Surgical Results of Arterial Switch Operation for Taussig-Bing Anomaly

Mark D. Rodefeld, MD, Mark Ruzmetov, MD, PhD, Palaniswamy Vijay, PhD, MPH, Andrew C. Fiore, MD, Mark W. Turrentine, MD, and John W. Brown, MD Section of Cardiothoracic Surgery, James W. Riley Hospital for Children and Indiana University School of Medicine, Indianapolis, Indiana; and Section of Cardiothoracic Surgery, St. Louis University School of Medicine, St. Louis, Missouri

Background. A variety of definitive operations have been used to manage patients with double-outlet right ventricle and subpulmonary ventricular septal defect (Taussig-Bing anomaly). This study identifies the impact of the position of the great arteries and use of a staged surgical approach on the outcome after the arterial switch operation in children with Taussig-Bing anomaly. Methods. From 1986 through July 2005, 34 patients with Taussig-Bing anomaly underwent the arterial switch operation. The median age at operation was 21 days. Based on position of the great arteries, patients were divided into group I (side by side; n ⴝ 16) and group II (anteroposterior; n ⴝ 18). Aortic arch obstruction was present in 18 patients (53%), of whom 16 had prior repair with aortic arch reconstruction. Abnormal coronary artery patterns were present in 9 patients (27%). Results. There were 4 early deaths and 1 late death (3 from group I and 2 from group II). The actuarial survival rate was 85% at 15 years (81% in group I and 89%

in group II). Right ventricular outflow tract obstruction (mean gradient, 46.0 ⴞ 5.5 mm Hg) developed in 5 cases (2 from group I and 3 from group II). One patient underwent reoperation for residual aortic arch obstruction. Freedom from reoperation was 80% at 15 years, and thereafter 85% in group I and 75% in group II. Statistical analysis of potential risk factors revealed no significant identifiers for death or need for reoperation between groups. Conclusions. The arterial switch operation remains our preferred choice of treatment for children with TaussigBing anomaly. The position of the great arteries has no effect on postoperative morbidity and mortality. In the presence of aortic arch obstruction, staged arch reconstruction followed soon thereafter by early intracardiac repair has yielded excellent outcomes in our experience.

I

morphologic left ventricle to the aorta (or neoaorta) and the morphologic right ventricle to the pulmonary artery (or neopulmonary artery). The options for anatomic repair are determined by great artery orientation, internal cardiac morphology [3], and associated lesions, which include aortic coarctation, small ascending aorta relative to the pulmonary artery, multiple VSDs, straddling mitral valve, and tricuspid septal leaflet attachment to the interventricular septum. The evolution of surgical repair for the Taussig-Bing DORV has progressed from atrial baffle operations with intraventricular partition [4], Damus-Kaye-Stansel procedure [5, 6], and Rastelli-type intracardiac baffle and right ventricle-pulmonary artery conduit repair [4, 7, 8] to the arterial switch operation (ASO) with VSD closure [9 –12] and intraventricular repair [10, 13, 14]. In addition, Fontan-type procedures may be proposed as a solution for even more complex forms. Of the intraventricular repairs, one (Patrick-McGoon operation) has been used for anteroposterior great artery anatomy by tunneling left ventricular flow anterior to the pulmonary valve, whereas the other (Kawashima operation) is used for side-by-side great artery anatomy by

n 1949, Taussig and Bing [1] reported on a morphologic syndrome consisting of transposed aorta, subpulmonary ventricular septal defect (VSD), and levoposition of the pulmonary artery. They emphasized that overriding of the pulmonary artery was an integral part of the malformation. Lev and associates [2] coined the term “Taussig-Bing heart” in 1950 and subsequently introduced the concept of a spectrum of Taussig-Bing hearts depending on the degree of pulmonary artery override (right-sided, intermediate, and left-sided). Despite this controversy, most authors of surgical reviews describe the Taussig-Bing heart as double-outlet right ventricle (DORV), subpulmonary VSD, and subarterial conus, perhaps more because of established usage rather than an endorsement of one interpretation over the other. Whatever the definition, the goal of therapy is anatomic correction whereby the resultant repair connects the Accepted for publication Oct 27, 2006. Presented at the Poster Session of the Fifty-second Annual Meeting of the Southern Thoracic Surgical Association, Orlando, FL, Nov 10 –12, 2005. Address correspondence to Dr Rodefeld, Section of Cardiothoracic Surgery, Indiana University School of Medicine, 545 Barnhill Dr, EH 215, Indianapolis, IN 46202-5123; e-mail: [email protected].

