Arterial Switch Operation: Step-by-Step Reconstruction

Arterial Switch Operation: Step-by-Step Reconstruction

image

The arterial switch operation (ASO) is the anatomical repair for d-transposition of the great arteries (d-TGA) and selected related forms of ventriculo-arterial discordance. The operation restores normal ventriculo-arterial concordance by connecting the left ventricle to the systemic circulation and the right ventricle to the pulmonary circulation.

In d-TGA, the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle, creating two parallel circulations. Survival before repair depends on adequate mixing through the atrial septum, ventricular septum, or ductus arteriosus. The arterial switch operation corrects this physiology by transecting and switching the great arteries, transferring the coronary arteries to the neoaortic root, reconstructing the neopulmonary artery, and performing the Lecompte maneuver to create an anterior pulmonary arterial pathway.

The contemporary ASO has excellent long-term outcomes. Large institutional series report low early mortality, low late mortality, and durable survival into adolescence and adulthood [1,2]. A systematic review including 151 studies and more than 30,000 patients found high short-, medium-, and long-term survival after ASO, supporting the operation as the definitive repair for most neonates with d-TGA [3]. Despite these results, ASO is not simply a “completed” neonatal repair. Long-term surveillance is required because late complications may involve the neopulmonary pathway, branch pulmonary arteries, neoaortic root, neoaortic valve, coronary arteries, rhythm, and associated arch repair sites [4,5].

1. Indications

The arterial switch operation is the standard definitive repair for most neonates with:

  • d-TGA with intact ventricular septum
  • d-TGA with ventricular septal defect
  • d-TGA with selected outflow tract considerations
  • Taussig–Bing anomaly, when the VSD can be baffled appropriately to the neoaorta
  • d-TGA or Taussig–Bing anomaly with coarctation or arch hypoplasia, when single-stage repair is anatomically feasible

The preferred timing is usually in the neonatal period. Early repair preserves left ventricular preparedness for systemic work and avoids prolonged cyanosis, unstable mixing physiology, and progressive hypoxemia-related morbidity. Early ASO is particularly important in d-TGA with intact ventricular septum because the left ventricle may decondition as pulmonary vascular resistance falls after birth.

Relative cautions include severe late left ventricular regression, coronary anatomy in which safe transfer is not achievable, severe extracardiac comorbidity precluding cardiopulmonary bypass, or complex intracardiac anatomy in which another strategy may offer a more reliable systemic outflow.

2. Physiological Rationale

The physiological problem in d-TGA is not inadequate ventricular function, but malconnection of the ventricles to the great arteries. The morphologic right ventricle ejects into the aorta, and the morphologic left ventricle ejects into the pulmonary artery. Therefore, systemic venous blood tends to recirculate to the body and pulmonary venous blood tends to recirculate to the lungs.

Effective systemic oxygen delivery depends on mixing at one or more levels:

  • Atrial septal communication
  • Ventricular septal defect
  • Patent ductus arteriosus
  • Bronchopulmonary collateral flow in selected settings

The ASO restores the normal series circulation:

  • The left ventricle becomes the systemic ventricle
  • The right ventricle becomes the pulmonary ventricle
  • The former pulmonary root becomes the neoaortic root
  • The former aortic root contributes to the neopulmonary pathway
  • The coronary arteries are transferred to the neoaortic root

This anatomical correction allows long-term physiology to approximate normal circulation, provided that coronary perfusion is intact and both outflow pathways remain unobstructed.

3. Preoperative Evaluation

Preoperative planning must define the anatomy, physiology, coronary transfer strategy, and associated lesions.

3.1 Segmental Anatomy

Echocardiography should confirm:

  • Atrial situs
  • Ventricular morphology
  • Ventriculo-arterial discordance
  • Great artery relationship
  • Presence, size, and location of VSD
  • LVOT and RVOT geometry
  • Atrioventricular valve morphology and competence
  • Semilunar valve morphology and size discrepancy

In Taussig–Bing anomaly, the spatial relationship between the VSD, semilunar valves, and outflow tracts is central. The VSD must be baffled to the neoaorta without creating LVOT obstruction, RVOT obstruction, atrioventricular valve distortion, or residual shunting.

