Article

PDF
Access to the PDF text
Advertising


Free Article !

Archives of cardiovascular diseases
Volume 110, n° 2
pages 124-134 (février 2017)
Doi : 10.1016/j.acvd.2016.11.002
Received : 29 August 2016 ;  accepted : 4 November 2016
Transposition of the great arteries: Rationale for tailored preoperative management
Transposition des gros vaisseaux : rationnel pour une prise en charge préopératoire sur-mesure
 

Pierre-Emmanuel Séguéla a, b, , François Roubertie c, Bernard Kreitmann c, Philippe Mauriat b, Nadir Tafer b, Zakaria Jalal a, Jean-Benoit Thambo a
a Pediatric and Congenital Cardiology Unit, Bordeaux University Hospital, Bordeaux, France 
b Pediatric Intensive Care Unit, Bordeaux University Hospital, Bordeaux, France 
c Cardiac Surgery Unit, Bordeaux University Hospital, Bordeaux, France 

Corresponding author. Department of Pediatric Cardiology, Hôpital Haut Lévêque, Bordeaux University Hospital, avenue de Magellan, 33600 Pessac, France.
Summary

As preoperative morbi-mortality remains significant, care of newborns with transposition of the great arteries is still challenging. In this review of the literature, we discuss the different treatments that could improve the patient's condition into the preoperative period. Instead of a standardized management, we advocate personalized care of these neonates. Considering the deleterious effects of hypoxia, special attention is given to the use of non-invasive technologies to assess oxygenation of the tissues. As a prolonged preoperative time with low cerebral oxygenation is associated with cerebral injuries, distinguishing neonates who should undergo early surgery from those who could wait longer is crucial and requires full expertise in the management of neonatal congenital heart disease. Finally, to treat these newborns as soon as possible, we support a planned delivery policy for foetuses with transposition of the great arteries.

The full text of this article is available in PDF format.
Résumé

La morbi-mortalité préopératoire des nouveau-nés ayant une transposition des gros vaisseaux est relativement conséquente, ce qui fait que leur prise en charge reste difficile. Dans cette revue de la littérature, nous discutons des différentes thérapeutiques qui peuvent améliorer l’état préopératoire de ces patients. Plutôt qu’un traitement standard, nous prônons une prise en charge personnalisée de ces nouveau-nés. Du fait des effets néfastes de l’hypoxie, une attention toute particulière est portée à l’utilisation de techniques non invasives de monitorage de l’oxygénation tissulaire. Puisque la durée de l’hypoxie cérébrale préopératoire est prédictive de l’intensité des lésions cérébrales, la distinction des nouveau-nés qui doivent pouvoir bénéficier d’une chirurgie précoce de ceux qui peuvent attendre plus longtemps est cruciale. Ceci requiert un niveau d’expertise important dans le domaine des cardiopathies congénitales. Enfin, nous prônons une politique d’accouchement programmée en cas de transposition des gros vaisseaux afin de traiter ces nouveau-nés le plus rapidement possible.

The full text of this article is available in PDF format.

Keywords : Transposition of the great arteries, Prostaglandin, Balloon atrial septostomy, Near-infrared spectroscopy, Arterial switch operation

Mots clés : Transposition des gros vaisseaux, Prostaglandine, Atrioseptostomie, Spectroscopie dans le proche infra-rouge, Switch artériel

Abbreviations : ASO, BAS, CHD, IVS, NIRS, PGE1, PPHN, PVL, rSO2 , TGA, VSD


Introduction

Transposition of the great arteries (TGA) is the most common cyanotic congenital heart defect (CHD) presenting in the neonatal period, accounting for 5–9% of cardiac malformations [1, 2]. In TGA, the ventriculo-arterial connection is discordant, which means that the aorta arises from the morphological right ventricle, and the pulmonary artery arises from the morphological left ventricle (Figure 1). The pulmonary and systemic circulations are therefore in parallel rather than in series. As the deoxygenated blood is recirculated through the body (right ventricle–aorta connection) – whereas the oxygenated blood recirculates through the lungs (left ventricle–pulmonary artery connection) – at least two of the three possible communications between the pulmonary and systemic circulations are obligatory to support early survival: a patent ductus arteriosus, an atrial septal defect (always present during pregnancy) or a ventricular septal defect (VSD) (optional). Thus, TGA can be categorized based on the presence or absence of VSD. Usually, newborns with TGA with an intact ventricular septum (IVS) become cyanotic in the first days of life when the ductus arteriosus closes; among these, patients with reduced mixing opportunities (TGA-IVS with restrictive foramen ovale and/or closure of the ductus arteriosus) become symptomatic with extreme cyanosis early after birth. Leading inevitably to progressive hypoxia and acidosis, TGA is an almost always fatal when left untreated.



Figure 1


Figure 1. 

Schematic representation of transposition of the great arteries with an intact ventricular septum at birth. The aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. Thus, aortic blood saturation is poor and newborns become cyanotic. At birth, two foetal communications exist concomitantly: the foramen ovale and the ductus arteriosus. Ao: aorta; DA: ductus arteriosus; FO: foramen ovale; LV: left ventricle; PA: pulmonary artery; RV: right ventricle.

Zoom

The physiological and anatomical correction of TGA is the finest example of the successful evolution of the surgical treatment of CHD. Indeed, the advent of the arterial switch operation (ASO) allowed better postoperative survival and outcomes than atrial switch procedures [3]. However, and even if data are scarce, preoperative mortality (describing a fatal adverse evolution during the time between birth and surgery) of newborns with TGA ranges from 3.6% to 10.3% [4, 5, 6]. In comparison, in a retrospective study involving 19 European institutions, operative mortality was reported to be 6% [7]. Since the widespread use of balloon atrial septostomy (BAS) and prostaglandin E1 (PGE1) therapy, no new major technique – with the exception of extracorporeal circulatory assistance, which is fortunately rarely used – has improved the postnatal condition of these newborns. Nevertheless, current non-invasive technologies allow us to closely monitor these patients and to identify those who will probably benefit from early surgery. Conversely, ASO can be delayed in certain circumstances. In this review of the literature, we discuss the different aspects of the preoperative management of newborns with TGA.

Foetal considerations

In the normal foetus, oxygen saturation of the umbilical venous blood, which is preferentially directed through the foramen ovale into the left atrium, is about 85% [8] (Figure 2). Left ventricular blood, which is ejected into the ascending aorta, and consequently distributed to the brain, has a saturation of about 65%. In foetuses with TGA, pulmonary arterial blood saturation (ejected by the left ventricle) is very high. On the contrary, oxygen saturation of the blood delivered to the brain is about 45%. Thus, the brains of foetuses with TGA are exposed to a relative chronic hypoxia, which can explain a certain predisposition for neurological injuries after birth [9].