© 2007 by The Society of Thoracic Surgeons Published by Elsevier Inc

(Ann Thorac Surg 2007;83:1451–7) © 2007 by The Society of Thoracic Surgeons

0003-4975/07/$32.00 doi:10.1016/j.athoracsur.2006.10.072

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Surgical Results of Arterial Switch Operation for Taussig-Bing Anomaly: Is Position of the Great Arteries a Risk Factor?

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RODEFELD ET AL SURGICAL RESULTS OF TAUSSIG-BING ANOMALY

Ann Thorac Surg 2007;83:1451–7

Table 1. Associated Cardiac Anomalies Anomaly CARDIOVASCULAR

Intracardiac Secundum atrial septal defect Multiple ventricular septal defects Bicuspid aortic valve Subaortic stenosis Extracardiac Coarctation of aorta Interrupted aortic arch Hypoplastic aortic arch

Number of Patients

Percent

30 2 1 1

88 6 3 3

14 4 1

41 12 3

tunneling left ventricular flow posterior to the pulmonary valve [13, 15]. Because of intraventricular geometric factors that can lead to tunnel stenosis, the Patrick-McGoon operation has been largely replaced by the ASO. The Kawashima intraventricular repair is still favored by some surgeons for patients with side-by-side orientation of the great arteries [13, 15]. Since 1986, we have performed ASO to manage all patients presenting with Taussig-Bing anomaly (side-byside or anteroposterior great artery relationships). In the presence of aortic arch obstruction, we have utilized an early staged approach to repair these patients. The purpose of this retrospective study is to identify the impact of anatomic relationship of the great arteries and use of an early staged approach on outcomes after ASO in children with Taussig-Bing anomaly.

Material and Methods Study Patients Between January 1986 and July 2005, 34 infants and children underwent ASO surgical repair of Taussig-Bing DORV at James W. Riley Hospital for Children at Indiana University School of Medicine. After obtaining approval from our Institutional Review Boards and waiving the need to obtain patient consent for this study, a retrospective review of medical records was performed with regard to initial clinical features, pathophysiologic findings, surgical treatment, and hospital mortality. Data from outpatient visits and from patients who died after hospital discharge were obtained from physician records, hospital records, or death certificates. Taussig-Bing anomaly is defined as an anomalous ventriculoarterial connection with VSD and DORV. The VSD is subpulmonary in location and the outlet septum is malaligned. In addition, tricuspid-aorta discontinuities are present. The aorta may be positioned rightward and anterior (D-transposition) or alongside the pulmonary trunk (side-by-side orientation). The assigned anatomic diagnosis was based on a combination of twodimensional echocardiographic and angiographic evidence (by cardiologists) and surgical inspection (by surgeons). Based on position of the great arteries, patients were divided into group I (side-by-side; n ⫽ 16) and group II (anteroposterior; n ⫽ 18).

There were 20 boys (59%) and 14 girls (41%). The mean age at the time of surgery was 10.5 ⫾ 34.5 months, with a range of 3 days to 16 years (median age, 21 days). Twenty-six patients (77%) were neonates (n ⫽ 21) or infants younger than 3 months (n ⫽ 5). Associated anatomic lesions are listed in Table 1. Aortic arch obstruction, manifested as aortic coarctation (n ⫽ 14) or interrupted aortic arch (n ⫽ 4), was common (18 of 34 patients; 53%). Two patients had an additional muscular VSD. Prior palliative and concomitant cardiovascular operations are shown in Table 2. Twenty-two patients (65%) underwent previous palliative procedures. All patients (except 1 with coarctation and 1 with interruption of the aorta) with a coarctation of the aorta and with an interrupted aortic arch underwent early two-stage repair. All patients had favorably facing aortic and pulmonary artery sinuses of Valsalva for coronary artery transfer regardless of great artery relationship. The coronary artery anatomy was sinus I (left anterior descending, circumflex) – sinus II (right coronary artery) in 25 (type A, according to Yacoub and Radley-Smith [16]); sinus I (right, left anterior descending, and circumflex) in 2 (type B); sinus I (left anterior descending) – sinus II (circumflex, right coronary artery) in 5 (type D); and sinus I (right, left anterior descending) – sinus II (circumflex) in 2 (type E).

