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): Anne Marie Brecher Andreas E. Urban Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wetter, J. Articles by Urban, A. E. Search for Related Content PubMed PubMed Citation Articles by Wetter, J. Articles by Urban, A. E. Related Collections Congenital - cyanotic

Ann Thorac Surg 2004;77:41-46
© 2004 The Society of Thoracic Surgeons

---

Original article: cardiovascular

Results of arterial switch operation for primary total correction of the Taussig-Bing anomaly

^a Department of Paediatric Cardiothoracic Surgery, Sankt Augustin, Germany
^b Department of Paediatric Cardiology, German Paediatric Heart Centre, Deutsches Kinderherzzentrum, Sankt Augustin, Germany

Accepted for publication June 5, 2003.

^* 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 Results Comment References

 
BACKGROUND: This study evaluates the results of the arterial switch operation for early total repair of double-outlet right ventricle with subpulmonary ventricular septal defect (the Taussig-Bing heart).

METHODS: From 1986 through April 2003, 27 patients with Taussig-Bing anomaly underwent arterial switch operation. Twenty patients were neonates (n = 11) or infants younger than 3 months (n = 9). Obstruction of aortic arch (n = 19) or subaortic right ventricular outflow tract obstruction (n = 20) and unusual coronary artery patterns (n = 19) were common. Total correction as a single procedure was performed in 21 patients. Events are depicted by Kaplan-Meier curves.

RESULTS: There was 1 patient hospital death at 2 months after repair. One patient died late that was not cardiac related. Survival was 92% ± 6% at 8 months and remained constant thereafter. Four patients underwent reoperation (1 for residual aortic arch obstruction and 3 for subvalvular and valvular pulmonary stenosis). Freedom from reoperation decreased to stabilize at 83% ± 8% after 2 years. The risk to have right ventricular outflow tract obstruction develop was 33% ± 10% at 1 year, increasing slowly and leveling out at 57% ± 12% at year 5 and thereafter. Statistical analysis revealed no significant risk factor for death or need for reoperation.

CONCLUSIONS: The Taussig-Bing anomaly should be corrected in the neonatal period or in early infancy by arterial switch operation, closure of the ventricular septal defect, and simultaneous correction of associated cardiovascular anomalies as a one-stage procedure. Right ventricular outflow tract obstruction often complicates the postoperative course and is the main cause for reintervention.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Second to the Fallot type heart, the Taussig-Bing heart is the most common variant of the double-outlet right ventricle malformation. In the series of Wilkinson and colleagues [1], the Taussig-Bing heart variant accounted for 24% of all double-outlet right ventricle cases.

In their original communication in 1949, Taussig and Bing [2] described a double-outlet right ventricle with side-by-side position of the great arteries in which both the aorta and the pulmonary artery arise entirely from the right ventricle and are supported by bilateral coni. The ventricular septal defect (VSD) is located beneath both coni, close to the subpulmonary infundibulum, above the trabeculated septum marginal, and therefore remote from both arteries. In 1968, van Praagh [3] summarized these anatomic findings by pointing out the importance of the presence of a muscular subpulmonary infundibulum. Stellin and colleagues [4] emphasized that the Taussig-Bing anomaly is a spectrum of malformations defined by the presence or absence of a subpulmonary conus combined with subpulmonary VSD. This study encompasses all sorts of double-outlet right ventricles with subpulmonary VSD and without pulmonary stenosis, the aorta arising entirely, and the pulmonary trunk at least 50% from the right ventricle.

Infants with an early Taussig-Bing anomaly present with congestive heart failure and pulmonary hypertension. The condition of those with associated aortic coarctation or aortic arch interruption (more than 50% of cases [5, 6]) is usually so poor that urgent surgical intervention is required. In the past, banding of the pulmonary artery was the usual primary palliative procedure, with aortic arch repair in case of aortic obstruction. Complete correction was postponed until later in childhood.

Repair can be achieved by two different surgical approaches: either (1) by intraventricular rerouting of the left ventricular blood stream through a patch tunnel from the VSD to the aorta including resection of infundibular septum (Kawashima) [7], or (2) by arterial switch operation (ASO) with VSD closure. In addition, Fontan-type procedures may be proposed as a solution for even more complex forms.

Since 1986, we performed ASOs to manage all patients with Taussig-Bing anomaly who were referred to us. This article presents our results with particular emphasis on survival rate, rate of reoperation, and postoperative occurrence of right ventricular outflow tract obstruction (RVOTO).

