EJCTS Click here for details of sales representative
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

 Click here to read this article as a CME activity

Eur J Cardiothorac Surg 2008;34:711-717. doi:10.1016/j.ejcts.2008.06.019
Copyright © 2008, European Association for Cardio-thoracic Surgery. Published by Elsevier. All rights reserved.
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Julie Cleuziou
Klaus Holper
Christian Schreiber
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lange, R.
Right arrow Articles by Schreiber, C.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Lange, R.
Right arrow Articles by Schreiber, C.
Related Collections
Right arrow Congenital - acyanotic
Right arrow Great vessels

Risk factors for aortic insufficiency and aortic valve replacement after the arterial switch operation

Rüdiger Langea,1, Julie Cleuzioua,1,*, Jürgen Hörera, Klaus Holpera, Manfred Vogtb, Peter Tassani-Prellc, Christian Schreibera

a Department of Cardiovascular Surgery, German Heart Centre Munich, Technische Universität München, Munich, Germany
b Department of Paediatric Cardiology and Congenital Heart Disease, German Heart Centre Munich, Technische Universität München, Munich, Germany
c Department of Anaesthesia, German Heart Centre Munich, Technische Universität München, Munich, Germany

Received 11 September 2007; received in revised form 2 June 2008; accepted 11 June 2008.

* Corresponding author. Address: Department of Cardiovascular Surgery, German Heart Centre Munich, Lazarettstrasse 36, D-80636 Munich, Germany. Tel.: +49 89 12 18 4111; fax: +49 89 12 18 4123. (Email: cleuziou{at}dhm.mhn.de).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 Appendix A
 References
 
Objective: Long-term results after the arterial switch operation have shown that patients may develop aortic insufficiency, and that some even require aortic valve replacement. Methods: A retrospective review of 479 hospital survivors after the arterial switch operation (ASO) was performed. Echocardiographic findings were reviewed and the incidence, as well as the progression, of aortic insufficiency (AI) was investigated. The combined end point of the study was defined as the first documented occurrence of moderate or more aortic insufficiency or the need for aortic valve replacement (AVR). Results: Upon discharge from the hospital 15% of the patients showed an AI of at least grade I, progressing to 20.7% after 1 year. At a mean follow-up time of 9.3 ± 6 years, 249 patients (53%) were free from AI, trivial AI was present 179 patients (38%), mild AI in 34 patients (7.2%) and moderate AI in 7 patients (1.5%). There is a progression of AI with time after ASO (r = 0.26, p < 0.001). A total of 18 patients reached the combined end point, out of which 11 underwent an AVR at a mean time of 11.2 years after ASO. Freedom from the end point was 99.7 ± 0.3%, 97.5 ± 1%, 91.9 ± 2%, 84.6 ± 6% at 5, 10, 15 and 20 years, respectively. The following risk factors were identified by univariate analysis: Taussig-Bing anomaly (p = 0.01), ventricular septal defect (VSD) (p = 0.006), prior pulmonary artery banding (p = 0.004), age over 12 months at time of ASO (p = 0.001) and a postoperative incidence of trivial AI (p < 0.0001). Independent risk factors by multivariate analysis were the presence of a left ventricular outflow tract obstruction (p < 0.0001) and at least a trivial AI at 1 year after the ASO (p < 0.0001). Conclusion: The incidence of trivial or mild AI after the ASO is considerable and a progression over time is evident. However, severe AI and the need for AVR are rare. Patients with VSD or Taussig-Bing anomaly, and those with left ventricular outflow tract obstruction exhibit a higher risk of developing significant aortic insufficiency. Particularly patients who have developed an AI at 1 year after the ASO need to be under close observation.