Operative Technique In the presence of associated aortic arch obstruction, we have approached the majority of these patients with a closely staged combined operative approach. If aortic

Table 2. Previous and Concomitant Cardiovascular Operation Procedure Previous PAB PAB with atrial septostomy IAA repair with atrial septostomy Atrial septostomy CoA repair with PDA ligation CoA repair with PDA ligation and PAB IAA repair with PAB and atrial septostomy Total Concomitant ASD closure ASD closure with PDA ligation ASD and additional VSD closure CoA repair with ASD closure and PDA ligation IAA repair with ASD closure and PDA ligation Subaortic resection Lecompte maneuver

Group I (n ⫽ 16)

Group II (n ⫽ 18)

1 1 1 1 4 2

1 1 1 2 6 0

0

1

10

12

9 3 1 1

11 4 1 0

1

0

1 15

0 18

ASD ⫽ atrial septal defect; CoA ⫽ coarctation of the aorta; interrupted aortic arch; PAB ⫽ pulmonary artery banding; pattern ductus arteriosus; VSD ⫽ ventricular septal defect.

IAA ⫽ PDA ⫽

arch obstruction is present, we have performed early arch repair through thoracotomy, followed closely (1 to 3 weeks) by intracardiac repair through median sternotomy. This has the advantage of simplifying the overall repair at each procedure, yet does not preclude ASO within the neonatal time period. The surgical technique for ASO is well outlined in several previous reports. We perform the ASO using continuous full-flow bypass at 20°C. Myocardial protection is accomplished with intermittent dose of cold 4:1 blood: crystalloid cardioplegia administered every 20 to 30 minutes at 10 to 15 cc/kg. Cardioplegia is given into the aortic root before the aorta is opened and directly into the coronaries while the neoaorta is reconstructed and coronary transfer is being accomplished. The neoaorta and coronary anastomoses are carried out with 7-0 absorbable monofilament sutures in running fashion. Once the neoaortic anastomosis has been completed, the aortic cross-clamp is released, allowing the aortic root to distend. The coronary artery buttons are excised from their respective sinuses taking most of sinus tissue. The coronary buttons were mobilized for a distance of 4 to 6 mm and allowed to rotate to the location on the distended neoaortic root where they will reside without torsion or tension. The ideal location on the neoaortic root is marked with a fine suture. A stab wound is made at the mark, taking care not to injure the previously marked anterior neoaortic commissure. The aortic cross-clamp is reapplied while a 2.5-mm aortic punch is used to create a site for coronary implantation. The location of the neoaortic commissure is confirmed, and the opening is enlarged if necessary to accommodate the coronary buttons. Selecting the ideal location for the coronary buttons on the closed and distended neoaortic root has greatly reduced the incidence of left ventricular dysfunction that was observed early (1985 to 1989) in our experience, and subsequently dramatically improved our mortality risk. During this phase, the coronary buttons were reimplanted as the neoaortic anastomosis was completed. The change in coronary implantation technique has eliminated our need to reposition the coronary buttons once implanted. Once coronary artery button transfer is complete, the aortic cross-clamp is removed, and the patient is rewarmed while the neopulmonary valve is reconstructed with a generous pantaloon-shaped patch of fresh autologous pericardium 2.5 to 3.5 times larger than the combined area of the transferred coronary buttons. Using a large pericardial patch to reconstruct the neopulmonary root has greatly reduced our incidence of late supravalvar pulmonary artery stenosis. In 18 patients (14 coarctation and 4 interrupted aortic arch), the surgical procedures included prior (n ⫽ 16) or concomitant (n ⫽ 2) aortic arch repair: in 8, subclavian flap type of coarctation repair; in 7, direct anastomosis between the ascending and descending aortic segments; in 2 patients (with interrupted aortic arch), the left common carotid artery was divided, spatulated appropriately and anastomosed as a reverse flap to the descending thoracic aorta; and in 1 patient, synthetic patch