3.2 Coronary Anatomy

Coronary anatomy is one of the most important determinants of technical risk. Coronary anomalies, single coronary patterns, and intramural coronary arteries have been repeatedly identified as risk markers for mortality or morbidity after ASO [6,7].

The surgeon must define:

  • Number of coronary ostia
  • Sinusal origin of each coronary artery
  • Single ostium or separate ostia
  • Intramural course
  • High or remote take-off
  • Looping coronary patterns around the great arteries
  • Relationship between the proximal coronaries and planned neoaortic root
  • Feasibility of tension-free transfer after the Lecompte maneuver

The technical objective is a wide, tension-free, non-kinked, non-twisted, non-compressed coronary course after transfer. Coronary variants do not automatically preclude ASO, but they may require modified button design, extensive mobilization, unroofing, trapdoor reimplantation, hood augmentation, or other tailored strategies.

3.3 Pulmonary Arteries and Aortic Arch

The pulmonary artery anatomy requires careful evaluation because the native pulmonary root becomes the neoaortic root, and the native aortic root becomes part of the neopulmonary reconstruction.

Assessment should include:

  • Main pulmonary artery size
  • Branch pulmonary artery caliber and symmetry
  • Pulmonary bifurcation geometry
  • Ductal tissue near the pulmonary artery confluence
  • Risk of branch PA distortion after the Lecompte maneuver
  • Aortic arch sidedness and caliber
  • Coarctation, transverse arch hypoplasia, or interrupted arch
  • Relationship between arch repair and great artery reconstruction

When arch obstruction is present, single-stage ASO with arch reconstruction can achieve excellent survival, but associated VSD or arch obstruction increases the likelihood of later reintervention compared with simple d-TGA [1,8].

3.4 Preoperative Stabilization

The goals before surgery are to maintain systemic oxygen delivery, prevent end-organ injury, and optimize the patient for neonatal cardiopulmonary bypass.

Key measures include:

  • Prostaglandin E1 to maintain ductal patency when needed
  • Targeted ventilation and correction of acidosis
  • Avoidance of excessive pulmonary vascular resistance
  • Monitoring of systemic perfusion, lactate, urine output, and end-organ function
  • Neurologic assessment when clinically indicated
  • Balloon atrial septostomy when atrial-level mixing is inadequate

A restrictive atrial septum can produce profound hypoxemia despite ductal patency. In that setting, urgent balloon atrial septostomy remains an important stabilization strategy.

4. Operative Strategy

4.1 Exposure and Cardiopulmonary Bypass

The operation is performed through a median sternotomy.

Standard preparation includes:

  • Pericardial opening and suspension
  • Inspection of great artery relationship
  • Identification of coronary artery course before major mobilization
  • Arterial and venous cannulation
  • Initiation of cardiopulmonary bypass
  • Cooling according to institutional strategy
  • Aortic cross-clamping and cardioplegic arrest

Venous drainage is usually bicaval or right atrial, depending on the associated procedures. If arch reconstruction is required, the cannulation and perfusion strategy must also support cerebral and systemic protection.

4.2 Great-Artery Transection

The ascending aorta is transected above the sinotubular junction, leaving adequate proximal tissue for coronary button harvest and adequate distal tissue for neoaortic reconstruction.

The main pulmonary artery is transected proximal to the bifurcation, preserving sufficient tissue for the neoaortic root and later neopulmonary reconstruction.

Before division and mobilization, the surgeon should mark:

  • Commissural orientation
  • Coronary button orientation
  • Sinusal anatomy
  • Relative rotation between the great arteries

These marks help prevent malrotation during reconstruction, particularly after the Lecompte maneuver and after the heart is filled.

4.3 Coronary Button Harvest

The coronary buttons are harvested from the native aortic root with generous cuffs of sinus tissue.

Principles include:

  • Avoid small or tight buttons
  • Avoid injury to the coronary ostium
  • Mobilize the proximal epicardial coronary segments adequately
  • Preserve adventitial support
  • Avoid excessive skeletonization
  • Avoid torsion during mobilization
  • Recognize looping, single-ostium, or intramural patterns early

The button should be large enough to prevent ostial narrowing after reimplantation. A small button or purse-string effect at the anastomosis may create critical coronary stenosis.

