Ann Thorac Surg 2005;80:1943-1945
© 2005 The Society of Thoracic Surgeons
How to do it
Pulmonary Root Translocation for Repair of Taussig-Bing Anomaly with Interrupted Arch
Hong Gook Lim, MD
a
,
Jeong Ryul Lee, MD
a
,
*
,
Eun Jung Bae, MD
b
,
Curie Ahn, MD
c
a Department of Thoracic and Cardiovascular Surgery, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul National University Hospital Clinical Research Center, Xenotransplantation Research Center, Seoul, South Korea
b Department of Pediatrics, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul National University Hospital Clinical Research Center, Xenotransplantation Research Center, Seoul, South Korea
c Department of Internal Medicine, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul National University Hospital Clinical Research Center, Xenotransplantation Research Center, Seoul, South Korea
Accepted for publication May 19, 2004.
* Address correspondence to Dr Lee, Department of Thoracic and Cardiovascular Surgery, Seoul National University Children's Hospital, Seoul National University College of Medicine, 28 Yongon-dong, Jongro-gu, Seoul 110744, South Korea (Email: jrl{at}plaza.snu.ac.kr).
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Abstract
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Anterior translocation of the pulmonary root was used as a new approach to the staged repair of Taussig-Bing anomaly with an interrupted aortic arch. It was performed to construct the right ventricle outflow tract with intraventricular baffling of the left ventricle to the aorta as the second stage operation after repair of the interrupted arch and pulmonary artery banding. This technique allows minimization of pulmonary regurgitation and has the major theoretical advantage for growth potential, which could diminish the need for reoperation.
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Introduction
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Surgical repair of the Taussig-Bing anomaly with interrupted aortic arch is required in the neonatal period in cases of marked cyanosis and congestive heart failure. However, the short distance between the tricuspid and pulmonic valves and the short ascending aorta after aortoplasty make the correction technically difficult. To overcome these problems and to assure pulmonary valve competency, we performed pulmonary root translocation to the right ventricle (RV). We present the successful staged biventricular repair of an infant who had the Taussig-Bing anomaly with an interrupted aortic arch.
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Technique
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A 19-day-old infant boy, weighing 3.6 kg, was referred to our hospital because of cyanosis and heart failure. Arterial blood gas analysis showed moderate acidosis and severe hypoxia. A grade 3/6 pansystolic murmur was heard over the entire chest. Cardiomegaly with a cardiothoracic ratio of 0.8 and central lung haziness due to pulmonary congestion were observed on the chest roentgenogram. His vital signs were 74/40-170-30-38.4°C, and his urine output was attenuated. An echocardiogram revealed Taussig-Bing anomaly, type A interrupted aortic arch, atrial septal defect and patent ductus arteriosus. The great arteries had a side-by-side relationship and a large size discrepancy. Coronary pattern was a single coronary artery arising anteriorly from the right coronary sinus, too far to be transferred to the pulmonary artery. A short ascending aorta and a bad coronary artery anatomy precluded Jatene's switch procedure. Subpulmonary conus was present, both ventricles had sufficient sizes and volumes, insertion of the tricuspid and mitral valve chord was not abnormal, and the distance between the tricuspid and pulmonic valves was less than the diameter of the aortic valve. He underwent extended end-to-side aortoplasty and pulmonary artery banding as a first-stage operation after a brief period of hemodynamic resuscitation. Hypoplasia of the transverse arch made end-to-end anastomosis impossible. The intraoperative transesophageal echocardiogram showed a slightly decreased ventricular function and no subaortic obstruction. He was transferred to the intensive care unit with the sternum open. Subsequently, he could not be weaned from ventilatory support until 5 weeks after the first palliation due to repeated episodes of cardiopulmonary failure. The second-stage complete repair was performed at 5 weeks postoperatively. The pulmonary artery root was dissected from the RV with great care, so as not to damage the pulmonary valve or coronary arteries. This hole was closed using bovine pericardium. A right ventriculotomy was performed anteriorly and the ventricular septal defect position was confirmed. Generous myocardial resection was done at the conal septum to unobstruct the left ventricle exit to the aorta. A Dacron (C. R. Bard, Haverhill, PA) patch and 5.0 polypropylene interrupted pedgetted sutures were used to close the ventricular septal defect, thus diverting the blood from the left ventricle to the aorta. Given the short distance between the tricuspid and pulmonary valves, we chose the suture line of the patch in a way as to surround both the aorta and the pulmonary artery to secure the patent left ventricular outflow tract. The pulmonary root was translocated to the anterior aspect of the RV preserving the native pulmonary valve. The floor of the pulmonary tract was constructed by anastomosis of the posterior edge of the distal section and the edge of the incision of the RV. The right ventricular outflow tract (RVOT) was completed by creating a hood formation with bovine pericardium across the anterior aspect of the anastomosis. Then the primary closure of the atrial septal defect was done (Fig 1). The cardiopulmonary bypass time was 219 minutes, and the aortic cross-clamp time was 87 minutes. Immediate postoperative RV to arterial blood pressure ratio was 45/75. The sternum was closed on postoperative day 2. The postoperative echocardiogram showed good ventricular contraction with small baffle leakage. He was weaned from the ventilator on postoperative day 15, and he was transferred to a general ward on postoperative day 21. Then he suffered Candida infective endocarditis. Intravenous amphotericin B was started and continued for 8 weeks. He was discharged on postoperative day 94 with no evidence of infection. His echocardiogram at 1 year after discharge showed good contractility of both ventricles, mild pulmonary stenosis of 25 mm Hg, and trivial pulmonary regurgitation. Further follow-up was needed.

