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Ann Thorac Surg 2002;74:1986-1991
© 2002 The Society of Thoracic Surgeons

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Original article: cardiovascular

Late outcome after arterial switch operation for complete transposition of great arteries with left ventricular outflow tract obstruction

^a Cardiothoracic Centre, All India Institute of Medical Sciences, New Delhi, India

Accepted for publication July 22, 2002.

* Address reprint requests to Dr Sharma, B-404, Adarsh Palace, Block-5, Jaya Nagar, Bangalore, India.
e-mail: rsharmacvs{at}hotmail.com

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
BACKGROUND: Long-term follow-up of patients who underwent arterial switch operation for complete transposition of great arteries with anatomic left ventricular outflow tract obstruction (LVOTO) has rarely been brought into the focus.

METHODS: Of 299 patients who underwent an arterial switch operation between January 1991 and January 2001, 23 patients had anatomic LVOTO. Age ranged from 4 days to 18 years (median 90 days) and weight ranged from 2.6 to 35 kg (median 4.3 kg). Surgical management included arterial switch operation, closure of ventricular septal defect wherever indicated, and excision of LVOTO.

RESULTS: Among patients with preoperative LVOTO there were 2 early deaths and 8 patients had mild neoaortic regurgitation at the time of discharge. Follow-up ranged from 8 months to 9 years (mean 60 ± 12 months). In 4 patients who had mild neoaortic regurgitation at discharge, the regurgitation progressed to moderate or severe degree after a follow-up of 22 to 72 months. In 1 patient mild mitral regurgitation present at the time of discharge progressed to severe mitral regurgitation. This patient subsequently underwent double valve replacement.

CONCLUSIONS: Presence of preoperative anatomical LVOTO in patients undergoing arterial switch operation predicts high incidence of postoperative neoaortic regurgitation.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Anatomical left ventricular outflow tract obstruction (LVOTO) is not an infrequent association of complete transposition of great arteries (TGA) [1–5]. This association has often been considered to be a contraindication for anatomical repair in the past [6–8]. Recently, however, organic LVOTO in transposition patients has been found to be compatible with a successful outcome [4, 9–11].

Various surgical options are available to treat LVOTO in association with complete transposition of great arteries often associated with a ventricular septal defect. These options include atrial level repair with or without relief of LVOTO [6, 12], the Rastelli or Lecompte procedure [7, 8, 13, 14], and the arterial switch operation with relief of LVOTO [4, 9–11]. The advantages of having the left ventricle to support the systemic circulation outweigh the alternative option of atrial level repair with left ventricular outflow clearance. Furthermore atrial repair may not be suitable in presence of right ventricular dysfunction, tricuspid regurgitation, or arrhythmias [4]. The Rastelli or Lecompte procedures require an unrestrictive ventricular septal defect in the subarterial region whereby the left ventricle can be conveniently routed to the aorta. Smaller or remote septal defects may not be suitable for these repairs. In that case the only way to recruit the left ventricle as systemic pump is an excision of the LVOTO and an arterial switch. We herein analyze our experience with a group of patients having anatomic LVOTO in association with complete transposition and who underwent arterial switch operation as the Rastelli/Lecompte type of repair was not possible owing to a remote or absent ventricular septal defect.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Patients with dynamic LVOTO in the setting of TGA with intact ventricular septum, where the basis of LVOT gradient was a pressure differential between the left ventricle and the right ventricle and which was expected to resolve upon restoration of the ventricle to their normal roles, were not included. The primary requirement to submit a patient to the arterial switch operation was the presence of a pulmonary annulus diameter and pulmonary valve morphology acceptable in the aortic position. Specifically, any pulmonary annulus less than -3 Z value for the aortic annulus [15] was considered unsuitable. Any isolated pulmonary valvular stenosis producing a gradient in excess 40 mm Hg in the absence of a ventricular septal defect was also a potential disqualification. If the subvalvular LVOTO was severe and the ventricular septal defect was in a suitable position we performed a Rastelli operation. If the subvalvular LVOTO was mild to moderate with a normal pulmonary valve an arterial switch operation was performed even if the septal defect was suitable for a Rastelli operation.

