Asian Cardiovasc Thorac Ann 2005;13:190-198
© 2005 Asia Publishing EXchange Ltd
Outcomes after Arterial Switch Operation for Simple Transposition
Shahzad G Raja, MRCS,
Arjamand Shauq, MRCPCH1,
Markku Kaarne, MD
Department of Pediatric Cardiac Surgery
1 Department of Pediatric Cardiology Alder Hey Hospital Liverpool, United Kingdom
For reprint information contact: Shahzad G Raja, MRCS Tel: 44 141 201 0269 Fax: 44 141 201 9204 Email: drrajashahzad{at}hotmail.com, Department of Paediatric Cardiac Surgery, Royal Hospital for Sick Children, Yorkhill NHS Trust, Dalnair Street, Glasgow, G3 8SJ, United Kingdom.
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ABSTRACT
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Without intervention, babies born with transposed great arteries (TGA) are doomed to a rapid death. Jatene and coworkers deserve the credit for performing the first successful arterial switch operation (ASO) in a patient with TGA and ventricular septal defect (VSD) in 1975. Since then ASO has become the procedure of choice in most medical centers. This review article summarizes the historical aspects of arterial switch operation and assesses this procedure’s outcomes.
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INTRODUCTION
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Transposition of the great arteries (TGA) is a severe cardiac malformation in which the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. Alternative terminology describes this malformation as a cardiac anomaly with the combination of concordant atrioventricular and discordant ventriculoarterial connections.1–2 TGA is a lethal and relatively frequent malformation accounting for 5–7% of all congenital cardiac malformations.3 With a concordant atrioventricular connection, the physiologic effects are acute, and cyanosis and distress are usually obvious soon after birth. Survival depends on the mixing of blood between pulmonary and systemic circulations, mainly through a patent foramen ovale and assisted by a patent ductus arteriosus (PDA). Sometimes, a co-existent ventricular septal defect contributes to circulatory mixing. If left untreated, many infants die in the first week of life, and most die by age 1.4
The arterial switch operation (ASO) ensures "anatomic correction" of transposition of the great arteries at the arterial level. The term anatomic correction of transposition of the great arteries applies to all repairs connecting the right ventricle with the pulmonary artery and the left ventricle with the aorta. This repair can be accomplished at the ventricular5–7 or arterial level, either with1 or without coronary transfer.8–10 This article reviews the procedure now called the ASO, that is, anatomic correction of TGA at the arterial level with coronary transfer.
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HISTORICAL ASPECTS
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In 1954, Mustard and colleagues were the first to attempt unsuccessfully ASO.1 They used a monkey lung as an oxygenator and transferred only the left coronary artery. None of the patients survived. In the pre-cardiopulmonary bypass era, both experimental as well as clinical attempts to switch the great arteries without coronary transfer failed.1
Attempts to switch the great arteries along with the coronary arteries continued despite impressive results of the physiologic repair.1 Senning reported 3 patients with TGA who had en bloc transfer of pulmonary valve and artery and diversion of the left ventricle to the aorta through a VSD.1 Apart from efforts of Idriss and colleagues,11 other experimental techniques for switching great arteries with coronary transfer have also been reported.1
Jatene and associates performed the first successful ASO in a patient with TGA and a large VSD.1 This operation was restricted to patients with TGA and VSD, large PDA, or left ventricular outflow tract obstruction whose left ventricular pressure was at or close to systemic levels after birth.12
A number of techniques, avoiding mobilization of coronary arteries, were developed to reduce the high early operative mortality attributed partly to technical difficulties related to transfer of the coronary arteries. These techniques included baffling of the coronary arteries to a surgically created aorto-pulmonary window,13 end-to-side anastomosis of the proximal pulmonary artery to the ascending aorta with placement of a conduit from right ventricle to the distal pulmonary artery,1,10 and translocation of the entire aortic root including the proximal coronary arteries.14 However, the ASO with coronary artery transfer retained its original appeal. Lecompte and colleagues devised an important maneuver of transferring the distal pulmonary artery anterior to the ascending aorta thus facilitating direct anastomosis of the neopulmonary artery without conduit interposition.5
For patients with TGA and intact ventricular septum (IVS), most early attempts, with a few exceptions,15–16 at performing primary ASO failed, mainly because of left ventricular dysfunction. Yacoub and associates devised a two-stage approach for patients with TGA-IVS by first banding the main pulmonary artery (with or without systemic-pulmonary shunt) to stimulate the development of the left ventricular muscle mass, followed by an ASO several months later.17 The "rapid two-stage ASO" for TGA-IVS was later introduced by surgeons at the Children’s Hospital in Boston who, after performing the PA banding and systemic-pulmonary shunt as the first stage, did ASO within an average interval of 7 days.18
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OUTCOMES AFTER ARTERIAL SWITCH OPERATION FOR SIMPLE TRANSPOSITION AND TGA WITH VSD
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The neonatal ASO has become the surgical procedure of choice for correction of TGA with or without VSD, as demonstrated by encouraging early- and mid-term cardiac results19–22 as well as normal exercise capacity in most patients.23–24 This section reviews outcomes after ASO for simple transposition and TGA with VSD (Table 1
).
