Asian Cardiovasc Thorac Ann 2007;15:367-370
© 2007 Asia Publishing EXchange Ltd
Left Ventricular Outflow Tract after Kawashima Intraventricular Rerouting
Shigemitsu Iwai, MD,
Hajime Ichikawa, MD,
Norihide Fukushima, MD,
Yoshiki Sawa, MD
Division of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan
For reprint information contact: Shigemitsu Iwai, MD, Tel: 81 72 556 1220, Fax: 81 72 556 5682, Email: iwai{at}mch.pref.osaka.jp, Department of Cardiovascular Surgery, Osaka Medical Center and Research Institute for Maternal and Child Health, 840 Murodo-cho, Izumi, Osaka 594-1101, Japan.
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ABSTRACT
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Left ventricular outflow tract obstruction is a concern in the long term after Kawashima intraventricular rerouting for Taussig-Bing anomaly. This study assessed the late results and left ventricular outflow tract dimensions after intraventricular rerouting for Taussig-Bing anomaly in 6 children. Age at operation ranged from 8 months to 7 years. The shortest distance from the tricuspid valve to the pulmonary valve ranged from 8 to 18 mm, which was 79%–139% of the normal aortic annulus diameter. All patients survived the operation, but one died of chronic heart failure 4 months after repair. Three patients had no left ventricular outflow tract obstruction 15 to 31 years after repair, and 2 had significant obstruction at 9 and 14 years. One patient underwent successful revision of the intraventricular baffle; the distance between the tricuspid and pulmonary valves was 16 mm (108% of the normal aortic annulus) although it had been 8 mm (79%) at the initial repair. Late results of intraventricular rerouting were considered favorable.
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INTRODUCTION
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Current surgical approaches for Taussig-Bing anomaly include the arterial switch operation with ventricular septal defect (VSD) closure, and Kawashima intraventricular rerouting.1 Intraventricular repair is an attractive surgical option, particularly in patients with adequate distance between the tricuspid valve and the pulmonary valve. However, either the subaortic or the subpulmonary channel can become obstructed after this procedure because the outlet portion of the morphological right ventricle is divided into 2: one for the left ventricular outflow tract (LVOT) through the VSD, and the other for the right ventricular outflow tract. We reviewed our experience with intraventricular rerouting for Taussig-Bing anomaly and analyzed the long-term results with regard to LVOT obstruction.
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PATIENTS AND METHODS
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Since 1969, we have carried out Kawashima intraventricular rerouting for Taussig-Bing anomaly in 6 children. Age at operation ranged from 8 months to 7 years, with a mean of 35 months. The great arteries were side by side in 4 patients, and they had an oblique relationship in 2. Associated malformations were coarctation of the aorta in 2 patients, mild pulmonary stenosis in 2, and an additional muscular VSD in 1. The aortic arch had been reconstructed previously with a subclavian flap in 1 patient, and the pulmonary artery had been banded in 4 (Table 1
).
Intracardiac maneuvers were carried out via a right ventriculotomy under cardiopulmonary bypass and induced cardiac arrest. Intracardiac morphology was confirmed, paying particular attention to the narrowest distance from the tricuspid ring or chordae to the pulmonary valve ring (T-P distance). Subaortic musculature was resected, as appropriate, without injury to the aortic valve or tension apparatus of the tricuspid valve. An oval-shaped internal conduit was fashioned from prosthetic material. The predicted LVOT diameter, calculated as (T-P distance + patch width – 8)/
mm, was standardized to the normal aortic valve ring size: 16.6 x (body surface area)0.6. The previously banded pulmonary trunk in 4 patients was debanded. The right ventricular outflow tract was enlarged using a prosthetic patch. Postoperative cardiac catheterization was carried out at 6 months to 14 years (mean, 8 ± 5 years) after repair. Follow-up duration was 13 to 31 years (mean, 19 ± 7 years; Table 2
).