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Between May 1986 and April 2003, 27 consecutive patients with Taussig-Bing heart underwent arterial switch operation at our institution. Detailed diagnoses (see Table 1) were based on a combination of echocardiography and surgical inspection (n = 27). In 25 of these patients additional information was available from angiography. All patients had double-outlet right ventricle with subpulmonary VSD. Muscular discontinuity between pulmonary and mitral valve was documented in 23 patients. Four patients presented with an intermediate type of Taussig-Bing lesion with a pulmonary to mitral valve fibrous continuity and the pulmonary artery arising mainly from the right ventricle. A side-by-side relationship between the aorta and pulmonary artery was observed in 15 patients. The pulmonary artery was always larger than the aorta; a size ratio of more than 2:1 was observed in 14 patients.

Because of marked discrepancy between the size of the great arteries and the associated anomalies, the surgical technique had to be adapted to individual circumstances. In 15 cases, a "U"-shaped segment of the anterior wall of the native proximal transected pulmonary trunk was excised to reduce the circumference of the neo-aorta. A single, large pericardial patch was used to reconstruct the coronary donor areas. In 22 patients this patch had to be considerably larger than the excised coronary buttons to supplement the neopulmonary artery. In 9 patients with side-by-side great arteries, we shifted the pulmonary anastomosis into the right pulmonary artery to minimize the risk of compression of the anteriorly transferred coronary artery, as well as to decrease the tension on the pulmonary anastomosis. This was realized by closing the leftward end of the distal divided main pulmonary trunk and by extending the opening into the right pulmonary artery. The pulmonary artery was not translocated anteriorly (Lecompte maneuver) in 4 patients to prevent compression of the left coronary artery button. The VSD was closed through the right atrium in 7 patients, through a combined (transatrial and transpulmonary) approach in 5, through native pulmonary valve in 14, and through a right ventriculotomy in 1. Subaortic narrowing was resected in 20 patients.

In 13 patients obstruction of the aortic arch was repaired at the same time by resection and end-to-side anastomosis in 8 patients and plastic enlargement of the hypoplastic aortic arch by a pulmonary homograft patch in the last 5 patients. During aortic arch repair we continued coronary perfusion through a small cannula inserted in the proximal ascending aorta, which was used later for infusion of cardioplegic solution. The homograft angioplasty (from 1999) was achieved using a technique similar to that of Tchervenkov and collegaues [9] to avoid complete circulatory arrest. 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.

Data analysis
The data of the patients were compiled by review of clinical records, including echocardiographic and cardiac catheterization data. To assess follow-up, all available clinical records, electrocardiographic results, and echocardiographic and postoperative catheterization (n = 4) data were collected. The peak pressure gradient was calculated using the simplified Bernoulli equation: gradient = 4V², where V is the peak instantaneous transvalvular or transvascular Doppler velocity. Aortic insufficiency was graded by mapping the dimensions of the regurgitation jet with pulsed or color flow Doppler echocardiography [10]. Kaplan-Meier curves for actuarial survival, freedom from reoperation, and freedom from postoperative RVOTO occurrence were calculated using the GraphPad Prism software (GraphPad Prism version 2.0 10855; San Diego, CA). Univariate analysis with Fischer's exact test was used to compare risk factors. As appropriate, means are given with standard deviation and percentages with 95% confidence limits.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
Early postoperative course
The postoperative course was complicated in 17 patients (63%; 95% confidence limit: 42% to 81%). Hemodynamic instability required delayed sternal closure in 9 patients. Surgical reexploration was necessary in 6 patients because of sustained bleeding. Low cardiac output with renal insufficiency led to peritoneal dialysis in 4 patients. Three patients had pulmonary hypertensive crises develop. Necrotizing enterocolitis occurred in 1 newborn, which had to be treated surgically. Various forms of supraventricular arrhythmias complicated early postoperative course in 6 patients. Mean duration of endotracheal intubation was 154 ± 132 hours; this includes the length after reintubation for 4 infants.

Survival
There was 1 patient hospital death in a neonate who had a reoperation on postoperative day 9 because of residual aortic arch obstruction. The arch was enlarged by a patch, but heart failure persisted and the patient died 2 months later from multiorgan failure. One patient died late; he had undergone ASO at the age of 5 months. Eight months later he died from septicemia unrelated to the cardiac surgery. Actuarial survival was 92% ± 6% at 8 months and remained constant thereafter (Fig 1).