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EARLY MORTALITY AND SURVIVAL
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In recent years, major changes regarding timing for operation, surgical technique, and perioperative care have resulted in a considerable improvement in the early outcomes following ASO. Institutions that have extensive experience and are properly prepared for ASO in neonates report less than 5% early operative or hospital mortality in both simple TGA and TGA with VSD.25–30 This mortality rate is a major improvement compared with about 15% reported in earlier eras.19,25,26,28,31–35 By 6 to 12 months after ASO, the death rate is extremely low and survival declines minimally after that time.26 Five and 10-year survival is 90% even for high-risk patients.19,36–40 Although 15 to 20-year survival figures are still not available, it can be reasonably speculated that it will be about 90%.
Death following ASO is usually secondary to ventricular dysfunction resulting from imperfect transfer of coronary arteries to the neoaorta. In fact, translocation of the coronary arteries remains one of the most crucial aspects of the operation, and late mortality for the ASO appears to coincide with coronary artery events.41–44 Sudden death secondary to acute myocardial infarction has been reported in 1–2% of hospital survivors following the ASO and usually occurs within the first 6 months after repair.45 Right ventricular dysfunction secondary to severe pulmonary vascular disease is the only other important mode of death, accounting for less than 1% of all deaths.26
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RIGHT VENTRICULAR OUTFLOW TRACT OBSTRUCTION
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The most commonly encountered long-term morbidity following ASO is right ventricular outflow tract obstruction (RVOTO) with a reported incidence of 7% to 40%.19,25,27,29,46–62 Postoperative obstruction may occur at multiple levels following anatomic correction. Usually, obstruction occurs in the pulmonary trunk. Less frequently, RVOTO occurs at the bifurcation of the pulmonary trunk. Circumferential narrowing at the suture line may also occur. Pulmonary artery stenosis may be related to the technique of reconstruction of the proximal pulmonary arteries with a patch to fill the defects in the posterior wall where the coronary artery buttons were excised57,63–64 or to distortion of the main and peripheral pulmonary arteries as a result of the anterior placement of the bifurcation (Lecompte’s maneuver).5 Supravalvular pulmonary stenosis is often associated with growth failure of the valve annulus and neopulmonary valve stenosis. It also induces a disturbed vascularization with asymmetrical distribution of the pulmonary flow between the two pulmonary branches,29 so that a significant stenosis should be relieved early, either by balloon angioplasty or surgical patchplasty, to promote branch growth. Balloon dilation of these stenotic areas has met with limited success, and pulmonary arterioplasty often requires operative reintervention, which carries with it a significant mortality rate.63,65–68
Neopulmonary valve stenosis has been reported rarely in patients who have undergone either a one- or two-stage ASO.49 Its incidence varies from 4% to 11%.49,61 Wernovsky and associates52 reported that risk factors of supravalvular pulmonary stenosis and neopulmonary valve stenosis were associated with the coronary artery pattern and a younger age at operation. Inadequate mobilization of the branch pulmonary arteries with semilunar valve distortion, pulmonary artery banding, and the type of patch procedure used to correct the defects in the pulmonary artery wall (from the coronary artery buttons) have been suggested as technical factors that can lead to valvular stenosis.49 Neopulmonary valve stenosis tends to develop primarily during the first year after repair.19,49
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NEOPULMONARY VALVE REGURGITATION
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Neopulmonary valve regurgitation occurs after ASO with most studies using Doppler echocardiographic evaluation reporting incidence varying from 9% to 80%.61,69–71
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NEOAORTIC VALVE REGURGITATION AND STENOSIS