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aortoplasty of a primary anastomosis. After aortic reconstruction, the pulmonary artery was banded (n ⫽ 13) to reduce the distal pulmonary artery pressure to 50% or less of systemic pressure. The VSD was closed through the right atrium in 7 patients and through the pulmonary artery (neoaorta) in 27 patients. Our approach the Taussig-Bing VSD is from the left side of patient. After dividing the aorta and pulmonary artery for the switch approach, the VSD is closed by starting the patch with a running 6-0 polypropylene sutute on the right inferior aspect of the VSD and running the suture line from right to left, sewing away from the crest of the septum and away from the conduction tissue. The surgeon then carries the suture line anterior and superior to the base of the neoaortic valve. The Lecompte maneuver was performed in all but 1 patient. No tension was noted on the left pulmonary artery in this subset of patients. One had restrictive VSD that was enlarged anteriorly. One patient with subaortic stenosis underwent resection of a hypertrophic infundibular septum during repair.

Statistical Analysis Variables including demographics, previous palliative procedures, morphology, coronary artery pattern, and operative procedure related variables were assessed by means of univariate analysis utilizing ␹2 test and multivariate logistic regression analysis. In the analysis of risk factors for early death, variables with significance levels of 0.1 in univariate analysis were admitted to a multivariate logistic regression model. Factors with p values of less than 0.05 were considered significantly related to early death. Kaplan-Meier analysis was used for the actuarial survival rates and freedom from reoperation rate. Differences in survival curves were assessed by log-rank test. All analyses were performed with standard commercially available statistical software (SPSS, Chicago, Illinois). Early mortality was defined as death during initial hospitalization or within 30 days of operation. Any deaths later than that were defined as late mortality. In this series, all early deaths occurred during the initial hospitalization and all late deaths occurred after discharge from the initial hospitalization.

Results Early and Late Mortality There were 4 early deaths (3 from group I and 1 from group II (12%, 4 of 34). One of them had a single coronary artery (type B), 1 had type E coronary artery anatomy and multiple VSDs, and 1 had interrupted aortic arch. The first patient (from group II) died early in the series owing to myocardial ischemia related to coronary insufficiency. The other child, who had anteroposterior relation of great vessels and redundant atrioventricular valve tissue, died of multisystem organ failure. This patient could not be weaned from cardiopulmonary bypass and was placed on extracorporeal membrane oxygenation (ECMO) support for 23 days. The third death occurred in a 4-week-old

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patient who previously underwent repair of interrupted aortic arch. This patient had side-by-side orientation of the great vessels and type B coronary arterial pattern. An ASO was performed, and this patient died 6 hours later. Postmortem examination revealed a recent infarct of the entire left ventricle due to left coronary ostial stenosis. The fourth death was of a patient from group I who underwent ASO but during the postoperative period suffered a cardiac arrest with cardiopulmonary resuscitation and then continuing ECMO support. Sixteen days later, orthotopic cardiac transplantation was performed. The immediate postoperative course was complicated by development of refractory hypoxemia with persistent acidosis and pulmonary hypertension, and this patient subsequently died. There was 1 late death in group II at a mean follow-up of 5.1 ⫾ 3.8 years (range, 6 months to 16 years). This patient had undergone ASO repair at 21 days of age. This death occurred 1 year after initial repair and was due to viral pneumonia. Overall survival including operative mortality according to Kaplan-Meier analysis was 85% at 1, 5, and 15 years. Figure 1 shows the actuarial survival, including operative mortality, which was 81% and 89% at 15 years in patients in group I and group II, respectively. Statistical analysis did not reveal any significant risk factors for early, late, or overall mortality between both groups.

Reoperations Reoperation was necessary in 6 survivors without operative mortality (6 of 30; 20%). All patients were successfully reoperated at a mean interval of 2.0 ⫾ 1.7 years after primary repair. Right ventricular outflow tract obstruction (mean gradient, 46.0 ⫾ 5.5 mm Hg) developed in 5 patients (2 from group I and 3 from group II). Two patients underwent right ventricular outflow tract (RVOT) obstruction reconstruction for pulmonary stenosis with Gore-Tex (W.L. Gore & Assoc, Flagstaff, Arizona) patch arterioplasty, and 1 patient required residual VSD closure in addition to Gore-Tex patch arterioplasty. Two had late pulmonary artery stenosis; both had side-byside great vessel orientation. The stenoses were located

Fig 1. Kaplan-Meier estimated 15-year survival, including hospital mortality. (Diamonds ⫽ overall; squares ⫽ group I; triangles ⫽ group II.)