View larger version (15K): [in this window] [in a new window]   Fig 1. Kaplan-Meier estimate of survival of 27 patients after arterial switch operation for the Taussig-Bing heart. Vertical bars represent standard error of the mean (SEM).

View larger version (15K): [in this window] [in a new window]   Fig 2. Kaplan-Meier estimate of survival with freedom from reoperation for 27 patients after arterial switch operation for the Taussig-Bing heart. Vertical bars represent standard error of the mean (SEM).

At discharge from the hospital, 5 patients showed a peak echo-gradient of at least 30 mm Hg across the right ventricular outflow tract. At follow-up, RVOTO (echo-gradient 30 mm Hg) was present in 11 patients (44%; 95% confidence limit: 24% to 65%), with severity (gradient 50 mm Hg) in 4. In 1 of these patients whose gradient was greater than 60 mm Hg, reintervention was proposed to the parents but they did not accept it. For all patients, the site of obstruction was subvalvular or valvular, or both. Moreover there was right pulmonary artery stenosis in 1 patient and moderate bilateral pulmonary artery stenosis in another. The incidence of significant RVOTO was not influenced by the presence of aortic arch obstruction (p = 1.00), the side-by-side relationship of the great arteries (p = 1.00), or the fact that the right coronary artery crossed the infundibulum (p = 0.66). Right ventricular outflow tract obstruction evolved over time (Fig 3). Twelve patients remained free of obstruction during the period of observation, whereas the stenosis became insignificant in 1 patient. The risk to have RVOTO develop is high in the first postoperative year, then it decreases and stabilizes from the fifth year on.

View larger version (18K): [in this window] [in a new window]   Fig 3. Probabilities of freedom from occurrence of postoperative right ventricular outflow tract obstruction over time. The dashed lines indicate standard error of the mean (SEM).

	Comment

Top Abstract Introduction Patients and methods Results Comment References

 
The original definition of the Taussig-Bing anomaly [2, 3] has been extended in many surgical reports to encompass all sorts of double-outlet right ventricles with subpulmonary VSD. We also included 4 patients with pulmonary to mitral valve continuity in this study. Indeed, the surgical approach is identical.

The ASO is actually the most commonly used technique for two-ventricular repair of the Taussig-Bing malformation; when compared with the Kawashima operation, it can be used in a wider group of patients [11], in particular, neonates and very young infants. In several published series [6, 12–16], ASO was associated with a higher rate of mortality than in standard transposition of the great arteries with posterior-anterior position of the great arteries and figures varying between 7% and 48%. This increased risk was attributed to several factors: poor preoperative condition, complexity of the repair (especially caused by unusual coronary patterns), mismatched size of the great arteries, and associated cardiac lesions (in particular aortic arch obstruction).

The postoperative morbidity was very high in our experience. Noteworthy is that renal insufficiency is common and often requires peritoneal dialysis. This complicated postoperative course is to be expected as the primary complete repair concerns neonates or young infants in decompensated heart failure and pulmonary hypertension. Nevertheless all our patients survived the first 30 days after operation. Only 1 patient hospital death occurred 2 months after ASO. This low mortality was achieved, although the great majority of patients (74%) were newborns or very young infants and a subset of neonates with aortic arch obstruction equally.

Our current policy applied since 1996 without exception is to perform one-stage ASO complete repair with correction of associated lesions as soon as the diagnosis of Taussig-Bing heart has been established. We assume that delaying repair increases the incidence of pulmonary vascular disease, the adverse effects of hypoxemia, congestive heart failure, and size discrepancy between both great arteries. Banding of the pulmonary trunk can distort the underlying pulmonary valve and trigger subaortic stenosis, thereby predisposing the patient after ASO to the increased risk of regurgitation through the neo-aortic valve and to the RVOTO, and sometimes it can also be ineffective. Therefore, early one-stage complete repair should be preferred.