Figure 2


Figure 2. 

Schematic representation of foetal blood circulation in: A. A healthy foetus. Left ventricle ejects high saturated blood into the aorta. The brain receives a blood with a saturation of 65%; B. A foetus with transposition of the great arteries. Right ventricle ejects less oxygenated blood into the aorta. The brain is exposed to a blood with a saturation of 45%.

Zoom

Notwithstanding the fact that in TGA and during foetal life, the pulmonary circulation receives blood with high oxygen saturation, which may act as a vasodilator, persistent pulmonary hypertension of the newborn (PPHN) is relatively frequent. The first hypothesis to explain this is that high saturation of pulmonary blood could reduce the development of pulmonary smooth muscle cells and make pulmonary vessels less reactive to vasoactive stimuli. Secondly, it could be explained by the high saturation of ductal blood, which can induce a prenatal ductal constriction leading to high pulmonary vascular resistance [8].

A restricted foramen ovale was reported in approximately 20% of foetuses with TGA [10]. This restriction – not yet fully understood, but probably due to complex haemodynamic mechanisms affecting atrial filling patterns (pulmonary versus systemic venous returns), ductal arteriosus and/or ductus venous flows – may compromise early survival after birth.

Location of delivery

Despite the use of intravenous PGE1 therapy, early demise of neonates with TGA may occur in 4% and is related to inadequate interatrial communication [4]. In fact, a patent ductus arteriosus allows essentially unidirectional flow either from the aorta to the pulmonary arteries or opposite, according to respective pressure levels. However, in TGA, systemic oxygenation requires mixing, that is to say reciprocal exchanges between the two compartments. Adequate mixing is provided either by a large defect such as atrial septal defect or by the coexistence of two communications. Although prenatal diagnosis of TGA was shown to be efficient in reducing early mortality – by decreasing the required time for BAS – and although several echocardiographic foetal signs were proposed to detect high-risk foetuses, an urgent BAS is mandatory in up to 12% of patients [10, 11, 12]. Accordingly, some surgical centres developed a strategy of planned onsite deliveries to limit neonatal transport [11]. If, obviously, centralization (requiring in utero transport) is advantageous, deficiency of prenatal detection, or large countries with few specialized centres, make this policy sometimes impossible to achieve. When performed by specialist transport teams, long-distance transport (by road or air) of a newborn with TGA can be done relatively safely [13]. Indeed, in two Australian retrospective studies (totalling 234 patients), the reported mortality was 0.04% [13, 14]. BAS was performed before transport in 57% of patients and 54% received PGE1 infusion during transport. Few major complications were encountered and most newborns remain stable [14]. In a cohort of 202 neonates who received PGE1 during transport, a strong predictor of complications was PGE1 dose, with a cutoff of 0.05μg/kg/min [15]. Thus, PGE1 should always be administrated with the lowest effective dose to avoid adverse effects such as hypotension or apnoea. Whereas elective intubation exposes infants to the risk of mechanical malfunction, it is sometimes preferable for them to be intubated before transport [15]. Indeed, the space for potential resuscitation is frequently limited, especially on commercial aircraft [13]. Anyway, as demonstrated in a recent study, children with a prenatal diagnosis had a lower prevalence of preoperative brain injury, probably because of a better neonatal haemodynamic state through early use of PGE1 [16]. This last finding supports a policy of planned delivery in a tertiary centre with expertise in neonatal CHD management. This approach is also supported by the fact that morbidity is higher when admission occurs during the weekend [17].

Balloon atrial septostomy

When the foramen ovale is restrictive or even small, interatrial mixing is insufficient to allow adequate systemic oxygenation. BAS is thus needed to enlarge or create a bidirectional interatrial communication. This manoeuvre was first described in 1966 by Rashkind and consists of a disruption of the atrial septum via the passage of an inflated balloon-tipped catheter from the left to the right atrium through the foramen ovale (Figure 3) [18]. This procedure may be performed either in an intensive care unit under echocardiographic guidance or in the cardiac catheterization laboratory under fluoroscopic guidance, according to the standard practices of the unit. Similarly, either the femoral vein or the umbilical vein can be used for the venous approach. Because systemic anticoagulation is rarely administered during the procedure, BAS has been suspected to induce brain injuries such as intraventricular haemorrhage, white matter injury and periventricular leukomalacia (PVL), by displacing pre-existing thrombi [19]. This initial supposition was subsequently refuted by recent studies [20]. Indeed, in a meta-analysis involving 10,108 neonates with TGA, no association was found between BAS and perioperative brain injuries [21]. Furthermore, it was emphasized that neonates with TGA and restrictive atrial septal defect who require BAS had lower arterial oxygen saturations, lower Apgar scores and a greater incidence of metabolic acidosis [22]. As Petit et al. showed that preoperative brain injuries were associated with hypoxaemia and delay to surgery rather than BAS, these findings may support a relationship between brain vulnerability, postnatal stresses and neurological complications [23]. Consequently, the current trend is to limit BAS to newborns with restrictive foramen ovale, hypoxemia or clinical instability [24, 25]. Because mortality of the procedure can reach 3%, routine BAS is probably not now indicated, but it has to be considered at any time (or weighted against early surgery, see later) if there is any evidence of potential brain and/or somatic risk [26]. Finally, when performed “out-of-hours”, BAS leads to more adverse outcomes; this observation advocates again for a planned delivery policy [27].



Figure 3


Figure 3. 

Balloon atrial septostomy. At birth, when the foramen ovale is restrictive, atrial mixing is inadequate, leading to profound hypoxia. Then, a balloon atrial septostomy is mandatory to enlarge the atrial communication. A. Schematic representation of the manoeuvre. A balloon-tipped catheter is introduced via the inferior vena cava into the right atrium. After passing through the foramen ovale, the balloon is inflated into the left atrium and then pulled across the septum to enlarge the opening. Finally, the balloon is rapidly deflated and the catheter is removed. B. Angiographic images showing the different steps of the manoeuvre.