Fig 2. Kaplan-Meier estimated 15-year freedom from reoperation. (Diamonds ⫽ overall; squares ⫽ group I; triangles ⫽ group II.)

distally at the branch level, and reconstruction of the RVOT was performed with Gore-Tex patch with resection of an RVOT muscle bundle. One patient (from group II) underwent revision of coarctation repair owing to aortic arch obstruction. Overall freedom from reoperation was 93% at 1 year, 80% at 5 and 75% at 15 years (Fig 2) and thereafter 85% in group I and 75% in group II. Statistical analysis of contributing factors revealed no significant risk factors for need for reoperation between groups. The incidence of significant RVOT obstruction was not influenced by the presence of aortic arch obstruction for side-by-side (p ⫽ 0.68) or anteroposterior great arteries (p ⫽ 1.00), the side-by-side relationship of the great arteries (p ⫽ 0.92), the anteroposterior relationship of the great arteries (p ⫽ 0.71), or by the right coronary artery crossing the infundibulum for side-by-side (p ⫽ 0.84) or anteroposterior great arteries (p ⫽ 0.86). The difference between neonatal repair versus older repair was significant in patients with aortic arch obstruction (p ⬍ 0.001), but was not significant between single-stage versus staged repair (p ⫽ 0.88).

Follow-Up and Functional Status of Survivors Mean follow-up was 5.1 ⫾ 3.8 years (range, 6 months to 16 years). Follow-up included sequential noninvasive evaluations: two-dimensional echocardiography, Doppler study, electrocardiography, and radiographic studies. Twenty-six patients have had postoperative echocardiography only, and 3 patients have had both postoperative echocardiography and cardiac catheterization. All 29 survivors are in New York Heart Association functional class I, without medication and are in normal sinus rhythm. At last follow-up, Holter examination performed in 2 patients did not reveal major abnormalities, and Doppler studies showed no subaortic obstruction in 28 and a mild subaortic obstruction (gradient at rest less than 30 mm Hg) in 1 patient. Neoaortic incompetence was moderate in 3 (10%; 3 of 29), and trivial or mild in 26 patients (90%; 26 of 29). Right ventricular outflow tract obstruction (echocardiographic gradient more than 30 mm Hg) was present only in 2 patients (7%). There is no significant difference in neoaortic or neopulmonary obstruction and incompetence between groups.



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Table 3. Arterial Switch Operation With Ventricular Septal Defect Closure for Taussig-Bing Anomaly Patients (Literature Review) Great Artery Anatomy First Author

Year

No. of Patients

A/P

S/S

Reoperation

Early

Late

Serraf [7] Mavroudis [10] Comas [9] Masuda [25] Takeuchi [11] Wetter [12] Rodefeld (current)

1991 1996 1996 1999 2001 2004 2005

20 16 28 27 20 27 41

11 10 16 15 17 12 21

9 6 12 12 3 15 20

5 8 4 7 3 4 9

1 1 2 1 4 1 5

1 3 1 3 0 1 1

A/P ⫽ anteroposterior;

S/S ⫽ side-by-side.

Comment

aortic conus, with hypertrophied muscle in the RV possibly necessitating resection of the aortic conal septum and a significant suture load to stably affix the patch in the RV. Snoddy and associates [18] have reported that tunnel repair of the VSD in the small RV may result in RVOT obstruction. In this situation, a valved external conduit from the RV to the pulmonary artery may provide good hemodynamic results. Recently, Binet and colleagues [19] reported treating physiologically complete transposition of the great arteries by closing the VSD and repairing the transposition by means of the Damus-Kaye-Stansel technique. The long-term outcome of this approach is limited, however, by the suboptimal durability of valved external conduits. Reoperation will eventually be necessary due to structural deterioration of biological valved conduits in children [20]. The ASO, which was introduced as a corrective technique for simple transposition of the great arteries, has become the procedure of choice for patients with all forms of D-transposition including those with TaussigBing DORV. At our institution, ASO is currently the most commonly used technique for two-ventricle repair of Taussig-Bing DORV. The ASO is always feasible; however, intraventricular repair seems more attractive as it preserves the native aortic valve and avoids coronary dissection. That has led Yacoub and Radley-Smith [21] to propose a classification according to the extracardiac anatomy: when great arteries are side by side, an intraventricular repair may be performed; when the great arteries relation is more or less anteroposterior, arterial switch may be performed.