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Post-ASO neoaortic valve regurgitation is commonly an underestimated complication of anatomic repair of TGA. The anatomic pulmonary valve, with thin leaflets and little collagen and elastic tissue, must function as the neoaortic valve after ASO. Mild regurgitation has been found in about 35% of patients72–74 with moderate to severe regurgitation being demonstrated in 5% or fewer patients.21,70–76 Prevalence of aortic regurgitation in patients who have reached 20 years of age is not known, but may be appreciable.77 More importantly, the frequency of the regurgitation after ASO seems to increase with time48,52,55,58,59,78,79 and isolated cases have had significant regurgitation requiring valve replacement.27,80–82
It remains unclear why neoaortic regurgitation seems to appear with increasing frequency 2 to 4 years after the operation in subjects with an otherwise perfectly functional postoperative neoaortic valve. Studies concerning the size and growth of the neoaortic root and anastomosis have been published, but the simple measurement of the diameter of the vascular structures may be insufficient to outline the complex geometric modifications of the growing neoaortic root after ASO.74
Indeed, the late occurrence of neoaortic regurgitation in many patients and the results of the morphometric study suggest that the neoaortic root distortion should not be regarded as the result of a direct surgical injury, but rather as an effect of some degree of growth impairment, which is possibly magnified by the extensive remodeling caused by the opening of the trapdoors.74 Furthermore, the role of the discrepancy in caliber between the native aortic and pulmonary roots, e.g. in the cases with TGA-VSD and aortic coarctation, previous pulmonary artery banding and the presence of bicuspid pulmonary valve cannot be ruled out.74 Left ventricular outflow tract and neoaortic stenosis are rare in the literature.19,27,30,48,50,52,59,66,83,84
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CORONARY ARTERY OBSTRUCTION AND MYOCARDIAL PERFUSION
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Mobilization and translocation of the coronary arteries remain the most technically challenging aspects of the ASO. It carries the combined risk of primary ischemic injury and late problems with coronary artery kinking or ostial stenosis. The long-term patency and growth of the coronary arteries are crucial for the ASO to be considered the procedure of choice for the surgical management of TGA. Coronary artery obstruction has been documented in a disturbingly high number of asymptomatic TGA patients evaluated prospectively by angiography at 5 to 10-year follow-up.42,85 The prevalence of coronary events in literature varies from 2% to 11%.33,39,41,55,86,87 The coronary events most often occur immediately after the ASO and are the main cause of death or morbidity. 19,33,34,36,37,39,86,87–91 In the early postoperative period, coronary events are related to coronary anatomy and to surgical technique difficulties.19,33,34,41,55,86–88 Causes are probably anatomical kinking or torsion and extrinsic compression by biological glue that necessitated immediate coronary revision or reoperation.41 Late coronary mortality and myocardial infarction are rare and have a prevalence of less than 2% in most studies.33,34,45,55,85–88 Coronary revascularizations occur late, at least 1 year after ASO and most often after 3 years.33,41,42,85 Late coronary events are not related to intraoperative problems or early ischemic symptoms.42,85 Causes are probably progressive fibrocellular intimal thickening or stretching of the coronary artery with growth.43
Concern remains as to the long-term effect on myocardial perfusion from coronary artery mobilization and reimplantation. When compared with the intraatrial repair, the ASO offers the advantage of normalizing the reversed role of the two ventricles. The importance of this advantage depends on the assumption that the left ventricle is not affected by the operative procedure or postoperative complications. Myocardial perfusion studies following the ASO have shown a surprisingly high incidence of perfusion defects.89–94 These abnormalities suggest a reduction of regional coronary flow reserve, a physiologic variable that assesses the ability of coronary flow to increase under hyperemic stimulation. However, these perfusion defects generally lessen with exercise92 and are rarely correlated with