Zoom

Prostaglandin therapy

Intravenous PGE1, a potent vasodilator, is routinely used for reopening and maintaining the patency of the ductus arteriosus in neonates with TGA. Since its first use in the 1970s, this molecule has dramatically improved the management of neonates with ductal-dependent CHD [28]. Although this therapy is lifesaving in these patients, it has several possible side-effects. Indeed, PGE1 can cause relevant peripheral vasodilation and subsequently hypotension. Because PGE1 is a proinflammatory molecule, fever, leucocytosis and tissue oedema are extremely frequent. Neurological side-effects can result in jitteriness, seizure-like activities and apnoea. Respiratory depression was reported in 12% of neonates, with a higher incidence of apnoea in low-birth-weight neonates (<2.0kg) [29]. This PGE1-associated respiratory depression can be potentiated by the use of sedatives for procedures like BAS. As methylated xanthines such as aminophylline and caffeine citrate were proved to be efficient for reducing the incidence of apnoea, especially in neonates who receive concomitant sedation, these drugs are commonly used to prevent intubation for hypoventilation [30]. Caffeine is usually administered intravenously with a loading dose of 20mg/kg, followed by a 5mg/kg/d maintenance doses [31]. The mechanism of action of xanthines involves competing with adenosine receptors and thus inhibiting the action of adenosine (a sleep-promoting substance) on the central nervous system. Owing to the fact that the side-effects of PGE1 are dose-dependent, the lowest effective dose, which enables maintenance of ductal patency, must be defined for each patient to avoid complications. While in the published literature, PGE1 dose can reach 0.1μg/kg/min, some authors advocate for a very low dose (0.005μg/kg/min) [32]. In practice, an effective dose of 0.02–0.03μg/kg/min is generally administered [33, 34]. Prolonged PGE1 infusion should also be avoided because it is associated with longer preoperative mechanical ventilation and a longer duration of postoperative hospitalization [33, 35]. Long-term PGE1 treatment is also responsible for side-effects such as cortical hyperostosis, gastric-outlet obstruction and pseudo-Bartter syndrome [34]. In addition, tissue oedema may make it harder for a neonate to be weaned postoperatively from the ventilator, as well as impairing wound healing. Thus, withdrawal of PGE1 treatment may always be attempted after BAS. Unfortunately, studies failed to identify predictors of successful withdrawal, and the proportion of infants in whom PGE1 is restarted is approximately 50% [35, 36, 37]. Actually, no relationship was found between the size of the atrial septal defect and the ability to stop PGE1 treatment. As PGE1 was shown to relax pulmonary veins, the changes in pulmonary resistance caused by PGE1 may explain rebound hypoxaemia at discontinuation of the PGE1 infusion after BAS [35, 38, 39]. Another issue of PGE1 therapy is the putative risk of necrotizing enterocolitis associated with enteral feeding. While the physiological and nutritional benefits of early enteral feeding in critical term and pre-term neonates have been well demonstrated, feeding apprehension may persist because of a theoretical risk of intestinal hypoperfusion due to a ductal steal phenomenon [40]. In fact, a retrograde diastolic flow pattern in the descending aorta may potentially result in mesenteric ischaemia. This suspicion was sustained by the fact that in a retrospective study, an increased prevalence of necrotising enterocolitis was found in children with CHD [41]. As a consequence, preoperative nutritional practices vary widely between centres [40]. However, data from recent studies suggested that enteral feeding is well tolerated in ductus-dependent CHD [42, 43, 44]. Consequently, strict avoidance of enteral feeds, in term and pre-term neonates with TGA regardless of PGE1 therapy, seems to be unnecessary in most cases. Moreover, the lack of initiation of enteral feeding before surgery was shown to be significantly correlated with prolonged postoperative course [45]. Surprisingly, a minority of teams base their enteral feeding decisions on the ductal flow direction [42]. In this situation, the use of non-invasive monitoring of oxygen delivery may help to accurately assess haemodynamics and to apply a personalized feeding strategy. Measurement or regional oxygen saturation (rSO2 ) may also indicate the need for fluid loading in this context of frequent capillary leak syndrome (tissue oedema) and its potential subsequent hypovolemia leading to hypotension. Somatic measurements of rSO2 may be done by targeting renal or mesenteric vascular beds [46].

Pulmonary hypertension

PPHN is a critical cyanotic condition that results from the failure of the pulmonary vascular bed to decrease its resistance after birth. PPHN is associated with TGA in 3–12% of patients and accounts for substantial preoperative mortality in newborns with TGA [47, 48, 49]. Indeed, the synergetic combination of TGA and PPHN leads to profound hypoxemia, even in the presence of a wide ductus arteriosus and a successful BAS. The elevation of pulmonary vascular resistance is associated with pulmonary-to-aorta shunting across the ductus arteriosus, therefore decreasing pulmonary blood flow and right-to-left shunting at the atrial level [50]. The right-to-left shunting through the ductus arteriosus can be easily assessed using echocardiography in the colour Doppler mode. In this context, dilation of the ductus arteriosus by PGE1 could be deleterious because it increases ductal right-to-left shunting and consequently decreases the amount of blood bypassing the lungs [51]. Indeed, the systemic oxygen saturation may be decreased with PGE1 infusion, leading to exacerbation of hypoxia and amplification of pulmonary artery constriction. Thus, restricting the ductus arteriosus may be considered in this setting [51]. PPHN is more common among newborns with TGA-IVS compared with those with TGA-VSD [47]. In any case, pharmacological manipulation of the ductus arteriosus must be done with extreme caution, and echocardiographic monitoring, as well as continuous measurements of somatic and cerebral regional saturations and acid/base monitoring, are of crucial importance to guide the management. In PPHN, the pulmonary endothelial and vascular smooth muscle cell dysfunctions may be caused by multiple factors including hypoxia, inflammation and mechanical forces. Several mediating pathways such as endothelin-1, prostacyclin-cGMP, nitric oxide-cAMP, and the vascular endothelial growth factor have been suspected to be responsible for pulmonary vasoconstriction in this context [52, 53, 54, 55, 56].

According to some authors, the preoperative mortality of TGA with PPHN can reach 29% [47]. Usual preoperative management of TGA with PPHN includes adjusted mechanical ventilation, appropriate sedation, neuromuscular blockade, alkalinisation, inotropic support and pulmonary vasodilators [57]. These therapies are targeted to reduce pulmonary vascular resistance and must be started early after birth. Pulmonary vasodilators are mainly represented by iNO, which dramatically improved the prognosis [58]. However, it is well known that approximately 30% of newborns fail to respond, because the mechanism of PPHN appears to be multifactorial. Moreover, airway obstruction or oedema may decrease the response to iNO and atelectasis may cause intrapulmonary shunting and hypoxia, which is worsened by pulmonary vasodilators [47]. Other specific vasodilators such as sildenafil, bosentan or inhaled iloprost have been proposed in this context [59, 60]. In refractory cases and especially if there is ventricular dysfunction, the use of extracorporeal membrane oxygenation may be lifesaving [4, 50, 61]. If some concern existed about “deconditioning” the left ventricle with preoperative extracorporeal membrane oxygenation in TGA, no recent observation has supported this hypothesis. Finally, patients with TGA and PPHN tend to have poor postoperative outcomes compared to TGA with normal pulmonary pressure: ventilatory support and ICU stay are longer, and the need for postoperative extracorporeal membrane oxygenation (with its inherent morbidity) may be more frequent [47, 50].