The ASO has become our procedure of choice for the Taussig-Bing DORV and all other types of D-transposition of the great arteries. Some authors suggest that the Kawashima intraventricular repair is preferable for Taussig-Bing patients when the great vessels are side by side. Our experience with the Kawashima operation is limited. Our results indicate that there was no difference in Taussig-Bing patient outcome based on great vessel orientation. A literature survey showing the results of the ASO versus the intraventricular repair for Taussig-Bing repair is shown in Tables 3 and 4. Because individual patient factors must be taken into consideration to determine the best overall surgical approach, the decision as to which patients are selected for ASO versus intraventricular procedure can be difficult. Intraventricular repair was first performed in 1968 by Patrick and McGoon [14], and Williams [17] first reported the ASO for Taussig-Bing in 1981. Serraf and colleagues [7] reported 20 patients undergoing ASO and 7 patients having intraventricular repair. Kawashima and colleagues [13] reported 10 patients having intraventricular repair and 13 having ASO. Mavroudis and coworkers [10] reported 16 patients undergoing ASO and 4 having intraventricular repair. In aggregate, ASO with VSD closure appears to be the more frequently applied method of repair. Intraventricular diversion of left ventricular blood flow to the aorta may provide a physiologic repair; however, this operation is technically difficult to perform. It involves the insertion of a patch through the VSD to the

Table 4. Kawashima Intraventricular Repair for Taussig-Bing Anomaly Patients (Literature Review) Great Artery Anatomy

Death

First Author

Year

No. of Patients

A/P

S/S

Reoperation

Early

Late

Serraf [7] Kawashima [13] Mavroudis [10]

1991 1993 1996

7 10 4

1 1 0

6 9 4

2 1 2

1 0 0

1 0 0

A/P ⫽ anteroposterior;

S/S ⫽ side-by-side.

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Death

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These conclusions were then discussed by Sakata and Lecompte [3], who could not define any strict relation between the intervalvular distances and the relation of the great arteries. Van Praagh [22] commented that the surgical significance is that when the great arteries are anteroposterior, the aortic valve is very anterior and the VSD-to-aorta conduit (for Rastelli-type conduit repair or intraventricular repair) would have to run anteriorly and would cause iatrogenic pulmonary stenosis. With sideby-side great arteries, the conduit can pass posteriorly and allow unimpeded flow to the pulmonary valve. Based on this previous work, we have developed our guidelines for surgical decision making. Our approach is to first consider the relationship of the great arteries: if anteroposterior, an arterial switch is performed with closure of the VSD. If side-by-side orientation of the great vessels is present, then the tricuspid-pulmonary valve distance is evaluated; if less than aortic valve diameter or if there are abnormal tricuspid valve chordae present, ASO and VSD closure are performed; if this distance is greater, pulmonary artery banding is performed before 1 year of age to permit growth, and then a Rastelli-type intraventricular conduit repair is subsequently performed beyond 1 year of age. The coronary distribution in Taussig-Bing DORV is often quite different than that in transposition of the great arteries and may be a source of technical difficulties in ASO. In patients in the ASO group, coronary patterns were normal (Yacoub type A) when the great vessels were in an anteroposterior relationship. But when the great vessel orientation is side by side, almost exclusively, other types of coronary artery distribution are encountered (Yacoub type B, D or E). In a detailed pathologic study, Uemura and associates [23] found that a single coronary artery (type B) was present in 27% of hearts with a side-by-side great artery relationship. Associated aortic arch anomalies are frequently observed in Taussig-Bing DORV [7, 10, 23, 24]. Repair of the aortic arch obstruction in a one- or two-stage procedure remains controversial, although the one-stage procedure has recently become increasingly popular [9, 10]. However, analysis of the overall mortality of patients with associated aortic arch anomalies in this series in which a closely sequenced two-stage repair was utilized, the existence of aortic arch anomalies was not an incremental risk factor, provided that an adequate aortic arch repair was achieved. If aortic arch reconstruction is complicated by an inadequate luminal diameter and pulmonary artery banding is performed, biventricular outflow tract obstruction will result. Finally, as we have performed in several patients in the latter part of our series, a onestage repair, including aortic arch reconstruction, ASO, and closure of the VSD can certainly be successfully performed in selected patients. A one-stage approach has the advantage of avoiding multiple operations, the development of pulmonary vascular disease, and may be performed in a neonate with suitable ventricular function. However, the optimal strategy utilized depends upon an overall assessment of the patients’ intracardiac