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RESULTS
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All 6 patients survived the operative procedure. One patient (no. 6) who had an additional trabecular muscular VSD, died 4 months after repair due to chronic heart failure and septicemia. At postoperative cardiac catheterization, the end-diastolic volume of the left ventricle was 120% ± 57% (range, 77%–204%) of the anticipated normal value.2 The left ventricular ejection fraction was 0.58 ± 0.11 (range, 0.47–0.73). Right atrial pressure was 7 ± 2 mm Hg (range, 4–9 mm Hg), and left ventricular end-diastolic pressure was 11 ± 2 mm Hg (range, 9–12 mm Hg). Pulmonary arterial pressure was 15 ± 6 mm Hg (range, 0–21 mm Hg), and the cardiac index was 3.7 ± 0.8 L–1·min·m–2 (range, 2.9–4.8 L–1·min·m–2). The T-P distance at intraventricular rerouting ranged from 8 to 18 mm (mean, 13 ± 3 mm), these values were 79%–139% (mean, 115% ± 25%) of the normal aortic valve diameters. Left ventricular outflow tract diameters in frontal view at late cardiac catheterization were 81%–117% (mean, 96% ± 17%) of normal aortic valve diameters. In all cases where late catheterization was performed, LVOT diameter enlarged in association with the growth of the patients own tissue (Figure 1
).

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Figure 1. Diameter of left ventricular outflow tract (LVOT) compared with anticipated normal aortic valve diameter (N. AVD). The shortest distance from the tricuspid to the pulmonary valve at intraventricular rerouting (white dots) changed to the LVOT diameter measured in frontal view at late cardiac catheterization (black dots).
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Three patients had no LVOT obstruction 15, 16 and 31 years after repair. In 2 children with mild pressure gradients (18 and 20 mm Hg) across the constructed channel remaining soon after repair, the left ventricular-aortic pressure gradient became > 50 mm Hg after 9 and 14 years; one patient (no. 2) is in a stable condition awaiting revision, the other (no. 5) has already undergone revision of the intraventricular baffle. This patient was diagnosed with situs inversus, l-malposition double-outlet right ventricle, and a subpulmonic VSD at 1-month old. He underwent pulmonary banding at 3 months of age. Kawashima intraventricular rerouting, reconstruction of the right ventricular outflow tract, and de-banding of the pulmonary artery were performed at 3 years. Nine years after repair, LVOT obstruction and moderate aortic insufficiency were revealed by an echocardiogram. Revision of the intraventricular baffle to relieve LVOT obstruction, aortic valvuloplasty, and right ventricular outflow tract reconstruction were performed at 12 years of age; a calcified thick peel on the baffle was thought to be the major cause of LVOT obstruction. T-P distance was 16 mm (108% of normal aortic diameter), although it had been 8 mm (79%) at the initial repair. He did well after the revision; however, aortic regurgitation and LVOT obstruction gradually deteriorated again. Aortic valve replacement and relief of LVOT obstruction was performed at 16 years of age. The internal conduit was narrowed and twisted with severe calcification. The previous conduit was removed as much as possible. Two hemispherical pieces of equine pericardium were sutured cranially and caudally. The 2 patches were sutured together in the middle of the LVOT (Figure 2
). Thereafter the pressure gradient across the LVOT reduced from 60 to 20 mm Hg.

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Figure 2. Operative findings at 2nd revision of intraventricular (IV) baffle (patient no. 5). The previous internal conduit was narrowed and twisted with severe calcification. Two hemispherical pieces of equine pericardium were sutured cranially and caudally. Ao = aorta, N. AVD = normal aortic valve diameter, PA = pulmonary artery, TV = tricuspid valve, VSD = ventricular septal defect.