electrocardiographic, echocardiographic, or angiographic changes, so that their clinical significance is questionable. The precise etiology of those abnormalities is undefined, but may be more related to the insult of open heart surgery itself than to the coronary manipulation involved in the arterial switch procedure. According to one study, these abnormalities reflect arteriolar or capillary processes below the resolution of coronary angiography, resulting from inhomogeneous myocardial protection, embolism, or other intraoperative insults.91 The rarity of regional left ventricular wall motion abnormalities is reassuring in comparison with scintigraphic studies.89,92,95,96 However, reduction of regional coronary flow reserve is a functional disorder which in pediatric patients is not accurately detected by echocardiography and angiocardiography. Exercise testing appears to be useful in detecting ischemic damage or exercise-induced ventricular arrhythmias possibly secondary to reduced coronary flow reserve.97 Many questions remain about long-term development of the coronary circulation after coronary reimplantation, including the evolution of atherosclerosis and coronary flow reserve.
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VENTRICULAR FUNCTION
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Left ventricular function is usually normal after ASO. A comparative study between the arterial and atrial switch showed that late postoperatively left ventricular ejection fraction was within the normal range in 98% of patients with simple TGA undergoing the arterial switch repair, but in 79% of those who underwent an artial switch repair.98 Similar results have been shown by other studies.30,99–101 Interestingly, preoperative dynamic left ventricular outflow tract obstruction, even with a gradient of up to 120 mm Hg, disappears after ASO.102,103
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GROWTH OF ARTERIES
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Although all currently available information indicates that aortic, pulmonary, and coronary anastomoses grow at a rate comparable to growth of the child,30,84,104 there is some concern that the arterial switch technique introduces possible growth interference at different levels, such as the pulmonary-aortic anastomosis and the introduction of aortic tissue due to coronary transfer. Each growth interference may have an impact on the aortic valve, the neo-aortic (pulmonary) sinuses, and the aortic root.105 Similar concerns have been raised about the growth of the main and branch pulmonary arteries.29 Disproportionate dilatation of the neo-aortic root has been reported after ASO.79,105 According to Hutter and associates,40,105 the neo-aortic valve and sinuses are larger than normal after the arterial switch. In the first year of life, there is rapid dilatation of the new aorta followed by active growth with tendency towards normalization of the valve and sinus size. However, this aortic dilatation by itself is rarely associated with significant insufficiency.105
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RHYTHM DISTURBANCES
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The use of an intraatrial baffling procedure such as the Mustard or Senning repairs for transposition of the great arteries has been associated with a high incidence of cardiac rhythm abnormalities.106–112 Sinus bradycardia, complicated by recurrent atrial flutter, is the most common management issue in this population and may contribute to late sudden death. These rhythm disturbances are thought to arise from trauma to the sinus node and atrial muscle from the extensive intraatrial suture lines required in the baffling procedure.113 During ASO, there is little intraatrial manipulation other than the repair of the atrial septal defect (either congenital or caused by balloon atrial septostomy). One of the major theoretical advantages of anatomic correction is that the limited atrial procedure should result in a significantly improved rhythm status of the survivors. The reported incidence of arrhythmias after arterial switch is 3% to 7%,20,114–115 which is much less compared to the 13% to 100% frequency of rhythm disturbances following atrial switch repair.20,106,115–121 However, as the follow-up is relatively short, one must remain vigilant in this regard, since such problems may become apparent after many years.
