Abstract/Free Full Text]
5. Boyadjiev K, Ho SY, Anderson RH, Lincoln Ch. The potential for subpulmonary obstruction in complete transposition after the arterial switch procedure: an anatomic study. Eur J Cardiothorac Surg 1990;4:214-218.[Abstract]
6. Urban AE, Brecher AM. The arterial switch repair and the obstructive right ventricular outflow tract: does it matter?. Thorac Cardiovasc Surg 1991;39(Suppl.):170-175.[Medline]
7. Nogi S, McCrindle BW, Boutin C, Williams WG, Freedom RM, Benson LN. Fate of the neopulmonary valve after the arterial switch operation in neonates. J Thorac Cardiovasc Surg 1998;115:557-562.[Abstract/Free Full Text]
8. Wetter J, Sinzobahamvya N, Blaschczok HC, Cho MY, Brecher AM, Grävinghoff LM, Urban AE. Results of arterial switch operation for primary total correction of the Taussig–Bing anomaly. Ann Thorac Surg 2004;77:41-47.[Abstract/Free Full Text]
9. Wetter J, Belli E, Sinzobahamvya N, Blaschczok HC, Brecher AM, Urban AE. Transposition of the great arteries associated with a ventricular septal defect: surgical results and long-term outcome. Eur J Cardiothorac Surg 2001;20:816-823.[Abstract/Free Full Text]
10. Böhm JO, Botha CA, Horke A, Hemmer W, Roser D, Blumenstock G, Uhlemann F, Rein JG. Is the Ross operation still an acceptable option in children and adolescents?. Ann Thorac Surg 2006;82:940-947.[Abstract/Free Full Text]
11. Krovetz LJ, Goldbloom S. Normal standards for cardiovascular data. II. Pressure and vascular resistances. Johns Hopkins Med J 1972;130:187-195.[Medline]
12. Reid C, Chantler C. Systemic hypertension. In: Anderson RH, Baker EJ, Macartney FJ, Rigby ML, Shinebourne EA, Tynan M, editors. Paediatric Cardiology. 2nd ed.. London: Churchill Livingstone; 2002. pp. 1809-1844.
13. Akiba T, Neirotti R, Becker AE. Is there an anatomic basis for subvalvular right ventricular outflow tract obstruction after an arterial switch repair for complete transposition? A morphometric study and review. J Thorac Cardiovasc Surg 1993;105:142-146.[Abstract]

This article has been cited by other articles:

				B. Alsoufi, S. Cai, W. G. Williams, J. G. Coles, C. A. Caldarone, A. M. Redington, and G. S. Van Arsdell Improved results with single-stage total correction of Taussig-Bing anomaly Eur. J. Cardiothorac. Surg., February 1, 2008; 33(2): 244 - 250. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Boulos Asfour Ehrenfried Schindler Andreas E. Urban Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sinzobahamvya, N. Articles by Urban, A. E. Search for Related Content PubMed PubMed Citation Articles by Sinzobahamvya, N. Articles by Urban, A. E. Related Collections Congenital - cyanotic