anatomy and severity of associated extracardiac anomalies. Patients with Taussig-Bing DORV face a higher risk of neoaortic incompetence from a mismatch of the large pulmonary artery and a small aorta. Minor neoaortic regurgitation is common after ASO, with reported rates ranging from 5% to 55% [24]. It has been speculated that resection of tissue of the neononcoronary sinus may lead to dilatation of the sinus of Valsalva and adjacent leaflet prolapse, which in turn leads to neoaortic insufficiency [7]. Moreover, the increased preoperative flow across the anatomic pulmonary valve may result in dilatation of the pulmonary valve annulus and postoperative neoaortic insufficiency, or reimplantation of the abnormal coronary arteries into the neoaorta may distort the architecture of the valve. Because the degree of neoaortic regurgitation present in most of our patients was hemodynamically insignificant, further follow-up will be required to determine whether trivial or mild regurgitation will eventually become clinically relevant. We conclude that Taussig-Bing DORV can be repaired by ASO and VSD closure in neonates and young infants with an excellent outcome. Staged correction of associated cardiac anomalies (especially aortic arch obstruction) closely followed by early intracardiac repair (1 to 3 weeks) had no detrimental influence on survival and later outcome. Therefore, we prefer to perform a twostage complete repair with each stage closely timed in the neonatal period. The position of the great arteries has no effect on postoperative morbidity and mortality. Right ventricular outflow tract obstruction often is the most commonly observed late complication and is a leading cause for reintervention. To determine secondary effects of neoaortic regurgitation and their clinical relevance, continued follow-up is mandatory after ASO repair of Taussig-Bing DORV.

References 1. Taussig HB, Bing RJ. Complete transposition of the aorta and levoposition of the pulmonary artery. Clinical, physiological, and pathological findings. Am Heart J 1949;37:551–9. 2. Lev M, Volk BM. The pathologic anatomy of the TaussigBing heart: riding pulmonary artery. Report of case. Bull Int Assoc Med Museums 1950;31:54 – 64. 3. Sakata R, Lecompte Y, Batisse A, Borromee L, Durandy Y. Anatomical repair of anomalies of ventriculoarterial connection associated with ventricular septal defect. I. Criteria of surgical decision. J Thorac Cardiovasc Surg 1986;92:913–30. 4. Pacifico AD, Kirklin JK, Colvin EV, Bargeron LM. Intraventricular tunnel repair for Taussig-Bing heart and related cardiac anomalies. Circulation 1986;74(Suppl 1):53– 60. 5. DeLeon SY, Ilbawi MN, Tubeszewski K, Wilson WR, Idriss FS. The Damus-Stansel-Kaye procedure: anatomical determinants and modifications. Ann Thorac Surg 1991;52:680 –7. 6. Lui RC, Williams WG, Trusler GA, et al. Experience with the Damus-Kaye-Stansel procedure for children with TaussigBing heart or univentricular hearts with subaortic stenosis. Circulation 1993;88:170 – 6. 7. Serraf A, Lacour-Gayet F, Bruniaux J, et al. Anatomic repair of Taussig-Bing hearts. Circulation 1991;84(Suppl 3):200 –5. 8. Kawashima Y, Matsuda H, Taniguchi K, Kobayashi J. Additional aortopulmonary anastomosis for subaortic obstruction in

9.

10.

11. 12. 13. 14. 15.