4.4 Coronary Transfer

The coronary arteries are reimplanted into the neoaortic root, which is the former pulmonary root.

The main technical objective is to create a coronary course that is:

  • Tension-free
  • Non-kinked
  • Non-compressed
  • Non-angulated
  • Hemostatic
  • Stable after cardiac filling and systemic pressure restoration

Common techniques include:

  • Trapdoor reimplantation
  • Open trapdoor technique
  • Pedicled button transfer
  • Pericardial hood augmentation
  • Unroofing for intramural coronary arteries

A trapdoor incision helps create a favorable take-off angle and reduces ostial distortion. In high or remote coronary take-off, hood augmentation may be required to relieve tension.

Coronary transfer is the central technical determinant of ASO. Early postoperative ventricular dysfunction, regional wall-motion abnormality, ventricular arrhythmia, ST-segment change, or difficulty separating from bypass should raise immediate concern for coronary insufficiency [5,9].

5. Special Coronary Patterns

5.1 Single Coronary Ostium

A single coronary ostium requires meticulous planning because one transfer site supplies both coronary distributions.

Technical priorities include:

  • Generous button harvest
  • Wide neo-ostium construction
  • Oblique orientation to avoid compression
  • Avoidance of stretching across the neoaortic root
  • Careful inspection after the Lecompte maneuver
  • Assessment after neoaortic reconstruction and cardiac filling

Even mild distortion may compromise a large myocardial territory.

5.2 Intramural Coronary Artery

An intramural coronary artery runs within the wall of the great artery before exiting externally. This is a high-risk pattern because incomplete mobilization or inadequate unroofing can leave a residual compressed or slit-like segment.

Important principles include:

  • Identify the intramural segment precisely
  • Unroof the intramural course completely
  • Create a wide opening without residual ostial narrowing
  • Avoid leaving a dynamic compressed segment
  • Consider open trapdoor or patch augmentation when needed

Partial unroofing is dangerous because it may leave a residual coronary narrowing that becomes clinically significant after reconstruction.

5.3 High or Remote Coronary Take-Off

High or remote coronary origin can create tension after transfer.

Management may require:

  • Extended mobilization
  • Modified button shape
  • Trapdoor extension
  • Pericardial hood augmentation
  • Adjustment of the reimplantation site on the neoaortic root

The reimplantation site should be selected according to the final coronary course, not simply according to the original sinus position.

6. Lecompte Maneuver

The Lecompte maneuver brings the branch pulmonary arteries anterior to the neoaorta.

Its purpose is to create a shorter and more direct neopulmonary pathway while avoiding posterior compression of the pulmonary arteries by the neoaorta.

Technical priorities include:

  • Avoid twisting of the branch pulmonary arteries
  • Avoid excessive tension on the pulmonary bifurcation
  • Ensure symmetric right and left PA alignment
  • Prevent compression between the neoaorta and surrounding structures
  • Preserve adequate space for the transferred coronary arteries

The Lecompte geometry must be assessed after reconstruction with the heart filled because pulmonary artery alignment may change substantially after separation from bypass. Neopulmonary and branch PA obstruction remain among the most frequent causes of late catheter or surgical reintervention after ASO [4,5,8].

7. Great-Artery Reconstruction

7.1 Neoaortic Reconstruction

The neoaorta is reconstructed by anastomosing the distal ascending aorta to the former pulmonary root.

Important considerations include:

  • Preserve neoaortic valve competence
  • Avoid distortion of the sinotubular junction
  • Avoid commissural traction
  • Maintain root symmetry
  • Avoid distortion of the coronary buttons by the neoaortic anastomosis

The former pulmonary valve becomes the neoaortic valve. Therefore, neoaortic root geometry has long-term importance. Progressive neoaortic root dilation and neoaortic regurgitation may develop over time, particularly in complex TGA, Taussig–Bing anatomy, aorto-pulmonary diameter mismatch, and patients with associated VSD or arch obstruction [8,10].