Key Words: Transposition of the great arteries • Aortic insufficiency • Arterial switch operation • Congenital heart defect


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 Appendix A
 References
 
The arterial switch operation (ASO) has been well established as the procedure of choice for the anatomical repair of the transposition of the great arteries (TGA). Long-term studies with large numbers of patients [1–4] have confirmed good long-term results with excellent quality of life. However, based on the experience of more than 20 years, specific long-term morbidity now comes to light and needs to be addressed and analysed [5–7]. The occasional occurrence of aortic root dilatation and the development of aortic insufficiency (AI) have been noticed, but the impact of this late complication is still unclear [8,9]. Furthermore, the potential need for a reoperation on the neoaortic valve could entail a surplus of morbidity [10,11]. Therefore, we analysed our long-term results after the ASO, with special emphasis on the incidence and progression of AI. The goal of this study was to determine risk factors associated with the combined end point of moderate or more AI or aortic valve replacement (AVR) after the ASO.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 Appendix A
 References
 
2.1 Patients
From 1983 to December 2006 a total of 512 patients underwent an ASO at the German Heart Centre Munich. Thirty-three patients (6.4%) died in hospital after the ASO and were not included in this study.

2.2 Operative data
The ASO was performed routinely with systemic hypothermia and low-flow perfusion. Until 1990, coronary reimplantation was performed according to the technique described by Quaegebeur et al. [12], named as the ‘button technique.’ After that, we switched exclusively to the ‘trap-door technique’ for coronary transfer. Thereby, two ‘trap-doors’ are incised in the neo-aorta leaving a complete circular ring of intact tissue below the suture line. Both coronary arteries are implanted into the neo-aorta through these ‘trap-doors’, so that they are re-implanted below the suture line of the aorta. The LeCompte maneuver was performed in all patients where the aortic position made it feasible. Since 1990, the pulmonary artery has been reconstructed with a pantaloon patch using glutaraldehyde preserved autologous pericardium. Before that, either a direct anastomosis had been performed or the pulmonary artery was augmented with two separate autologous pericardial patches. Operative data were obtained by reviewing the operative notes of all patients, especially focusing on morphological characteristics of the native pulmonary valve, the position of the aorta to the pulmonary artery, and the reimplantation technique of the coronary arteries as well as the reconstruction of the pulmonary artery.

2.3 Follow-up
Follow-up data were obtained by reviewing the patient charts and by contacting the referring paediatric cardiologist. Echocardiographic assessment was carried out postoperatively before discharge from the hospital and then yearly. Patients were followed-up either at the German Heart Centre Munich or at another paediatric cardiological centre. The quantification of AI was evaluated by colour Doppler imaging and graded as none (grade 0), trivial (grade I), mild (grade II), moderate (grade III) or severe (grade IV). Upon the first occurrence on echocardiography, a new onset of AI was assumed. Quantification was based on the following parameters: trivial aortic insufficiency (grade I): jet length less than one third of left ventricle (LV) length, LV normal sized. Mild aortic insufficiency (grade II): jet length one half of LV length, vena contracta less than 10% of aortic valve annulus diameter, no diastolic regurgitation from descending aorta. Moderate aortic insufficiency (grade III): jet length to the apex of LV, LV diameter normal or slightly enlarged, vena contracta less than 10–20% of aortic valve annulus, early to mid-diastolic regurgitation from descending aorta. Severe aortic insufficiency (grade IV): broad jet to the LV apex, LV diameter dilated, function hypercontractile or diminished, vena contracta >20% of aortic valve annulus, holodiastolic regurgitation from descending aorta [13]. Echocardiographic data were only used for analysis if there were at least two postoperative echocardiograms available. This was the case for 445 patients. A total of 2040 echocardiographic assessments were used for analysis of postoperative AI.

2.4 Statistical analysis
Descriptive statistics are described as frequencies and percentages for categorical variables and as medians with ranges or means with standard deviation for continuous variables. The univariate analysis was done using a univariate Cox regression analysis to estimate the probability of reaching the end point of moderate or more AI or AVR after ASO for each risk factor. The estimate started at time of the ASO and patients who did not reach the end point were censored at time of follow-up. Each variable reaching a statistic significance of <0.05 was analysed in a multivariate Cox regression model. Because of the high degree of covariance of variables, this analysis was performed repeatedly, removing variables stepwise, to find the most important risk factor. A correlation between the progression of aortic insufficiency and time was obtained for all patients who had at least two postoperative echocardiographic assessments using the Spearman correlation coefficient. Statistical analysis was done using SPSS statistical software (Version 15.0.1, SPSS Inc., Chicago, IL).