Preoperative conditions, neurological injuries and neuromonitoring

There is a growing recognition of neurodevelopmental impairments in children with CHD. If initial studies have focused on the responsibility of intraoperative factors – and especially cardiopulmonary bypass – to explain neurological lesions observed in this population [62, 63], recent studies seem to indicate a multifactorial origin. In a cohort of term infants either with TGA (n =13) or hypoplastic left heart syndrome (n =29), Licht et al. showed that before surgery, these newborns have smaller and structurally less mature brains than expected [64]. The total maturation score, a magnetic resonance imaging semiquantitative scoring system, was significantly lower than that in controls of similar gestational age. Moreover, the mean birth head perimeter was one standard deviation below the expected value for age. Basically, infants with TGA have a delay in brain development of approximately 1 month. These findings suggest that TGA produces abnormal foetal physiology that results in impaired cerebral blood flow and oxygen delivery to the developing brain. A recent meta-analysis supports this theory by reporting that 34% of newborns with TGA have brain lesions on neuroimaging before they undergo cardiac surgery [65]. Furthermore, Miller et al. showed that newborns with TGA have white matter injuries similar to those observed in premature newborns [66]. In fact, PVL is a form of white matter disease commonly found both in extreme premature infants and in children with CHD. In pre-terms, PVL is associated with the vulnerability of early differentiating oligodendroglia to perinatal hypoxia induced by immature lung development, oligodendrocytes being the glial cells responsible for central myelination [67, 68]. In neonates with TGA, the cerebral perfusion – therefore oxygen delivery to the brain – may be diminished due to the ductus arteriosus patency (which may be exaggerated with the use of PGE1) [69, 70]. As these neonates may present profound hypoxia and because their glial cells are more vulnerable, they frequently suffer from PVL. In a recent meta-analysis on neonates with TGA who did not undergo BAS, the prevalence of preoperative brain lesions on neuroimaging was 34%, mainly represented by white matter injuries [65]. Furthermore, in a retrospective study, Petit et al. showed that preoperative PVL identified by magnetic resonance imaging was not associated with BAS, but rather was correlated with the severity and the duration of preoperative hypoxia [23]. Because these lesions are responsible for cognitive dysfunction rather than motor incapacity, their incidence is clearly underestimated. Nevertheless, in a prospective magnetic resonance imaging study in 54 adolescents who had undergone ASO in the neonatal period, white matter injuries were found in 31%, higher than for premature infants thought to be at greater risk of PVL [71]. Moreover, neurological status was impaired in 10%, and its severity correlated with the grade of PVL. In this study, preoperative acidosis and hypoxia were the only independent patient-related risk factors for PVL. Hövels-Gürich et al. showed that after neonatal ASO, neurodevelopmental status in school-age children was related to deleterious effects of the perioperative management and particularly to severe preoperative acidosis and hypoxia [72]. These children are also more likely to demonstrate difficulties in exerting cognitive and behavioural inhibition, neurological disorders that are similar to autistic behaviours encountered in very low-birth-weight infants [73, 74].

Near-infrared spectroscopy (NIRS) applies the Beer Lambert law relating photon transmission to concentration of absorbers and scatters in biological tissues. Near-infrared light photons (700–1000nm) are produced by a light-emitting source placed on the patient's skin. The photons penetrate the body tissue of interest and a fraction is reflected toward the detectors. By measuring the quantity of returning photons as a function of wavelength, the spectral absorption of the underlying tissue is measured and the relative amounts of deoxyhaemoglobin and oxyhaemoglobin are calculated, thus giving the rSO2 , which is well correlated with mixed venous oxygen saturation [46, 75]. Cerebral rSO2 (rc SO2 ) depends on both oxygen delivery and brain oxygen consumption. Oxygen delivery is determined by arterial partial pressure of oxygen and cerebral blood flow, which directly depends on cardiac output and cerebral vascular resistance. After full-term birth, rc SO2 rapidly (in the first 15minutes) increases to values between 70% and 80% [76]. In piglets, cerebral anaerobic metabolism occurred with rc SO2 <45%, hypoxic ischaemic injury occurred with rc SO2 <40% and neuronal cell death at a rc SO2 <30% [77]. These data are concordant with the results of a study conducted by Hoffman et al. on neonates with hypoplastic left heart syndrome [78]. Actually, for these children who underwent Norwood stage 1 palliation in the neonatal period, the neurodevelopmental performance was strongly associated with the time spent with rc SO2 <45%. In TGA, this predictive value of preoperative NIRS to predict neurodevelopmental outcomes seems to be of great importance. Van der Laan et al. showed that for children with inadequate mixing defined as above, BAS drastically improves rc SO2 from a median of 42% to a median of 64% [79]. Therefore, a low NIRS value at birth should influence the decision to perform BAS. This improvement in rc SO2 values is also observed after ASO. Uebing et al. monitored 20 patients with TGA 24hours before and 48hours after surgery: rc SO2 rose from 56% before ASO to 80% 48hours after ASO [80]. Moreover, for these patients, the preoperative time spent with low rc SO2 (<35%) was correlated with a lower developmental quotient at 30–36 months of age [81]. Therefore, in case of low rc SO2 , these data suggest a potential benefit of early surgery in order to prevent future neurological complications. Although transcranial ultrasonography is a widely recognised tool for the non-invasive bedside cerebral imaging of the premature/sick full-term newborn, its use has been rarely reported in newborns with TGA [82]. However, in case of patent ductus arteriosus, the steal of blood from the cerebral arteries was described more than 30 years ago [83]. This phenomenon of ductal steal in premature infants was speculated to lead to compromised brain perfusion, therein contributing to cerebral injuries such as intraventricular haemorrhage. Recently, cerebral oxygenation, assessed with NIRS, was reported to be dependent on the diameter of the ductus arteriosus in pre-terms [84]. For children with TGA, assessing blood flow velocity in the cerebral arteries may therefore also guide the preoperative management (Figure 4). As a matter of fact, the detection of an abnormal diastolic retrograde flow can be an additional argument for early surgery. In conclusion, neonates with TGA have an immature brain, which is more sensitive to hypoxia than the brains of healthy newborns. Thereby, a full-term delivery should be always preferred when possible. Precise monitoring of both cerebral perfusion and oxygenation, by transcranial ultrasonography and NIRS, respectively, should influence the decision for BAS and/or surgery and guide the medical and surgical decisions. In this context, we propose a clinical decision algorithm based on these current monitoring technologies (Figure 5).



Figure 4


Figure 4. 