7.2 Neopulmonary Reconstruction

The neopulmonary artery is reconstructed using the native aortic root and the pulmonary artery bifurcation. Because the coronary buttons have been removed from the native aortic root, the anterior wall usually requires patch reconstruction. Autologous pericardium is commonly used.

Technical priorities include:

  • Create a wide and smooth anterior patch
  • Avoid narrowing at the supravalvar neopulmonary level
  • Avoid distortion of the branch PA origins
  • Remove or avoid ductal tissue that may contribute to later stenosis
  • Avoid branch PA torsion after Lecompte
  • Ensure no compression after sternal approximation

Pulmonary stenosis, supravalvar neopulmonary narrowing, and branch pulmonary artery obstruction are predictable late complications and should be systematically evaluated during follow-up [4,5,11].

8. Associated Procedures

8.1 VSD Closure

When a significant VSD is present, it is usually closed at the time of ASO.

The VSD closure must:

  • Direct LV outflow to the neoaorta
  • Avoid residual LVOT obstruction
  • Avoid atrioventricular valve distortion
  • Protect the conduction system
  • Avoid residual shunting

In Taussig–Bing anatomy, the VSD is part of the systemic outflow pathway. The baffle must direct left ventricular flow to the neoaorta without creating subaortic obstruction or compromising atrioventricular valve function.

8.2 Aortic Arch Repair

When coarctation or arch hypoplasia coexists, single-stage repair may include:

  • Coarctation resection
  • Extended end-to-end arch reconstruction
  • Patch augmentation in selected cases
  • Ductal tissue excision
  • Cerebral and visceral protection strategies

The arch reconstruction must be planned together with the ASO because arch geometry, neoaortic reconstruction, coronary course, and pulmonary artery alignment are interdependent. Complex TGA with VSD and/or arch obstruction has excellent long-term survival, but late reintervention risk remains higher than in simple d-TGA [1,8].

8.3 Atrial Septal Management

An atrial communication may be enlarged, closed, or partially closed depending on exposure and physiology. Once normal series circulation is restored, a large residual atrial communication is usually unnecessary. However, the atrial septum may require attention if it affects venous drainage, exposure, postoperative filling, or residual shunt physiology.

9. Weaning from Cardiopulmonary Bypass

Before separation from bypass, the team must assess anatomy and physiology.

Key priorities include:

  • Adequate biventricular function
  • Sinus rhythm or stable rhythm
  • Satisfactory coronary perfusion
  • No regional wall-motion abnormality
  • No significant neoaortic regurgitation
  • No LVOT obstruction
  • No significant neopulmonary or branch PA obstruction
  • No important residual VSD
  • No significant bleeding from coronary buttons or patch lines

Coronary insufficiency may present as:

  • ST-segment changes
  • Regional wall-motion abnormality
  • Global ventricular dysfunction
  • Ventricular arrhythmias
  • Low cardiac output
  • Rising lactate
  • Difficulty separating from bypass

If coronary compromise is suspected, it must be addressed immediately. Delayed recognition may be catastrophic.

10. Early Postoperative Management

Early postoperative management focuses on coronary perfusion, ventricular recovery, pulmonary vascular resistance, rhythm, and detection of residual obstruction.

10.1 Coronary Perfusion

Coronary insufficiency is the most feared early complication.

Monitoring includes:

  • Continuous ECG surveillance
  • Assessment of ST-segment changes
  • Serial lactate
  • Ventricular function by echocardiography
  • Regional wall-motion assessment
  • Hemodynamic response to inotropes and afterload changes

Management priorities include:

  • Maintain adequate diastolic pressure
  • Avoid severe hypotension
  • Treat coronary spasm if suspected
  • Maintain sinus rhythm when possible
  • Correct anemia, hypoxemia, and acidosis
  • Investigate persistent ventricular dysfunction urgently

Late coronary events are uncommon but clinically important. Coronary anomalies, single ostium, intramural course, and early postoperative ischemic signs justify particularly vigilant surveillance [5,6,9].

10.2 Pulmonary Vascular Resistance

After ASO, the right ventricle supports the pulmonary circulation. Elevated pulmonary vascular resistance can increase RV afterload and impair cardiac output.