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 Appendix A
 References
 
3.1 Patients
From the 479 survivors, 302 (63%) presented with transposition of the great arteries (TGA) and intact ventricular septum (IVS), 141 (29.4%) with TGA and ventricular septal defect (VSD) and 36 (7.5%) with either a Taussig-Bing anomaly (TB) or another complex anatomy with double outlet right ventricle (DORV). Mean age at time of ASO was 11 days (range 2 days–13.5 years); mean weight was 3.5 kg (2.1–57 kg). Associated cardiac anomalies were present in 83 patients (17%); 43 (9%) of these presented with an obstruction of the aortic arch and 9 (2%) with obstruction of the left ventricular outflow tract (LVOTO). Prior to ASO, surgery had been performed in 61 patients (13%), pulmonary artery banding being the most common in 47 patients (10%), either as a unique surgical procedure or combined with an atrial septectomy, or the repair of an aortic obstruction or the placement of a systemic-to-pulmonary artery shunt. A morphological tricuspid native pulmonary valve was found in 449 patients (94%), a bicuspid valve in 21 patients (4%), a quadricuspid valve in 2 patients (0.4%) and a dysplastic valve in one patient. Demographic data of the patients are depicted in Table 1 .


View this table:
[in this window]
[in a new window]

  		Table 1 Demographic data of 479 hospital survivors undergoing the arterial switch operation
 
3.2 Incidence of aortic insufficiency and aortic valve replacement
After ASO, at time of discharge from the hospital, a total of 72 patients (15%) showed an AI of grade I or more. One year after ASO the rate of trivial AI had increased to 20.7% (99 patients). At a mean follow-up time of 9.3 ± 6 years (median 9.3 years), 249 patients (53%) were free from AI, trivial AI (grade I) was present in 179 patients (38%), mild AI (grade II) in 34 patients (7.2%) and moderate AI (grade III) in 7 patients (1.5%). At any time during follow-up, 272 patients (57%) showed an AI of at grade I or more, whereas 64 patients (13.4%) of grade II or more. Fig. 1 shows the development and progression of AI over a period of 20 years after ASO including a total of 2040 echocardiographic observations. There is a steady increase in AI over time (p < 0.001). Patients with TB/DORV had a higher incidence of developing moderate or more AI (n = 3, 8.3%) or requiring AVR (n = 3, 8.3%) over time (p = 0.01). No patient with TGA IVS exhibited more than mild AI at last follow-up and 4 (1.3%) required AVR (p = 0.003). Four patients (2.8%) with TGA + VSD showed moderate or more AI at last follow-up and another four underwent AVR after ASO (p = 0.1). Although in our patient population, there were only nine patients with associated LVOTO, one of them (11%) required AVR and another patient developed moderate AI at 7.6 years after ASO (p = 0.005).


Figure 1
View larger version (21K):
[in this window]
[in a new window]

  		Fig. 1. Box plot showing the development of aortic insufficiency over time. The boxes represent 2040 observations of AI in 479 patients after the arterial switch operation.

 
Aortic valve replacement was necessary in 11 patients (2.3%) at a mean time of 11 ± 4 years after ASO (Table 2 ). Four patients underwent isolated aortic valve replacement with a mechanical valve prosthesis. As an additional procedure to AVR, two patients had relief of a supravalvar aortic stenosis with a patch, one patient had replacement of the ascending aorta with a mechanical composite valved conduit, one patient had resection of a LVOTO, one patient had replacement of the mitral valve, and another patient had a conduit placement between the right ventricle and the pulmonary artery. The latter patient and another patient who underwent an isolated reduction of a large ascending aorta without replacement of the aortic valve, were followed-up at another cardiac centre and reoperated there.