Doppler recordings of the anterior cerebral artery in three full-term newborns with transposition of the great arteries and patent ductus arteriosus. Diastolic velocity depends directly on the importance of ductal steal phenomenon. A. Normal pattern of Doppler velocities in a newborn with small ductal steal phenomenon. Systolic velocities are high. B. Moderate ductal steal phenomenon resulting in null diastolic values. Systolic velocities are high. C. Spectral waveforms showing a reverse diastolic flow confirming a severe ductal steal phenomenon. Systolic velocities are too low.

Zoom



Figure 5


Figure 5. 

Proposal for clinical decision making in newborns with transposition of the great arteries with intact ventricular septum according to current monitoring technologies. Neonates with persistent pulmonary hypertension of the newborn are excluded from this algorithm. ASO: arterial switch operation; BAS: balloon atrial septostomy; FO: foramen ovale; PGE1: prostaglandin E1; rc SO2 : cerebral regional oxygen saturation; rs SO2 : somatic regional oxygen saturation; TGA: transposition of the great arteries; TTE: transthoracic echocardiography; US: ultrasound.

Zoom

Surgery

According to the previously presented discussion, it becomes clear that the preoperative period presents a time of risk for neonates with TGA. It is therefore important to examine its duration. Even for TGA-IVS, there are no formal recommendations and a wide variety of practices is noted. For instance, in a cohort of 1196 patients with TGA-IVS having undergone ASO, the median age at surgery was 6 days and the mean age was 22.9 days (interquartile range 1, 8 days) [85]. The optimal timing for surgery remains controversial. Previously, it was usual to wait until after the first week of life, to improve renal, lung and liver functions. The difficulty lay in the fact that the risk of delayed ASO was thought to be significantly increased beyond 2–3 weeks of age. This was attributed to failure of the left ventricle to support systemic pressures after surgery. Indeed, as pulmonary resistance declined with age, the left ventricle was supposed to undergo preoperative deconditioning, explaining that late ASO was associated with higher mortality [86]. Some authors have considered age>3 weeks to be a contraindication to primary ASO and advocated a two-stage approach, with pulmonary banding as the first stage [87]. According to other studies, such a 3-week delay seemed not to provide excessive mortality [88]. In fact, the ability to use postoperative extracorporeal membrane oxygenation may add safety in performing delayed corrective surgery. Thus, primary ASO may be performed in infants aged 3 to 8 weeks, with comparable outcomes to those in neonates [89]. Nonetheless, late ASO was significantly associated with longer mechanical ventilation and in-hospital stay. Recently, Anderson et al. showed that performing ASO in the very first days of life was strongly associated with better outcomes and reduced hospital costs [17]. Although methodologically questionable (a retrospective study of 140 cases, over a 10-year period, with an operative age ranging from 2–12 days, 97%<10 days), this study is interesting. It is reported that between the age of 1 and 3 days, for every day later the surgery was performed, the odds of a major morbidity decreased by 46% (ranging from 3% to 70%); conversely, for age older than 3 days, for every day later the surgery was performed, the odds of a major morbidity increased by 47% (ranging from 23% to 66%). In this study, as previously discussed, major morbidity was also more frequent when admission occurred during a weekend. To determine which patient could benefit from early surgery, NIRS monitoring seems to be highly interesting. Considering the significant associated neurological morbidity, clinical instability is probably an indication for early surgery. Conversely, a stable haemodynamic status allows waiting for at least several days. In case of cerebral stroke, it is usual to delay ASO for 3–4 weeks to reduce the risk of extension of the neurological damage due to heparinization and cardiopulmonary bypass [90]. All of these notions support the fact that the timing of surgery should likely be adapted for each patient.

Conclusions

After the surgical revolution of ASO and to reduce morbi-mortality – which remains significant – we have now to improve the preoperative care of neonates with TGA. Instead of a standardized course of care, personalized preoperative management seemed to be highly beneficial for these patients. Therefore, as for PGE1 therapy, which should be discussed for each infant, BAS is not always mandatory. If echocardiographic monitoring is still essential both to assess cardiac shunting and to detect a possible ductal steal, multisite NIRS monitoring allows a continuous non-invasive assessment of circulatory states. In these newborns with frequent, profound hypoxia, a two-site NIRS approach (cerebral/somatic) offers early detection of organ-specific oxygen debt. Thus, NIRS should influence the decision for early surgery in case of poor preoperative cerebral oxygenation, a condition associated with neurological injuries. Finally, a specific and coordinated healthcare pathway is required to optimize the preoperative status of these neonates.

Disclosure of interest

The authors declare that they have no competing interest.