16.

the Rastelli-type repair for the Taussig-Bing malformation. Ann Thorac Surg 1987;44:662– 4. Comas JV, Mignosa C, Cochrane AD, Wilkinson JL, Karl TR. Taussig-Bing anomaly and arterial switch: aortic arch obstruction does not influence outcome. Eur J Cardiothorac Surg 1996;10:1114 –9. Mavroudis C, Backer CL, Muster AJ, Rocchini AP, Rees AH, Gevitz M. Taussig-Bing anomaly: arterial switch versus Kawashima intraventricular repair. Ann Thorac Surg 1996; 61:1330 – 8. Takeuchi K, McGowan FX, Moran AM, et al. Surgical outcome of double-outlet right ventricle with subpulmonary VSD. Ann Thorac Surg 2001;71:49 –53. Wetter J, Sinzobahamvya N, Blaschczok HC, et al. Results of arterial switch operation for primary total correction of the Taussig-Bing anomaly. Ann Thorac Surg 2004;77:41–7. Kawashima Y, Matsuda H, Yagihara T, et al. Intraventricular repair for Taussig-Bing anomaly. J Thoracic Cardiovasc Surg 1993;105:591–7. Patrick DL, McGoon DC. An operation for double-outlet right ventricle with transposition of the great arteries. J Cardiovasc Surg 1968;9:537– 42. Kawahira Y, Yagihara T, Uemura H, et al. Ventricular outflow tracts after Kawashima intraventricular rerouting for double outlet right ventricle with subpulmonary ventricular septal defect. Eur J Cardiothorac Surg 1999;16:26 –31. Yacoub MH, Radley-Smith R. Anatomy of the coronary arteries in transposition of the great arteries and methods for their transfer in anatomical correction. Thorax 1978;33:418 –24.


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17. Williams WG, Freedom RM, Culhan JAG, et al. Early experience with arterial repair of transposition. Ann Thorac Surg 1981;32:8 –15. 18. Snoddy JW, Parr EL, Robertson LW, Mauck HP, McCue CM, Lower RR. Successful intracardiac repair of the Taussig-Bing malformation in 2 children. Ann Thorac Surg 1978;25:158 – 63. 19. Binet JP, Lacour-Gayet F, Conso JF, Dupuis C, Bruniaux J. Complete repair of the Taussig-Bing type of double-outlet right ventricle using the arterial switch operation without coronary translocation. J Thorac Cardiovasc Surg 1983;85: 272–5. 20. Kanter K, Anderson R, Lincoln C, Firmin R, Rigby M. Anatomic correction of double-outlet right ventricle with subpulmonary ventricular septal defect (the “Taussig-Bing” anomaly). Ann Thorac Surg 1986;41:287–92. 21. Yacoub MH, Radley-Smith R. Anatomic correction of the Taussig-Bing anomaly. J Thorac Cardiovasc Surg 1984;88: 380 – 8. 22. Van Praagh R. What is the Taussig-Bing malformation? Circulation 1968;38:445–9. 23. Uemura H, Yagihara T, Kawashima Y, et al. Coronary arterial anatomy in double-outlet right ventricle with subpulmonary VSD. Ann Thorac Surg 1995;59:591–7. 24. Masuda M, Kado H, Shiokawa Y, et al. Clinical results of arterial swith operation for double-outlet right ventricle with subpulmonary VSD. Eur J Cardiothorac Surg 1999; 15:283– 8.

The Society of Thoracic Surgeons: Forty-Fourth Annual Meeting Please mark your calendars for the Forty-Fourth Annual Meeting of The Society of Thoracic Surgeons, to be held in Fort Lauderdale, Florida, from January 28 –30, 2008. The program will provide in-depth coverage of surgical topics selected to enhance and broaden the knowledge of cardiothoracic surgeons. Attendees will benefit from traditional Abstract Presentations, as well as Surgical Forums, Breakfast Sessions, and Surgical Motion Pictures. Parallel sessions will focus on specific subspecialty interests. Advance registration forms, hotel reservation forms, and details regarding transportation arrangements, as well as the complete meeting program, will be mailed to Society members this fall. Also, complete meeting information will be available on the Society’s Web site

© 2007 by The Society of Thoracic Surgeons Published by Elsevier Inc

at www.sts.org. Nonmembers who wish to receive information on the Annual Meeting may contact the Society’s secretary, Douglas E. Wood. Douglas E. Wood, MD Secretary The Society of Thoracic Surgeons 633 N. Saint Clair St, Suite 2320 Chicago, IL 60611-3658 Telephone: (312) 202-5800 Fax: (312) 202-5801 e-mail: [email protected] website: www.sts.org

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0003-4975/07/$32.00

CARDIOVASCULAR