This also holds true for patients with associated aortic arch obstruction. The ASO for transposition of the great arteries with concomitant repair of aortic coarctation through median sternotomy is currently the standard procedure in specialized centers. Overall, it carries a much lower operative risk (ie, 19% to 20% [6, 17, 18]) than the classic two-stage approach (ie, 31% to 64% [19]). Equally one should expect similar outcomes for repair of the Taussig-Bing anomaly; the single-stage ASO with relief of aortic arch obstruction should give overall better results than the two-staged strategy. Although the numbers are small in our series, the early one-stage repair provided statistically similar early and late results whether aortic obstruction was present (n = 13) or absent (n = 8). The survival is identical. There is no significant statistical difference in the rate of reoperation and in RVOTO occurrence. We agree with Comas and colleagues [6] that concomitant repair of aortic arch obstruction does not adversely affect the outcome. Thus a single-stage procedure should be promoted. However, staged repair is to be considered when multiple VSDs or other complex intracardiac anomalies that are difficult to address during ASO are present.

Right ventricular outflow obstruction remains the most frequent cause of reoperation after ASO, with a relatively early occurrence within the first 2 postoperative years and as much as 10% to 20% of cases in the literature [6, 13, 19–23]. The obstruction is usually in the pulmonary trunk. Insufficient mobilization of pulmonary arteries and the Lecompte maneuver have been advocated as possible triggering factors. These causes can hardly be evoked for our experience as the level of obstruction in our patients was subvalvular and valvular. The mismatch in size between both great arteries has been postulated to be an incremental risk factor for developing neopulmonary stenosis [20, 21]. The aortic annulus is usually hypoplastic in patients with transposition of the great arteries, VSD, and aortic arch obstruction. In this series, the pulmonary artery was always larger than the aorta, a ratio of more than 2:1 in size being observed in 52% of patients (14 of 27). All 4 patients who had to undergo reoperation had a small aortic annulus at the time of ASO. Akiba and colleagues [23] suggested that this mismatch may set off a process of increasing adaptive infundibular hypertrophy.

Whatever pathogenesis is involved, it is clear that the obstruction evolves over time (Fig 3). Resection of the obstructing subaortic conus at the time of ASO indeed relieved the obstruction in the majority of patients, as only 5 of 20 patients with preoperative subaortic stenosis still had a significant RVOTO at the time of hospital discharge. The subvalvular pulmonary stenosis became evident afterward with the other patients. Right ventricular outflow tract obstruction incidence mainly increased in the first year after repair and stabilized after 5 years, with an overall 57% of patients being affected. We believe that this is the first time that actuarial RVOTO occurrence after ASO for the Taussig-Bing lesion has been estimated. Authors usually report rates of reoperation for this complication. Our experience better reflects the real incidence of postoperative RVOTO as measured by echo-Doppler in this complex heart anomaly.

It is common that after arterial switching the right coronary artery passes in front of the pulmonary artery and crosses the right ventricular outflow tract. If a transannular patch enlargement becomes necessary, conduit insertion is sometimes the only way to relieve obstruction without causing damage to the coronary artery. Unusual coronary artery patterns are much more frequent with the Taussig-Bing heart than in patients with transposition of the great arteries [24]. In 8 patients we noted an anterior origin of the right coronary artery. In these patients, extensive mobilization of this vessel is necessary to prevent tethering. This underlines the fact that coronary translocation remains the most challenging aspect of ASO especially in patients with the Taussig-Bing heart. All survivors have retained normal sinus node functions so far, and no patient has presented with signs of myocardial ischemia. The problem of side-by-side relationship of the great arteries and coronary translocation of unusual coronary artery pattern was surgically addressed so that it did not adversely affect the outcome in this series.

Minor neo-aortic regurgitation is common after ASO, ranging from 5% to 55% [25]. Patients with the Taussig-Bing heart face a higher risk of neo-aortic incompetence from a mismatch of the large pulmonary artery and a small aorta as previously mentioned. It has been speculated that resection of tissue of the neo-noncoronary sinus may lead to dilatation of the sinus of Valsalva and adjacent leaflet prolapse, which in turn leads to neo-aortic insufficiency [20]. Moreover, the increased preoperative flow across the anatomic pulmonary valve may result in dilatation of the pulmonary valve annulus and postoperative neo-aortic insufficiency, or reimplantation of the abnormal coronary arteries into the neo-aorta may distort the architecture of the valve. Because the amount of neo-aortic regurgitation present in most of our patients was hemodynamically insignificant, further follow-up data will be required to determine whether trivial or mild regurgitation will eventually become clinically relevant, but an increase in the degree of insufficiency since discharge was seen in 40% of the cohort.