Based on the rejection criteria, 4 patients in this time period underwent a Senning repair with either pulmonary valvotomy (n = 3) or a left ventricle to pulmonary artery conduit (n = 1). Two patients also underwent treatment along the lines of univentricular repair (bidirectional Glenn shunt plus atrial septectomy and interruption of main pulmonary artery and enlargement of the ventricular septal defect) due to preoperatively and intraoperatively determined unresectable LVOTO and remote ventricular septal defect making them unsuitable for a Rastelli type repair One patient with a subarterial ventricular septal defect and subvalvular pulmonary stenosis underwent a Rastelli repair as the LVOT was predicted intraoperatively to become unacceptably narrow if the left ventricle was routed to the pulmonary valve as would be the case if an arterial switch operation was chosen as the treatment.

Twenty-three of the 299 patients who underwent an arterial switch operation between January 1991 and January 2001 and who were noted to have anatomic LVOTO form the basis of the study. Preoperative and postoperative echocardiograms, catheterization studies, operative notes, and follow-up cardiac clinic files were evaluated. Median age of this group was 90 days (range 4 days to 18 years) and median weight was 4.3 kg (range 2.6 to 35 kg). Sixteen of the 23 patients had an associated ventricular septal defect (VSD), and 2 had the Taussig Bing anomaly. Causes of subvalvular LVOTO included accessory tricuspid valve tissue prolapsing through the VSD (n = 2), accessory mitral valve tissue (n = 6), discrete/diffuse fibromuscular tissue (n = 10), septal malalignment (n = 2), and endocardial cushion tissue (n = 1). Two patients had valvular pulmonary stenosis. The mean peak systolic gradient across the left ventricular outflow tract was 52 ± 16.5 mm Hg (range 16 to 90 mm Hg, median 60 mm Hg). None of the patients had had a palliative pulmonary artery banding.

Surgical management was performed according to standard surgical technique [16]. Intraoperative transesophageal echocardiography was performed in all patients before and after surgical correction. On transesophageal echocardiography an impression was formed about pulmonary annulus diameter, leaflet pliability and thickness, and the exact anatomic basis and proximity of the subvalvular obstructive tissue to the pulmonary valve leaflets. The pulmonary annular diameter was compared with the predicted diameter [15] and the Z value was calculated. If the above findings favored a pulmonary valve usable in the systemic circulation, preparations proceeded on the line of an arterial switch operation, namely, pulmonary artery mobilization up to lobar branches, ligament/ductus division, and marking sutures on the pulmonary trunk at the proposed site of coronary transfer. After aortic and bicaval cannulation, cardioplegic arrest was achieved and left ventricle was vented through the right superior pulmonary vein. A right atriotomy was made to locate the VSD and, if any, tissue prolapsing into the left ventricular outflow tract. Pulmonary valve leaflets were visualized through the VSD and in 3 patients resection of the subvalvular membrane or fibrous tissue could be partially undertaken through the VSD. The VSD was then closed. The aorta was transected and so was the pulmonary artery. In all the patients, further clearance of the left ventricular outflow tract was then undertaken through the pulmonary (neoaortic) valve. Pulmonary valve was inspected, and if finally deemed usable as the future aortic valve, coronary button excision and transfer was undertaken followed by the Lecompte maneuver and reconstruction of the ascending aorta. Aortic clamp was then removed after deairing the left side of the heart.

Perfusate temperature in excess of 32°C was ensured at the release of aortic clamp so that cardiac action resumed immediately to counteract the effect of any neoaortic valve incompetence. Pulmonary artery reconstruction was then completed in the routine fashion.

Operative survivors had a predischarge echocardiogram. Subsequently they were followed up in the outpatient clinic at periodic intervals. At each visit a detailed clinical and echocardiographic evaluation was performed. Valvular regurgitation or stenosis was quantified according to the reported criteria [17, 18].