Management includes:

  • Adequate oxygenation
  • Normocapnia
  • Avoidance of acidosis
  • Gentle lung recruitment
  • Appropriate sedation and analgesia
  • Selective pulmonary vasodilators when indicated

10.3 Afterload and Neoaortic Valve Care

Systemic hypertension may increase neoaortic valve stress and bleeding risk, whereas hypotension may compromise coronary perfusion. Postoperative management must balance:

  • Adequate systemic pressure for coronary perfusion
  • Avoidance of excessive afterload
  • Maintenance of ventricular output
  • Protection of neoaortic valve competence

10.4 Rhythm Management

Sinus rhythm supports ventricular filling and coronary perfusion.

Important rhythm issues include:

  • Junctional rhythm
  • Supraventricular tachycardia
  • Ventricular ectopy
  • AV block
  • Ischemia-related arrhythmias

Persistent arrhythmia after ASO should prompt evaluation for myocardial ischemia, electrolyte disturbance, ventricular dysfunction, or residual hemodynamic lesions.

11. Outcomes

Contemporary ASO outcomes are excellent. In a 25-year institutional experience of 618 patients, early mortality was 2.8% and late mortality was 0.9%; reintervention was more frequent in patients with VSD or arch obstruction than in simple TGA [1]. A systematic review of 151 studies reported survival of approximately 92% in the short term, 90% in the medium term, and 87% beyond 20 years [3]. Another long-term series demonstrated survival of 96.6% at 23 years and freedom from reoperation of 81.9% at 23 years [2].

Complex anatomy remains relevant. Anatomical risk factor analysis has shown that complex anatomy, coronary anomalies, and prolonged bypass time are associated with operative mortality or cardiac morbidity [6]. In patients with TGA, VSD, and/or aortic arch obstruction, 25-year conditional survival after ASO was 96.7%, but neoaortic regurgitation and root dilation became important late surveillance targets [8].

Mid-term functional status is generally favorable. In a 155-patient series, late mortality was 2.9%, 18% required surgical or catheter reintervention, and most reinterventions were for right-sided obstruction. At last follow-up, 92% were in functional class I, 95% were free of arrhythmias, and 95% had preserved left ventricular ejection fraction [11].

12. Late Complications and Surveillance Targets

ASO patients require lifelong congenital cardiology follow-up. The major late issues are predictable and should be incorporated into structured surveillance.

12.1 Neopulmonary and Branch PA Obstruction

Neopulmonary stenosis and branch PA stenosis are among the most common causes of reintervention after ASO. Contributing mechanisms include:

  • Lecompte-related branch PA stretching or torsion
  • Supravalvar neopulmonary narrowing
  • Inadequate anterior patch size
  • Residual ductal tissue
  • Pulmonary artery confluence distortion
  • Compression after great-artery reconstruction

Patients with VSD, arch obstruction, or Taussig–Bing anatomy may have higher reintervention risk than those with simple d-TGA [1,8].

12.2 Neoaortic Root Dilation and Neoaortic Regurgitation

The pulmonary root becomes the neoaortic root and is exposed to systemic pressure. Over time, neoaortic root dilation and neoaortic regurgitation may develop.

Risk markers include:

  • Taussig–Bing anatomy
  • VSD
  • Aorto-pulmonary diameter mismatch
  • Prior pulmonary artery banding
  • Early postoperative neoaortic regurgitation
  • Longer follow-up duration
  • Complex TGA with arch obstruction

In complex TGA with VSD and/or arch obstruction, neoaortic regurgitation reached a cumulative incidence of 41.6% at 25 years, and 24.1% of patients had neoaortic root dilation with a sinus z-score ≥3 at last follow-up [8]. These data support continued imaging surveillance into adolescence and adulthood.

12.3 Coronary Complications

Coronary complications are uncommon but potentially catastrophic. They may present early as difficulty separating from bypass, ventricular dysfunction, or arrhythmia, or later as ischemia, ventricular dysfunction, syncope, arrhythmia, or sudden death.