We conclude that the Taussig-Bing heart can be repaired by ASO and VSD closure in neonates and young infants (< 3 months) with a good outcome. Simultaneous correction of associated cardiac anomalies (especially aortic arch obstruction) had no detrimental influence on survival and later outcome. Therefore we recommend early one-stage complete repair. It should be kept in mind that the risk of reoperation for RVOTO, despite initial resection of subaortic stenosis, persists for a long time (as long as 5 years in this series). To determine secondary effects of neo-aortic regurgitation and their clinical relevance, continued follow-up is mandatory after ASO repair of Taussig-Bing lesion.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

1. Wilkinson J.L., Wilcox B.R., Anderson R.H. The anatomy of double-outlet right ventricle. In: Anderson R.H., Macartney F.J., Shinebourne E.A., Tynan M., eds. Paediatric Cardiology, Vol 5. Edinburgh: Churchill Livingstone, 1981:397-407.
2. Taussig H.B., Bing R.J. Complete transposition of the aorta and a levoposition of the pulmonary artery. Am Heart J 1949;37:551-559.[Medline]
3. van Praagh R. What is the Taussig-Bing malformation?. Circulation 1968;39:445-449.
4. Stellin G., Zuberbuhler J.R., Anderson R.H., Siewers R.D. The surgical anatomy of the Taussig-Bing malformation. J Thorac Cardiovasc Surg 1987;93:560-569.[Abstract]
5. Parr G.V., Waldhausen J.A., Bharati S., Lev M., Fripp R., Whitman V. Coarctation in Taussig-Bing malformation of the heart. Surgical significance. J Thorac Cardiovasc Surg 1983;86:280-287.[Abstract]
6. Comas J.V., Mignosa C., Cochrane A.D., Wilkinson J.L., Karl T.R. Taussig-Bing anomaly and arterial switch operation: aortic arch obstruction does not influence outcome. Eur J Cardiothorac Surg 1996;10:1114-1119.[Abstract]
7. Kawashima Y., Fujita T., Miyamoto T., Manabe H. Intraventricular re-routing of blood for the correction of Taussig-Bing malformation. J Thorac Cardiovasc Surg 1971;62:825-829.[Medline]
8. Wetter J., Belli E., Sinzobahamvya N., Blaschczok H.C., Brecher A.M., Urban A.E. 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]
9. Tchervenkov C.I., Korkola S.J., 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]
10. Perry G.J., Helmcke F., Nanda N.C., Byarad C., Soto B. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Coll Cardiol 1987;9:952-959.[Abstract]
11. Mavroudis C., Backer C.L., Muster A.J., Rocchini A.P., Rees A.H., Gevitz M. Taussig-Bing anomaly: arterial switch versus Kawashima intraventricular repair. Ann Thorac Surg 1996;61:1330-1338.[Abstract/Free Full Text]
12. Takeuchi K., McGowan F., Moran A., et al. Surgical outcome of double-outlet right ventricle with subpulmonary VSD. Ann Thorac Surg 2001;71:49-53.[Abstract/Free Full Text]
13. Daebritz S.H., Nollert G., Sachweg J.S., Engelhardt W., von Bernuth G., Messmer B. Anatomical risk factors for mortality and cardiac morbidity after arterial switch operation. Ann Thorac Surg 2000;69:1880-1886.[Abstract/Free Full Text]
14. Haas F., Wottke M., Poppert H., Meisner H. Long-term survival and functional follow-up in patients after arterial switch operation. Ann Thorac Surg 1999;68:1692-1697.[Abstract/Free Full Text]
15. Wernovsky G., Mayer J.E., Jonas R.A., et al. Factors influencing early and late outcome of the arterial switch operation for transposition of the great arteries. J Thorac Cardiovasc Surg 1995;109:289-302.[Abstract/Free Full Text]
16. Feinstein J.A., Housen T.J. Complete transposition of the great arteries. In: Moller J.H., ed. Perspectives in pediatric cardiology: surgery of congenital heart disease. Pediatric Cardiac Care Consortium 1984–1995, Vol 6. Armonk, NY: Futura Publishing Company, Inc, 1998:179-205.
17. Planché C., Serraf A., Comas J.V., Lacour-Gayet F., Bruniaux J., Touchot A. Anatomic repair of transposition of the great arteries with ventricular septal defect and aortic arch obstruction. J Thorac Cardiovasc Surg 1993;105:925-933.[Abstract]
18. Tchervenkov C.I., Tahta S.A., Cecere R., Beland M.J. Single-stage arterial switch with aortic arch enlargement for transposition complexes with aortic arch obstruction. Ann Thorac Surg 1997;64:1776-1781.[Abstract/Free Full Text]
19. Masuda M., Kado H., Shiokawa Y., et al. Clinical results of arterial switch operation for double-outlet right ventricle with subpulmonary VSD. Eur J Cardiothorac Surg 1999;15:283-288.[Abstract/Free Full Text]
20. Serraf A., Roux D., Lacour-Gayet F., et al. Reoperation after the arterial switch operation for transposition of the great arteries. J Thorac Cardiovasc Surg 1995;110:892-899.[Abstract/Free Full Text]
21. Nakanishi T., Momoi N., Satoh M., et al. Growth of the neopulmonary valve annulus after arterial switch operation in transposition of the great arteries. Circulation 1996;94(Suppl 9):II27-31.
22. Gandhi S.K., Pigula F.A., Siewers R.D. Successful reintervention after the arterial switch procedure. Ann Thorac Surg 2002;73:88-93.[Abstract/Free Full Text]
23. Akiba T., Neirotti R., Becker A.E. 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]
24. Gordillo L., Faye-Petersen O., de la Cruz M.V., Soto B. Coronary arterial patterns in double-outlet right ventricle. Am J Cardiol 1993;71:1108-1110.[Medline]
25. Jenkins K.J., Hanley F.L., Colan S.D., Mayer J.E., Castaneda A.R., Wernovsky G. Function of the anatomic pulmonary valve in the systemic circulation. Circulation 1991;84(Suppl III):173-179.