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Fig 1. Schematic presentations showing pulmonary root translocation. (A) Pulmonary root dissected out and its origin closed with a bovine pericardial patch. (B) Pulmonary root sutured to the superior aspect of the right ventriculotomy preserving native pulmonary valve. (C) Right ventricular outflow tract completed by creating a hood formation with bovine pericardium across the anterior aspect of the anastomosis. (DP = Dacron patch; PH = pericardial hood; PP = pericardial patch; PT = pulmonary trunk; VSD = ventricular septal defect.)
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Comment
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Current corrective surgical approaches for the Taussig-Bing heart include arterial switch with ventricular septal defect closure and intraventricular repair, as described by Kawashima [1]. Nevertheless, the neonatal arterial switch operation demonstrates several morbidities such as neo-aortic regurgitation and residual RVOT obstruction [1]. The Kawashima intraventricular repair for side-by-side great arteries seems to be an attractive method, because it preserves the native aortic valve and avoids coronary dissection [2]. In this particular case, the remaining intact ascending aorta was too short for the arterial switch procedure, because the side wall of the proximal ascending aorta was used to repair the aortic interruption, and the short distance between the tricuspid and pulmonic valves precluded Kawashima repair. Moreover, the Rastelli approach is suboptimal, especially in children, because they are almost certain to outgrow their conduit and require conduit replacement [3]. In addition, valve function deteriorates in valved tissue conduits used in the pulmonary circulation, and the RV does not always tolerate chronic pulmonary regurgitation well [4]. Lecompte designed an operation in which a valveless pulmonary artery is brought directly to the RV by transection of the aorta [5]. He used an anterior monocusp patch to complete the RVOT reconstruction, which had potential problems such as pulmonary stenosis, pulmonary regurgitation, and RV dysfunction. Experience with the Ross procedure has shown that the pulmonary root can be excised and relocated without compromising valve integrity [6]. Given the success of this procedure, it is likely that the Taussig-Bing anomaly can be repaired by translocating the pulmonary root with similar efficacy. In our operation, by dissecting the pulmonary root out, we elongated the pulmonary artery trunk. This maneuver, associated with adequate dissection of the hilar pulmonary branches, allowed the pulmonary root to be implanted in the RVOT without tension. Therefore this technique obviates the need for the aortic transection necessary in Lecompte's procedure. Furthermore our technique renders no pulmonary regurgitation, which optimizes postoperative hemodynamics, theoretically providing a better outcome for the patient. There are reports on pulmonary root translocations [7, 8], but our technique differs from those because it was applied to repair the Taussig-Bing anomaly as a second-stage operation after aortoplasty and pulmonary artery banding. The translocation of this pulmonary root was performed because some expansion was noticed after dissection from its original position, and we anticipated some growth of this structure, which eventually could prevent conduit replacement reoperations. We believe that pulmonary root translocation is a preferable approach. The primary advantage of this technique is that the native tissue is used for RVOT reconstruction. Based on outcomes after pulmonary autograft aortic valve replacement [6], we believe that translocation of the native root will probably translate into growth potential and preserved valve function. These factors should contribute to minimizing the likelihood of reoperation related to RVOT obstruction or pulmonary regurgitation with RV dysfunction [3, 4].
In conclusion, pulmonary root translocation allows some growth of the pulmonary root, which may decrease or eliminate the need for reoperation and offers an alternative repair for the Taussig-Bing anomaly.
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References
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- Mavroudis C, Backer CL, Muster AJ, Rocchini AP, Rees AH, Gevitz M. Taussig-Bing anomalyarterial switch versus Kawashima intraventricular repair. Ann Thorac Surg 1996;61:1330-1338.[Abstract/Free Full Text]
- Serraf A, Lacour-Gayet F, Bruniaux J, et al. Anatomic repair of Taussig-Bing hearts Circulation 1991;84(Suppl III):200-205.
- Reddy VM, Rajasinghe HA, McElhinney DB, Hanley FL. Performance of right ventricle to pulmonary artery conduits after repair of truncus arteriosusa comparison of Dacron housed porcine valves and cryopreserved allografts. Semin Thorac Cardiovasc Surg 1995;7:133-138.[Medline]
- Ilbawi MN, Idriss FS, DeLeon SY, et al. Factors that exaggerate the deleterious effects of pulmonary insufficiency on the right ventricle after tetralogy repair J Thorac Cardiovasc Surg 1987;93:36-44.[Abstract]
- Lecompte Y, Neveux JY, Leca F, et al. Reconstruction of the pulmonary outflow tract without prosthetic conduit J Thorac Cardiovasc Surg 1982;84:727-733.[Abstract]
- Reddy VM, Rajasinghe HA, McElhinney DB, et al. Extending the limits of the Ross procedure Ann Thorac Surg 1995;60:S600-S603.
- McElhinney DB, Reddy MR, Hanley FL. Pulmonary root translocation for biventricular repair of double-outlet left ventricle with absent subpulmonic conus J Thorac Cardiovasc Surg 1997;114:501-503.[Free Full Text]
- da Silva JP, Baumgratz JF, da Fonseca L. Pulmonary root translocation in transposition of great arteries repair Ann Thorac Surg 2000;69:643-645.[Abstract/Free Full Text]