Surveillance is particularly important in patients with:

  • Single coronary ostium
  • Intramural coronary artery
  • High or remote coronary origin
  • Early postoperative ischemia
  • Unexplained ventricular dysfunction
  • Ventricular arrhythmia
  • Symptoms during exercise

Advanced imaging with CT or CMR may be required to define the coronary course and evaluate ostial patency, particularly when echocardiographic windows are insufficient [5,9].

12.4 Aortic Arch Obstruction

In patients requiring arch reconstruction at the time of ASO, residual or recurrent arch obstruction must be monitored. Surveillance should include upper and lower extremity blood pressure assessment, echocardiographic arch gradients, and cross-sectional imaging when arch geometry is unclear.

12.5 Exercise Capacity and Adult Follow-Up

Most ASO survivors have good functional status, but adult follow-up should assess:

  • Exercise capacity
  • Rhythm
  • Coronary perfusion when clinically indicated
  • Neoaortic root dimension
  • Neoaortic valve function
  • Branch PA anatomy
  • Ventricular function
  • Residual arch obstruction

Adult congenital heart disease follow-up is recommended for all ASO patients, with advanced imaging by CT or CMR used selectively to evaluate coronary arteries, great-vessel geometry, and ventricular performance [5,9,12].

13. Follow-Up Program

A structured follow-up program should include:

Echocardiography

  • LV and RV function
  • Neoaortic valve regurgitation
  • Neoaortic root dimension
  • LVOT and RVOT gradients
  • Branch PA flow acceleration
  • Residual VSD
  • Arch gradient when relevant

Cross-Sectional Imaging

CMR or CT can assess:

  • Coronary artery course and patency
  • Neoaortic root and ascending aorta
  • Branch pulmonary artery anatomy
  • RV size and function
  • Arch geometry
  • Pulmonary artery distortion after Lecompte maneuver

Functional Assessment

In later childhood, adolescence, and adulthood:

  • Exercise testing
  • Rhythm monitoring when indicated
  • Symptom assessment
  • Ischemia evaluation when clinically appropriate
  • Lifelong adult congenital heart disease follow-up

14. Special Anatomical Scenarios

14.1 d-TGA with VSD

ASO with VSD closure is appropriate when the VSD can be closed without causing LVOT obstruction or atrioventricular valve distortion. Large VSDs may preserve LV preparedness but may also be associated with pulmonary overcirculation, heart failure, pulmonary hypertension, and more complex outflow anatomy.

14.2 Taussig–Bing Anomaly

Taussig–Bing anomaly is a form of double-outlet right ventricle with subpulmonary VSD and transposition-type physiology. Repair commonly involves:

  • Arterial switch
  • VSD baffling from LV to neoaorta
  • Coronary transfer
  • Lecompte maneuver
  • Relief or prevention of outflow obstruction
  • Arch repair when indicated

These patients may have higher complexity because of VSD geometry, great artery relationship, coronary patterns, and associated arch obstruction. Late surveillance should focus on RVOT/branch PA obstruction, neoaortic regurgitation, neoaortic root dilation, and coronary anatomy [8,12].

14.3 d-TGA with Arch Hypoplasia or Coarctation

When arch obstruction is present, single-stage neonatal repair may be required.

The repair must address:

  • Ventriculo-arterial discordance
  • Coronary transfer
  • Arch obstruction
  • Ductal tissue
  • Cerebral and visceral perfusion strategy
  • Pulmonary artery alignment after Lecompte maneuver

Late surveillance is particularly important because arch obstruction and pulmonary artery stenosis may recur or evolve over time.

15. Core Concept

The arterial switch operation is an anatomical correction, but its success depends on precise technical execution. The most important determinant is safe coronary transfer. The second major determinant is unobstructed reconstruction of both great-artery pathways, particularly the neopulmonary artery and branch pulmonary arteries.