This article has been cited by other articles:

				Y. Hirata, J. M. Chen, J. M. Quaegebeur, and R. S. Mosca Should We Address the Neopulmonic Valve? Significance of Right-Sided Obstruction After Surgery for Transposition of the Great Arteries and Coarctation Ann. Thorac. Surg., October 1, 2008; 86(4): 1293 - 1298. [Abstract] [Full Text] [PDF]

				K. Agematsu, M. Aoki, Y. Naito, and T. Fujiwara Surgical Palliation for Taussig-Bing Anomaly with Multiple Lesions Asian Cardiovasc Thorac Ann, October 1, 2008; 16(5): 412 - 413. [Abstract] [Full Text] [PDF]

				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]

				N. Sinzobahamvya, H. C. Blaschczok, B. Asfour, C. Arenz, M. J. Jussli, E. Schindler, J. Photiadis, and A. E. Urban Right ventricular outflow tract obstruction after arterial switch operation for the Taussig-Bing heart Eur. J. Cardiothorac. Surg., May 1, 2007; 31(5): 873 - 878. [Abstract] [Full Text] [PDF]

				M. D. Rodefeld, M. Ruzmetov, P. Vijay, A. C. Fiore, M. W. Turrentine, and J. W. Brown Surgical Results of Arterial Switch Operation for Taussig-Bing Anomaly: Is Position of the Great Arteries a Risk Factor? Ann. Thorac. Surg., April 1, 2007; 83(4): 1451 - 1457. [Abstract] [Full Text] [PDF]

				M. Griselli, S. P. McGuirk, C.-S. Ko, A. J.B. Clarke, D. J. Barron, and W. J. Brawn Arterial switch operation in patients with Taussig-Bing anomaly -- influence of staged repair and coronary anatomy on outcome Eur. J. Cardiothorac. Surg., February 1, 2007; 31(2): 229 - 235. [Abstract] [Full Text] [PDF]

				M. Pocar, E. Villa, A. Degandt, P. Mauriat, P. Pouard, and P. R. Vouhe Long-Term Results After Primary One-Stage Repair of Transposition of the Great Arteries and Aortic Arch Obstruction J. Am. Coll. Cardiol., October 4, 2005; 46(7): 1331 - 1338. [Abstract] [Full Text] [PDF]

				T. P. Graham Jr The year in congenital heart disease J. Am. Coll. Cardiol., June 2, 2004; 43(11): 2132 - 2141. [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): Anne Marie Brecher Andreas E. Urban Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wetter, J. Articles by Urban, A. E. Search for Related Content PubMed PubMed Citation Articles by Wetter, J. Articles by Urban, A. E. Related Collections Congenital - cyanotic