View this table:
[in this window]
[in a new window]

  		Table 2 Postoperative occurrence of aortic insufficiency and aortic valve replacement for 479 hospital survivors after the arterial switch operation
 
Two patients died after AVR. One of them presented with severe AI and additional severe mitral regurgitation and consecutive advanced dilatation of the left ventricle with severely impaired left ventricular function. During preoperative cardiac catheterisation the patient went into cardiogenic shock, cardiopulmonary resuscitation was necessary and the patient died eventually after emergency replacement of the aortic and mitral valve in multiorgan failure. The second patient died suddenly 2 years after AVR at home without any prodromi. Both patients had a TGA + VSD.

Freedom from moderate or more AI or AVR was 99.7 ± 0.3%, 97.5 ± 1%, 91.9 ± 2%, 84.6 ± 6% at 5, 10, 15 and 20 years, respectively (Fig. 2 ). Comparing the patients according to their initial pathology, patients with TB/DORV exhibited the highest likelihood of developing AI (p < 0.001, compared to TGA IVS and p < 0.04, compared to TGA + VSD). Patients with TGA IVS and TGA + VSD also differed significantly in freedom from moderate or more AI or AVR (p = 0.02). At 5, 10, 15 and 20 years after ASO, freedom from moderate or more AI or AVR was 99.3 ± 0.7%, 97.2 ± 2% and 77.7 ± 17% for TGA IVS; 99 ± 1%, 94.9 ± 2%, 88.3 ± 4% and 83.1 ± 6% for TGA+VSD; and 96.2 ± 4%, 92 ± 5%, 71 ± 12% and 60.8 ± 14% for TB/DORV, respectively (Fig. 3 ).


Figure 2
View larger version (10K):
[in this window]
[in a new window]

  		Fig. 2. Freedom from moderate or more AI or AVR for 479 survivors after the arterial switch operation.

 

Figure 3
View larger version (17K):
[in this window]
[in a new window]

  		Fig. 3. Freedom from moderate or more AI or AVR for 479 hospital survivors after ASO, separated for three diagnoses. DORV: double outlet right ventricle, IVS: intact ventricular septum, TB: Taussig-Bing anomaly, TGA: transposition of the great arteries, VSD: ventricular septal defect.

 
3.3 Risk factors
In the univariate Cox regression analysis, the following parameters were found to be predictors for moderate or more AI or AVR: TB/DORV (p = 0.01), the presence of a VSD (p = 0.006), or a LVOTO (p = 0.005), age over 12 months at time of ASO (p = 0.001), prior PAB (p = 0.004) and the presence of AI at discharge or at 1 year after ASO (p < 0.0001, Table 3 ). Because of the high degree of covariance between patients with TB/DORV, a VSD, PAB and age over 12 months at time of ASO, it was not possible to further discriminate by multivariate analysis which of the latter parameters had the strongest influence on AI or AVR. A bicuspid native pulmonary valve, the position of the aorta to the pulmonary artery and the coronary anatomy were not determinants for the development of an AI or the need for AVR. The multivariate Cox regression model revealed that only the presence of a LVOTO and at least trivial AI at 1 year after ASO were independent risk factors for the development of a moderate AI or the need for AVR (Table 3, Fig. 4 ).


View this table:
[in this window]
[in a new window]

  		Table 3 Risk factors for moderate or more aortic insufficiency or aortic valve replacement after the arterial switch operation for 479 hospital survivors
 

Figure 4
View larger version (12K):
[in this window]
[in a new window]

  		Fig. 4. Freedom from moderate or more AI or AVR for 479 patients after ASO, comparing patients with at least trivial AI at 1 year after ASO to patients without AI at 1 year after ASO.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
Appendix A
 References
 