References

Ferencz C., Rubin J.D., McCarter R.J., and al. Congenital heart disease: prevalence at livebirth. The Baltimore-Washington Infant Study Am J Epidemiol 1985 ;  121 : 31-36 [cross-ref]
Marek J., Tomek V., Skovranek J., Povysilova V., Samanek M. Prenatal ultrasound screening of congenital heart disease in an unselected national population: a 21-year experience Heart 2011 ;  97 : 124-130 [cross-ref]
Bull C., Yates R., Sarkar D., Deanfield J., de Leval M. Scientific, ethical, and logistical considerations in introducing a new operation: a retrospective cohort study from paediatric cardiac surgery BMJ 2000 ;  320 : 1168-1173 [cross-ref]
Soongswang J., Adatia I., Newman C., Smallhorn J.F., Williams W.G., Freedom R.M. Mortality in potential arterial switch candidates with transposition of the great arteries J Am Coll Cardiol 1998 ;  32 : 753-757 [cross-ref]
Turon-Vinas A., Riverola-de Veciana A., Moreno-Hernando J., and al. Characteristics and outcomes of transposition of great arteries in the neonatal period Rev Esp Cardiol (Engl Ed) 2014 ;  67 : 114-119 [cross-ref]
Garne E., Loane M.A., Nelen V., and al. Survival and health in liveborn infants with transposition of great arteries – a population-based study Congenit Heart Dis 2007 ;  2 : 165-169 [cross-ref]
Sarris G.E., Chatzis A.C., Giannopoulos N.M., and al. The arterial switch operation in Europe for transposition of the great arteries: a multi-institutional study from the European Congenital Heart Surgeons Association J Thorac Cardiovasc Surg 2006 ;  132 : 633-639 [cross-ref]
Rudolph A.M. Aortopulmonary transposition in the fetus: speculation on pathophysiology and therapy Pediatr Res 2007 ;  61 : 375-380 [cross-ref]
Licht D.J., Wang J., Silvestre D.W., and al. Preoperative cerebral blood flow is diminished in neonates with severe congenital heart defects J Thorac Cardiovasc Surg 2004 ;  128 : 841-849 [cross-ref]
Jouannic J.M., Gavard L., Fermont L., and al. Sensitivity and specificity of prenatal features of physiological shunts to predict neonatal clinical status in transposition of the great arteries Circulation 2004 ;  110 : 1743-1746 [cross-ref]
Bonnet D., Coltri A., Butera G., and al. Detection of transposition of the great arteries in fetuses reduces neonatal morbidity and mortality Circulation 1999 ;  99 : 916-918 [cross-ref]
Punn R., Silverman N.H. Fetal predictors of urgent balloon atrial septostomy in neonates with complete transposition J Am Soc Echocardiogr 2011 ;  24 : 425-430 [inter-ref]
Paul S., Resnick S., Gardiner K., Ramsay J.M. Long-distance transport of neonates with transposition of the great arteries for the arterial switch operation: a 26-year Western Australian experience J Paediatr Child Health 2015 ;  51 : 590-594 [cross-ref]
Woods P., Browning Carmo K., Wall M., Berry A. Transporting newborns with transposition of the great arteries J Paediatr Child Health 2013 ;  49 : E68-E73
Meckler G.D., Lowe C. To intubate or not to intubate? Transporting infants on prostaglandin E1 Pediatrics 2009 ;  123 : e25-e30
Peyvandi S., De Santiago V., Chakkarapani E., and al. Association of prenatal diagnosis of critical congenital heart disease with postnatal brain development and the risk of brain injury JAMA Pediatr 2016 ;  170 : e154450
Anderson B.R., Ciarleglio A.J., Hayes D.A., Quaegebeur J.M., Vincent J.A., Bacha E.A. Earlier arterial switch operation improves outcomes and reduces costs for neonates with transposition of the great arteries J Am Coll Cardiol 2014 ;  63 : 481-487 [cross-ref]
Deshpande S., Wolf M.J., Kim D.W., Kirshbom P.M. Simple transposition of the great arteries Pediatric and congenital cardiology, cardiac surgery and intensive care London: Springer-Verlag (2014).  1919-1939
McQuillen P.S., Hamrick S.E., Perez M.J., and al. Balloon atrial septostomy is associated with preoperative stroke in neonates with transposition of the great arteries Circulation 2006 ;  113 : 280-285 [cross-ref]
Applegate S.E., Lim D.S. Incidence of stroke in patients with d-transposition of the great arteries that undergo balloon atrial septostomy in the University Healthsystem Consortium Clinical Data Base/Resource Manager Catheter Cardiovasc Interv 2010 ;  76 : 129-131 [cross-ref]
Polito A., Ricci Z., Fragasso T., Cogo P.E. Balloon atrial septostomy and pre-operative brain injury in neonates with transposition of the great arteries: a systematic review and a meta-analysis Cardiol Young 2012 ;  22 : 1-7 [cross-ref]
Doshi H., Venugopal P., MacArthur K. Does a balloon atrial septostomy performed before arterial switch surgery increase adverse neurological outcomes? Interact Cardiovasc Thorac Surg 2012 ;  15 : 141-143 [cross-ref]
Petit C.J., Rome J.J., Wernovsky G., and al. Preoperative brain injury in transposition of the great arteries is associated with oxygenation and time to surgery, not balloon atrial septostomy Circulation 2009 ;  119 : 709-716 [cross-ref]
Hornung T.S., O'Sullivan J.J. Should we standardise the pre-operative management of babies with complete transposition? Cardiol Young 2000 ;  10 : 458-460
Lorts A., Krawczeski C.D. Perioperative care of a child with transposition of the great arteries Curr Treat Options Cardiovasc Med 2011 ;  13 : 456-463 [cross-ref]
Campbell B. Interventional Procedure Consultation Document – balloon or blade atrial septostomy in neonates  : National Institute for clinical excellence (2011). 
Vimalesvaran S., Ayis S., Krasemann T. Balloon atrial septostomy performed “out-of-hours”: effects on the outcome Cardiol Young 2013 ;  23 : 61-67 [cross-ref]
Elliott R.B., Starling M.B., Neutze J.M. Medical manipulation of the ductus arteriosus Lancet 1975 ;  1 : 140-142 [cross-ref]
Lewis A.B., Freed M.D., Heymann M.A., Roehl S.L., Kensey R.C. Side effects of therapy with prostaglandin E1 in infants with critical congenital heart disease Circulation 1981 ;  64 : 893-898 [cross-ref]
Lim D.S., Kulik T.J., Kim D.W., Charpie J.R., Crowley D.C., Maher K.O. Aminophylline for the prevention of apnea during prostaglandin E1 infusion Pediatrics 2003 ;  112 : e27-e29
Park H.W., Lim G., Chung S.H., Chung S., Kim K.S., Kim S.N. Early caffeine use in very low birth weight infants and neonatal outcomes: a systematic review and meta-analysis J Korean Med Sci 2015 ;  30 : 1828-1835 [cross-ref]
Yucel I.K., Cevik A., Bulut M.O., and al. Efficacy of very low-dose prostaglandin E1 in duct-dependent congenital heart disease Cardiol Young 2015 ;  25 : 56-62 [cross-ref]
Butts R.J., Ellis A.R., Bradley S.M., Hulsey T.C., Atz A.M. Effect of prostaglandin duration on outcomes in transposition of the great arteries with intact ventricular septum Congenit Heart Dis 2012 ;  7 : 387-391 [cross-ref]