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DISCUSSION
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In patients with Taussig-Bing anomaly, Kawashima intraventricular rerouting is attractive for patients with side-by-side great arteries, especially those with unusual coronary artery anatomy or a pulmonary valve that is not considered adequate to function as a systemic valve. Intraventricular rerouting preserves the native aortic valve and avoids coronary dissection.2,3 These patients are at risk of developing subaortic stenosis from the intracardiac left ventricle-to-aorta baffle. The arterial switch operation, suitable for patients with an anteroposterior relationship of the great artery, is one of the attractive surgical options in patients with side-by-side arteries.4–7 These patients are at risk of aortic insufficiency from prior pulmonary artery banding and use of the pulmonary valve as the neoaortic valve. Although the arterial switch operation may be feasible for some patients with a side-by-side relationship, our preference has been intraventricular rerouting in view of the lower mortality and morphologic characteristics including the pattern of the coronary arteries.8
Yacoub and colleagues4 reported that pulmonary artery banding may produce further right ventricular hypertrophy with an increase in size of the conal septum, which can result in progressive subaortic stenosis. As a result of this, they recommended that after banding in this subset of patients, definitive repair should not be delayed beyond the age of 2 to 3 years. In our series, the mean age at operation was 2.9 years, and the relatively older age of the patients is due to prior pulmonary artery banding. However, there was no subaortic stenosis after banding in our cases, and the subpulmonary space was large enough to place an internal conduit.
Regarding LVOT obstruction after intraventricular rerouting, Serraf and colleagues3 reported progressive LVOT obstruction in 2 patients who had undergone intraventricular rerouting early in infancy (3 and 4 months of age). In one case, re-operation for LVOT obstruction was performed 1 month after intraventricular rerouting. The other patient died 8 months after repair. They recommended that intraventricular rerouting be performed in patients > 1 year of age. Mavroudis and colleagues6 reported one re-operation for baffle stenosis 9 months after intraventricular rerouting in an 11-month-old patient. Kawahira and colleagues9 reported one re-operation for progressive LVOT obstruction 10.8 years after initial repair. They suspected that use of a heart-shaped internal conduit, which seemed to result from inadequate conal resection, was a possible cause of obstruction in the long term.
In our series, 2 patients had significant LVOT obstruction with pressure gradients across the channel of 61 mm Hg after 14 years, and 72 mm Hg after 9 years. One patient had undergone the initial operation at 8 months of age, and this was the only case in our experience in which intraventricular rerouting was performed at < 1 year of age; progression of LVOT obstruction occurred 8 years after repair. The other patient underwent the initial operation at 3 years of age. Although the ratio of T-P distance to normal aortic valve ring size at intraventricular rerouting was 79%, which was the lowest value in our series, the pressure gradient across the channel was < 20 mm Hg up to 3 years after repair. T-P distance had increased by 108% of the normal aortic diameter at revision, and the calcified thick peel on the baffle was thought to be the major cause of LVOT obstruction. However, it must be noted that the T-P distance is a crucial indication for Kawashima intraventricular rerouting. Even in the original Taussig-Bing anomaly, the pulmonary valve may ride on the left ventricle over the interventricular septum to various degrees. The superior suture line of the tunnel patch may be around the pulmonary valve annulus in the left ventricle. In such cases, both the left and right ventricular outflow tracts could become obstructed concurrently after this procedure. Deciding on the operation only by the position of the great arteries is dangerous, and it is preferable that the T-P distance is greater than the anticipated normal size of the aortic orifice. Therefore, if a pressure gradient remains across the constructed channel after the repair, long-term follow-up over 10 years is necessary, as in our cases.
We used a Dacron or Hemashield vascular prosthesis cut in an oval shape as a tunnel in most patients. It was suspected that turbulent flow within the constructed channel was closely associated with proliferation of intimal fibrous tissue. In one patient who underwent re-operation, we used an oval-shaped Hemashield vascular prosthesis at re-operation, but the conduit became narrowed and twisted with severe calcification, and relief of LVOT obstruction was required again. Therefore, we used 2 hemisphere-shaped pieces of equine pericardium to avoid turbulent flow. It is important to select an optimal patch without turbulent flow in the constructed channel, especially if the operation is performed in younger patients and for re-operations. Despite this late LVOT obstruction, it was concluded that the long-term results of Kawashima intraventricular rerouting were favorable.
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REFERENCES
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