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
There were two early deaths. The first patient died of multiorgan failure on the fifth postoperative day and the second patient succumbed to renal failure on the seventh postoperative day. Two patients required permanent pacemaker implantation for complete heart block. There was no other major perioperative morbidity. Predischarge echocardiography performed 5 to 7 days postoperatively, revealed mild regurgitation across the neoaortic valve in 8 patients. The profile of these patients is shown in Table 1. In addition, 1 patient had developed mild mitral regurgitation. There was no residual flow across the ventricular septal defect. At discharge only 1 patient had a residual gradient (20 mm Hg) across the neoaortic valve. Follow-up ranged from 8 months to 9 years (mean 60 ± 12 months). In 4 of the patients who had mild regurgitation at discharge the neoaortic regurgitation progressed to moderate or severe degree after a follow-up of 22 to 72 months (Table 2). In the remaining 4 patients with initial mild regurgitation the neoaortic regurgitation did not progress after a follow-up of 18 to 40 months. Freedom from development of moderate or severe neoaortic regurgitation was 60.5% ± 8.6% at 8 years. Functionally all patients except 1 were in New York Heart Association functional class I. One patient (no. 1, Table 1) with severe neoaortic regurgitation was in NYHA class II. This patient had undergone resection of severely narrowed LVOT and developed significant dilatation of the neoaortic root with severe neoaortic regurgitation (Fig 1). In the same patient mild mitral regurgitation present at the time of discharge from the hospital had progressed to severe regurgitation after a follow-up of 72 months. This patient underwent successful double valve replacement. At the time of reoperation the aortic root was dilated and all the three leaflets of the neoaortic valve were thick, noncoapting, and rolled up. The other patient (no. 4, Table 2) who underwent pulmonary valvotomy for bicuspid pulmonary valve developed severe neoaortic regurgitation (follow-up 55 month). Presently he is asymptomatic but echocardiography shows evidence of left ventricular dysfunction. He is scheduled for aortic valve replacement. In the other patient (no. 5, Table 2), who had bicuspid pulmonary valve but did not require valvotomy, the gradients (20 mm Hg) at the time of discharge have progressed to 40 mm Hg after a follow-up of 40 months. No other patient had developed fresh gradients on follow-up.

View larger version (99K): [in this window] [in a new window]   Fig 1. (A) Preoperative left ventriculogram in patient no. 1, Table 1. There is severe subvalvular narrowing. (LV= left ventricle; PA = pulmonary artery.) (B) Postoperative cineangiogram of the same patient after 64 months. Aortic root angiogram shows significantly dilated aortic root with severe neoaortic regurgitation.

	Comment

Top Abstract Introduction Patients and methods Results Comment References

In our experience with arterial switch operation in the category of patients who did not have preoperative LVOTO neoaortic regurgitation was present only in 15 patients (total number of patients 217) and it was not more than mild in severity in any patient over a follow-up period of 10 years. In contrast to this in patients whose preoperative LVOTO had required excision, the incidence of neoaortic regurgitation has been high (8 out of 23). Among 8 patients neoaortic regurgitation has progressed in 4 and has become severe enough to require reoperation in 2. Previous publications on this subject [4, 9] have not experienced aortic valve incompetence to this degree. Similar to our experience, however, one other group of investigators [20] has reported correlation between the existence of preoperative LVOTO and the development of postoperative neoaortic regurgitation.

Potentially any arterial switch operation, not necessarily with LVOT abnormality that requires resection, may result in development of neoaortic regurgitation by way of (1) interference with integrity of the sinotubular junction during coronary transfer, and (2) downsizing of the dilated proximal main pulmonary artery to the size of the distal aorta in patients with large VSD. One factor peculiar to the group with preoperative important LVOTO may be introduction of the pulmonary valve and proximal main pulmonary artery into the systemic circulation in patients in whom the pulmonary artery pressure has remained low for a significant length of time. This may a probable factor in patients with coexistent severe LVOTO where the protected pulmonary valve and thin-walled main pulmonary artery may respond to systemic arterial pressure by a dilatory response. Dilatation of the neoaortic root has been documented in 1 of our patient (no. 1, Table 1) who had undergone aortography before reoperation (Fig 1). This points to expansion of the aortic root to the systemic pressure as one of the possible mechanisms for development of neoaortic regurgitation. In other patients undergoing arterial switch operation for TGA with significant VSD, however, residual dilatation of the root has not contributed to the development of neoaortic regurgitation. This suggests that it may be the sudden exposure to unaccustomed high pressure rather than a preexisting dilated root that could be the causative factor for neoaortic regurgitation.

Other factors that may possibly be implicated in the causation of neoaortic regurgitation in our experience may be pulmonary valvotomy (n = 1), subvalvular resection with consequent loss of support for the aortic valve cusps (n = 2), and chronic damage to the pulmonary valve leaflet tissue by prolapsing atrioventricular valve tissue (n = 1). Other reasons of neoaortic regurgitation in this subset of patients may be surgical manipulation through the neoaortic valve, which may produce damage of the neoaortic leaflets not visible macroscopically during operation, and residual turbulent flow through the valve even in the absence of significant gradient across the neoaortic valve.

In summary the increased incidence of progressive neoaortic regurgitation in patients with transposition of the great arteries plus LVOTO treated along the line of the arterial switch operation warrants a relook at this approach vis a vis other options such as the Nikaidoh Bex procedure [21–24]. In the absence of published long-term results of this option, however, the question as to the preferred approach remains open for hearts in which a Rastelli-type repair is not readily feasible.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

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