Talosi G., Katona M., Turi S. Side-effects of long-term prostaglandin E(1) treatment in neonates Pediatr Int 2007 ;  49 : 335-340 [cross-ref]
Beattie L.M., McLeod K.A. Prostaglandin E2 after septostomy for simple transposition Pediatr Cardiol 2009 ;  30 : 447-451 [cross-ref]
Oxenius A., Hug M.I., Dodge-Khatami A., Cavigelli-Brunner A., Bauersfeld U., Balmer C. Do predictors exist for a successful withdrawal of preoperative prostaglandin E(1) from neonates with d-transposition of the great arteries and intact ventricular septum? Pediatr Cardiol 2010 ;  31 : 1198-1202 [cross-ref]
Finan E., Mak W., Bismilla Z., McNamara P.J. Early discontinuation of intravenous prostaglandin E1 after balloon atrial septostomy is associated with an increased risk of rebound hypoxemia J Perinatol 2008 ;  28 : 341-346 [cross-ref]
Jones R.L., Qian Y., Wong H.N., Chan H., Yim A.P. Prostanoid action on the human pulmonary vascular system Clin Exp Pharmacol Physiol 1997 ;  24 : 969-972 [cross-ref]
Walch L., Labat C., Gascard J.P., de Montpreville V., Brink C., Norel X. Prostanoid receptors involved in the relaxation of human pulmonary vessels Br J Pharmacol 1999 ;  126 : 859-866 [cross-ref]
Howley L.W., Kaufman J., Wymore E., and al. Enteral feeding in neonates with prostaglandin-dependent congenital cardiac disease: international survey on current trends and variations in practice Cardiol Young 2012 ;  22 : 121-127 [cross-ref]
McElhinney D.B., Hedrick H.L., Bush D.M., and al. Necrotizing enterocolitis in neonates with congenital heart disease: risk factors and outcomes Pediatrics 2000 ;  106 : 1080-1087 [cross-ref]
Willis L., Thureen P., Kaufman J., Wymore E., Skillman H., da Cruz E. Enteral feeding in prostaglandin-dependent neonates: is it a safe practice? J Pediatr 2008 ;  153 : 867-869 [inter-ref]
Iannucci G.J., Oster M.E., Mahle W.T. Necrotising enterocolitis in infants with congenital heart disease: the role of enteral feeds Cardiol Young 2013 ;  23 : 553-559 [cross-ref]
Becker K.C., Hornik C.P., Cotten C.M., and al. Necrotizing enterocolitis in infants with ductal-dependent congenital heart disease Am J Perinatol 2015 ;  32 : 633-638
Wheeler D.S., Dent C.L., Manning P.B., Nelson D.P. Factors prolonging length of stay in the cardiac intensive care unit following the arterial switch operation Cardiol Young 2008 ;  18 : 41-50
Scott J.P., Hoffman G.M. Near-infrared spectroscopy: exposing the dark (venous) side of the circulation Paediatr Anaesth 2014 ;  24 : 74-88 [cross-ref]
Roofthooft M.T., Bergman K.A., Waterbolk T.W., Ebels T., Bartelds B., Berger R.M. Persistent pulmonary hypertension of the newborn with transposition of the great arteries Ann Thorac Surg 2007 ;  83 : 1446-1450 [cross-ref]
Kumar A., Taylor G.P., Sandor G.G., Patterson M.W. Pulmonary vascular disease in neonates with transposition of the great arteries and intact ventricular septum Br Heart J 1993 ;  69 : 442-445 [cross-ref]
El-Segaier M., Hellstrom-Westas L., Wettrell G. Nitric oxide in neonatal transposition of the great arteries Acta Paediatr 2005 ;  94 : 912-916 [cross-ref]
Sallaam S., Natarajan G., Aggarwal S. Persistent pulmonary hypertension of the newborn with D-transposition of the great arteries: management and prognosis Congenit Heart Dis 2016 ;  11 : 239-244 [cross-ref]
Masutani S., Seki M., Taketazu M., Senzaki H. Successful management of the persistent pulmonary hypertension of the newborn with transposition of the great arteries by restricted patency of the ductus arteriosus: a simple and rational novel strategy Pediatr Cardiol 2009 ;  30 : 1003-1005 [cross-ref]
Endo A., Ayusawa M., Minato M., Takada M., Takahashi S., Harada K. Endogenous nitric oxide and endothelin-1 in persistent pulmonary hypertension of the newborn Eur J Pediatr 2001 ;  160 : 217-222 [cross-ref]
Ivy D.D., Ziegler J.W., Dubus M.F., Fox J.J., Kinsella J.P., Abman S.H. Chronic intrauterine pulmonary hypertension alters endothelin receptor activity in the ovine fetal lung Pediatr Res 1996 ;  39 : 435-442 [cross-ref]
Mata-Greenwood E., Grobe A., Kumar S., Noskina Y., Black S.M. Cyclic stretch increases VEGF expression in pulmonary arterial smooth muscle cells via TGF-beta1 and reactive oxygen species: a requirement for NAD(P)H oxidase Am J Physiol Lung Cell Mol Physiol 2005 ;  289 : L288-L289
Mata-Greenwood E., Meyrick B., Soifer S.J., Fineman J.R., Black S.M. Expression of VEGF and its receptors Flt-1 and Flk-1/KDR is altered in lambs with increased pulmonary blood flow and pulmonary hypertension Am J Physiol Lung Cell Mol Physiol 2003 ;  285 : L222-L231
Geiger R., Berger R.M., Hess J., Bogers A.J., Sharma H.S., Mooi W.J. Enhanced expression of vascular endothelial growth factor in pulmonary plexogenic arteriopathy due to congenital heart disease J Pathol 2000 ;  191 : 202-207 [cross-ref]
Chang A.C., Wernovsky G., Kulik T.J., Jonas R.A., Wessel D.L. Management of the neonate with transposition of the great arteries and persistent pulmonary hypertension Am J Cardiol 1991 ;  68 : 1253-1255 [cross-ref]
Luciani G.B., Chang A.C., Starnes V.A. Surgical repair of transposition of the great arteries in neonates with persistent pulmonary hypertension Ann Thorac Surg 1996 ;  61 : 800-805 [cross-ref]
Goissen C., Ghyselen L., Tourneux P., and al. Persistent pulmonary hypertension of the newborn with transposition of the great arteries: successful treatment with bosentan Eur J Pediatr 2008 ;  167 : 437-440 [cross-ref]
Avila-Alvarez A., Bravo-Laguna M.C., Bronte L.D., Del Cerro M.J. Inhaled iloprost as a rescue therapy for transposition of the great arteries with persistent pulmonary hypertension of the newborn Pediatr Cardiol 2013 ;  34 : 2027-2029 [cross-ref]
Jaillard S., Belli E., Rakza T., and al. Preoperative ECMO in transposition of the great arteries with persistent pulmonary hypertension Ann Thorac Surg 2005 ;  79 : 2155-2158 [cross-ref]
Bellinger D.C., Wypij D., du Plessis A.J., and al. Developmental and neurologic effects of alpha-stat versus pH-stat strategies for deep hypothermic cardiopulmonary bypass in infants J Thorac Cardiovasc Surg 2001 ;  121 : 374-383 [cross-ref]
Bellinger D.C., Wypij D., duPlessis A.J., and al. Neurodevelopmental status at eight years in children with dextro-transposition of the great arteries: the Boston Circulatory Arrest Trial J Thorac Cardiovasc Surg 2003 ;  126 : 1385-1396 [cross-ref]
Licht D.J., Shera D.M., Clancy R.R., and al. Brain maturation is delayed in infants with complex congenital heart defects J Thorac Cardiovasc Surg 2009 ;  137 : 529-536[discussion 36–7].  [cross-ref]