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ENLARGED BRONCHIAL ARTERIES
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Abnormally enlarged bronchial arteries are frequently identified at postoperative catheterization after ASO despite early repair and may explain continuous murmurs or persistent cardiomegaly in patients with otherwise normal noninvasive findings.30,122–124 These vessels are probably intrinsic to transposition and not related to the duration or degree of cyanosis before repair or to a decreased pulmonary blood flow to one lung or the other because of hypoplastic pulmonary artery. The shunt is sometimes significant, necessitating catheter-directed therapy with coil embolization.122
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FUNCTIONAL STATUS
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Exercise performance is significantly reduced after the Mustard or Senning atrial baffle operation for transposition of the great arteries.125–126 One of the expected benefits of ASO is that exercise performance would be improved after a more anatomically correct repair of this defect. Available data on exercise performance in this population demonstrates that cardiopulmonary performance during exercise is generally excellent after ASO.92–93,97,127 However, even though essentially all surviving patients are fully active and without limitation,127–128 evidence of stress-induced myocardial ischemia continues to be a concern in this population.24,94,127 Continued monitoring of exercise performance, especially for ischemia, would appear to be warranted as this population ages and begins to participate in more vigorous athletic activities.127
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NEURODEVELOPMENTAL STATUS
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Neonatal ASO with combined circulatory arrest and low flow bypass is associated with neurological impairment, but not with reduced development as assessed by formal testing of motor, cognitive, language, and behavioral functions.129 At 8-year follow-up in one patient cohort, overall physical and psychosocial health status was similar to that of general population, according to the Mean Physical Health Summary and the Mean Psychosocial Summary scores; however, increased problems with attention, learning, speech, and developmental delay are reported by parents.130 A recently published, single-center, randomized controlled trial to assess developmental, neurologic, and speech outcomes 8 years after ASO has revealed that the use of total circulatory arrest to support vital organs while performing ASO is generally associated with greater functional deficits than is use of low-flow cardiopulmonary bypass, although both strategies are associated with increased risk of neurodevelopmental vulnerabilities.131
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REOPERATION
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Reoperative probability for a variety of complications has ranged from 5% to 30% in the literature.19,22,34,66,67,89,132–136 Neopulmonary stenosis or RVOTO is the single most common complication requiring reintervention.82 Complications other than neopulmonary stenosis after ASO severe enough to require reintervention are distinctly uncommon.137 Compression of esophagus137 and left main bronchus138–139 has been reported after arterial switch. The mechanism of left bronchial compression after ASO may relate to the placement of the proximal ascending aorta posterior to the transected pulmonary artery.138–139 The left main bronchus is intimately related to the left pulmonary artery and the descending thoracic aorta as it courses beneath the aortic arch. The mobilization and posterior displacement of the ascending aorta behind the left pulmonary artery as the neoaorta may allow it to impinge upon the left main bronchus or may permit compression of the bronchus between the ascending and descending aorta.138–139 Other reported complications requiring reintervention are aortic arch obstruction66 and neoaortic insufficiency.27,80–82 Aortic arch obstruction seems to be limited to that patient population in whom an aortic coarctation was present and an extensive aortic reconstruction comprised a portion of the initial operation. This problem appears, at least in the short term, amenable to balloon angioplasty techniques for correction.66
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CONCLUSIONS
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The arterial switch operation has been universally recognized as the therapy of choice for children born with TGA. As experience with this operation has increased, mortality has been lowered and is consistently below 10% in most contemporary series. Most children who have undergone ASO have also enjoyed normal growth, development, and cardiac function. In contrast to the former atrial switch procedures, ASO has the advantages of maintenance of sinus node function and preservation of the left ventricle as the systemic ventricle and the mitral valve as the systemic atrioventricular valve. However, ASO involves translocation of the coronary arteries — the pulmonary valve becomes the systemic outflow valve — and the pulmonary arteries may become distorted because of their atypical relationship to the great vessels. All of these are associated with early as well as delayed complications. Incidence of late reintervention, whether therapeutic cardiac catheterization or operation, is common in this patient population. Therefore, it is important to realize that even though almost three decades have passed since the first ASO was performed and morbidity and mortality have been lowered, one must remain vigilant to identify newly emerging problems, since such unrecognized problems may become apparent only after follow-up of many years.
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ABSTRACT
INTRODUCTION