A durable ASO creates:

  • A competent neoaortic valve
  • A tension-free coronary circulation
  • An unobstructed systemic outflow
  • A smooth neopulmonary pathway
  • Symmetric branch pulmonary arteries
  • Stable biventricular function
  • Durable physiology suitable for lifelong surveillance

One-Paragraph Synopsis

The arterial switch operation anatomically corrects d-transposition of the great arteries by switching the great arteries, transferring the coronary arteries to the neoaortic root, and using the Lecompte maneuver to establish an anterior neopulmonary pathway. The operation restores the left ventricle as the systemic ventricle and the right ventricle as the pulmonary ventricle. Contemporary outcomes are excellent, with low early mortality and strong long-term survival, but the operation requires precise coronary transfer and careful reconstruction of both great-artery pathways. Late surveillance should focus on neopulmonary and branch PA obstruction, neoaortic root dilation, neoaortic regurgitation, coronary complications, rhythm, exercise capacity, and residual or recurrent arch obstruction in patients with associated arch repair.

References

[1] Fricke TA, d’Udekem Y, Richardson M, Thuys C, Dronavalli M, Ramsay JM, Wheaton G, Grigg LE, Brizard CP, Konstantinov IE. Outcomes of the arterial switch operation for transposition of the great arteries: 25 years of experience. Ann Thorac Surg. 2012;94(1):139-145.

[2] Lim HG, Kim WH, Lee JR, Kim YJ. Long-term results of the arterial switch operation for ventriculo-arterial discordance. Eur J Cardiothorac Surg. 2013;43(2):325-334.

[3] Morfaw F, Leenus A, Mbuagbaw L, Anderson LN, Dillenburg R, Thabane L. Outcomes after corrective surgery for congenital dextro-transposition of the arteries using the arterial switch technique: a scoping systematic review. Syst Rev. 2020;9(1):231.

[4] Vargo P, Mavroudis C, Stewart RD, Backer CL. Late complications following the arterial switch operation. World J Pediatr Congenit Heart Surg. 2011;2(1):37-42.

[5] Kirzner J, Pirmohamed A, Ginns J, Singh HS. Long-term management of the arterial switch patient. Curr Cardiol Rep. 2018;20(8):68.

[6] Daebritz SH, Nollert G, Sachweh JS, Engelhardt W, von Bernuth G, Messmer BJ. Anatomical risk factors for mortality and cardiac morbidity after arterial switch operation. Ann Thorac Surg. 2000;69(6):1880-1886.

[7] Villafañe J, Lantin-Hermoso MR, Bhatt AB, Tweddell JS, Geva T, Nathan M, Elliott MJ, Vetter VL, Paridon SM, Kochilas LK, Jenkins KJ, Beekman RH, Wernovsky G, Towbin JA. D-transposition of the great arteries: hot topics in the current era of the arterial switch operation. J Am Coll Cardiol. 2014;64(5):498-511.

[8] Baruteau AE, Vergnat M, Kalfa D, Delpey JG, Ly M, Capderou A, Lambert V, Belli E. Long-term outcomes of the arterial switch operation for transposition of the great arteries and ventricular septal defect and/or aortic arch obstruction. Interact Cardiovasc Thorac Surg. 2016;23(2):240-246.

[9] Moe TG, Bardo DME. Long-term outcomes of the arterial switch operation for d-transposition of the great arteries. Prog Cardiovasc Dis. 2018;61(3-4):360-364.

[10] Baruteau AE, Vergnat M, Kalfa D, Delpey JG, Ly M, Capderou A, Lambert V, Belli E. Long-term outcomes of the arterial switch operation for transposition of the great arteries and ventricular septal defect and/or aortic arch obstruction. Interact Cardiovasc Thorac Surg. 2016;23(2):240-246.

[11] Rodríguez Puras MJ, Cabeza-Letrán L, Romero-Vazquiánez M, Santos de Soto J, Hosseinpour R, Gil Fournier M, Alvarez Madrid A, González A, Pérez P, Gallego P. Mid-term morbidity and mortality of patients after arterial switch operation in infancy for transposition of the great arteries. Rev Esp Cardiol. 2014;67(3):181-188.

[12] Villafañe J, Lantin-Hermoso MR, Bhatt AB, Tweddell JS, Geva T, Nathan M, Elliott MJ, Vetter VL, Paridon SM, Kochilas LK, Jenkins KJ, Beekman RH, Wernovsky G, Towbin JA. D-transposition of the great arteries: hot topics in the current era of the arterial switch operation. J Am Coll Cardiol. 2014;64(5):498-511.