Khalil A., Suff N., Thilaganathan B., Hurrell A., Cooper D., Carvalho J.S. Brain abnormalities and neurodevelopmental delay in congenital heart disease: systematic review and meta-analysis Ultrasound Obstet Gynecol 2014 ;  43 : 14-24 [cross-ref]
Miller S.P., McQuillen P.S., Hamrick S., and al. Abnormal brain development in newborns with congenital heart disease N Engl J Med 2007 ;  357 : 1928-1938 [cross-ref]
Salmaso N., Jablonska B., Scafidi J., Vaccarino F.M., Gallo V. Neurobiology of premature brain injury Nat Neurosci 2014 ;  17 : 341-346 [cross-ref]
Overby P. Neurologic complications and neuromonitoring in pediatric congenital heart disease Pediatric and congenital cardiology, cardiac surgery and intensive care London: Springer-Verlag (2014).  3299-3307
Miller S.P., McQuillen P.S., Vigneron D.B., and al. Preoperative brain injury in newborns with transposition of the great arteries Ann Thorac Surg 2004 ;  77 : 1698-1706 [cross-ref]
Back S.A., Riddle A., McClure M.M. Maturation-dependent vulnerability of perinatal white matter in premature birth Stroke 2007 ;  38 : 724-730 [cross-ref]
Heinrichs A.K., Holschen A., Krings T., and al. Neurologic and psycho-intellectual outcome related to structural brain imaging in adolescents and young adults after neonatal arterial switch operation for transposition of the great arteries J Thorac Cardiovasc Surg 2014 ;  148 : 2190-2199 [cross-ref]
Hovels-Gurich H.H., Seghaye M.C., Schnitker R., and al. Long-term neurodevelopmental outcomes in school-aged children after neonatal arterial switch operation J Thorac Cardiovasc Surg 2002 ;  124 : 448-458 [cross-ref]
Calderon J., Bonnet D., Courtin C., Concordet S., Plumet M.H., Angeard N. Executive function and theory of mind in school-aged children after neonatal corrective cardiac surgery for transposition of the great arteries Dev Med Child Neurol 2010 ;  52 : 1139-1144 [cross-ref]
Limperopoulos C., Bassan H., Sullivan N.R., and al. Positive screening for autism in ex-preterm infants: prevalence and risk factors Pediatrics 2008 ;  121 : 758-765 [cross-ref]
Nagdyman N., Ewert P., Peters B., Miera O., Fleck T., Berger F. Comparison of different near-infrared spectroscopic cerebral oxygenation indices with central venous and jugular venous oxygenation saturation in children Paediatr Anaesth 2008 ;  18 : 160-166
Pichler G., Binder C., Avian A., Beckenbach E., Schmolzer G.M., Urlesberger B. Reference ranges for regional cerebral tissue oxygen saturation and fractional oxygen extraction in neonates during immediate transition after birth J Pediatr 2013 ;  163 : 1558-1563 [inter-ref]
Kurth C.D., Levy W.J., McCann J. Near-infrared spectroscopy cerebral oxygen saturation thresholds for hypoxia-ischemia in piglets J Cereb Blood Flow Metab 2002 ;  22 : 335-341 [cross-ref]
Hoffman G.M., Brosig C.L., Mussatto K.A., Tweddell J.S., Ghanayem N.S. Perioperative cerebral oxygen saturation in neonates with hypoplastic left heart syndrome and childhood neurodevelopmental outcome J Thorac Cardiovasc Surg 2013 ;  146 : 1153-1164 [cross-ref]
van der Laan M.E., Verhagen E.A., Bos A.F., Berger R.M., Kooi E.M. Effect of balloon atrial septostomy on cerebral oxygenation in neonates with transposition of the great arteries Pediatr Res 2013 ;  73 : 62-67 [cross-ref]
Uebing A., Furck A.K., Hansen J.H., and al. Perioperative cerebral and somatic oxygenation in neonates with hypoplastic left heart syndrome or transposition of the great arteries J Thorac Cardiovasc Surg 2011 ;  142 : 523-530 [cross-ref]
Toet M.C., Flinterman A., Laar I., and al. Cerebral oxygen saturation and electrical brain activity before, during, and up to 36hours after arterial switch procedure in neonates without pre-existing brain damage: its relationship to neurodevelopmental outcome Exp Brain Res 2005 ;  165 : 343-350 [cross-ref]
van Wezel-Meijler G., Steggerda S.J., Leijser L.M. Cranial ultrasonography in neonates: role and limitations Semin Perinatol 2010 ;  34 : 28-38 [cross-ref]
Perlman J.M., Hill A., Volpe J.J. The effect of patent ductus arteriosus on flow velocity in the anterior cerebral arteries: ductal steal in the premature newborn infant J Pediatr 1981 ;  99 : 767-771 [cross-ref]
Dix L., Molenschot M., Breue J., and al. Cerebral oxygenation and echocardiographic parameters in preterm neonates with a patent ductus arteriosus: an observational study Arch Dis Child Fetal Neonatal Ed 2016 ;  101 (6) : F520-F526
Jacobs J.P., Jacobs M.L., Mavroudis C., and al. Transposition of the great arteries: lessons learned about patterns of practice and outcomes from the congenital heart surgery database of the society of thoracic surgeons World J Pediatr Congenit Heart Surg 2011 ;  2 : 19-31 [cross-ref]
Norwood W.I., Dobell A.R., Freed M.D., Kirklin J.W., Blackstone E.H. Intermediate results of the arterial switch repair. A 20-institution study J Thorac Cardiovasc Surg 1988 ;  96 : 854-863
Lacour-Gayet F., Piot D., Zoghbi J., and al. Surgical management and indication of left ventricular retraining in arterial switch for transposition of the great arteries with intact ventricular septum Eur J Cardiothorac Surg 2001 ;  20 : 824-829 [cross-ref]
Kang N., de Leval M.R., Elliott M., and al. Extending the boundaries of the primary arterial switch operation in patients with transposition of the great arteries and intact ventricular septum Circulation 2004 ;  110 : II123-II127
Edwin F., Mamorare H., Brink J., Kinsley R. Primary arterial switch operation for transposition of the great arteries with intact ventricular septum – is it safe after three weeks of age? Interact Cardiovasc Thorac Surg 2010 ;  11 : 641-644 [cross-ref]
Eagle K.A., Guyton R.A., Davidoff R., and al. ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery) Circulation 2004 ;  110 : e340-e437



© 2016  Elsevier Masson SAS. All Rights Reserved.
EM-CONSULTE.COM is registrered at the CNIL, déclaration n° 1286925.
As per the Law relating to information storage and personal integrity, you have the right to oppose (art 26 of that law), access (art 34 of that law) and rectify (art 36 of that law) your personal data. You may thus request that your data, should it be inaccurate, incomplete, unclear, outdated, not be used or stored, be corrected, clarified, updated or deleted.
Personal information regarding our website's visitors, including their identity, is confidential.
The owners of this website hereby guarantee to respect the legal confidentiality conditions, applicable in France, and not to disclose this data to third parties.
Close
Article Outline