Ever since long-term results after ASO have become available, the occurrence of AI became increasingly evident. In the present study, we showed that there is a progression of AI in the long-term after ASO and that the development of moderate or more AI or the need for AVR is closely related to a number of risk factors, namely the presence of a VSD, prior PAB, older age at operation and the underlying morphology being TB/DORV. Since these risk factors are more or less interrelated to each other, only the presence of any degree of AI at 1 year after ASO and the association of a LVOTO turned out as independent factors. However, the incidence of higher degree AI, even requiring AVR, remains a rare complication after ASO and its reported occurrence varies considerably, obviously also depending on the time of follow-up. In studies with a follow-up time of up to 5 years after ASO, the incidence of AI or AVR ranges between 0.3% [14] and 5.1% [3,6,15,16]. Looking at a more recent study with a longer follow-up time (6.4 years) the prevalence of any AI is reported as high as 14.9%. However, in the same study the prevalence is reduced to 5.9% when only the incidence of more than trivial AI is considered [17]. Other studies, describing the prevalence of more than moderate AI (grade III/IV) and the need for AVR in the long-term vary from 2.7% [18] to 4.9% [19] at a follow-up time of up to 8.8 years. It becomes obvious that the development of AI after ASO is a time-dependent phenomenon and, therefore, studies with a longer follow-up report a higher incidence of AI. In our patient population, the median follow-up time was 9.3 years and the incidence of any AI at the latest examination was found to be 38%. Similar results have been described after a follow-up time of a median of 8.2 years, with an incidence of any AI of 35% [20]. Excluding patients with trivial AI in our series, however, reduces the incidence of AI to 7.2%. But still, the freedom from moderate or more AI (grade III/IV) or AVR continuously decreases over time in our study and decreases to 84.6% at 20 years. Hence, in the future, more patients after ASO can be expected to present with relevant AI, requiring subsequent AVR. To date, aortic valve replacement is still rare after ASO and ranges between 1.4% [20] and 2.4% [15]. Likewise, in our population, only 2.3% of the patients required AVR at a mean time of 11.2 years after ASO. Although the incidence of AVR is rare, it should not be underestimated, as our results show that mortality after AVR is substantial. A reason for these poor results could be a too late referral, when left ventricular function is already impaired. We therefore advise a continuous follow-up of patients after ASO even if in good clinical condition and an early referral for AVR.

The aetiology of AI after ASO is presumably multifactorial and different risk factors have been identified. Aortic root dilatation is a common finding after the ASO, but no consistent correlation with the occurrence of AI has been found [15,18,20]. Only one study could demonstrate that patients with aortic root dilatation had a higher risk of developing AI, although AI was mostly trivial to mild [16]. It has been suggested that neo-aortic root enlargement after ASO mirrors that reported after the Ross, Norwood and Damus-Kaye-Stansel procedure where the pulmonary valve functions in the systemic circulation [16]. But unlike the Ross procedure, the infringement on the neo-aorta occurs at the sinus and the sinu-tubular junction after ASO and not at the ventriculo-aortic junction. However, it has been shown that the pulmonary artery in TGA shows a clear trend in reduction of actin staining smooth muscle cells in the media throughout the first year of life, potentially promoting root dilatation following ASO [21]. Since this is an age dependent phenomenon, it could also explain the finding of the present investigation that older age at operation was a risk factor for the development of AI. In addition, the injury to the vasa vasorum, the presence of the various suture lines and the characteristics of the pulmonary vessel in high-pressure circulation has also been advocated to cause aortic root dilatation after the ASO [22]. In our study with a retrospective review of patient charts, we were not able to analyse the exact dimensions of the aortic root over time, as description and measurements were inconsistent. However, we have also noticed an increase of the aortic root in most patients after the ASO. One patient with AVR in our study even required a simultaneous replacement of the aortic root, suggesting that aortic root dilatation might have been responsible for the development of AI.

As the exact influence of aortic root dilation on the development of AI may not be totally clear, other strong risk factors for the occurrence of AI after ASO have emerged, such as the presence of a VSD or prior PAB which are also associated with an older age at the time of the ASO and with the diagnosis of TB/DORV [8,15]. High flow through the pulmonary valve before the ASO in patients with a VSD and distortion by the PAB have been discussed as potential mechanisms [23]. Furthermore these patients, in particular the ones with TB/DORV, usually exhibit a size discrepancy between the native pulmonary artery and the aorta, which has been found to be predictive for later development of AI [24]. Pathophysiologically, a distortion of the sinu-tubular junction caused by the downsizing of the dilated pulmonary artery to the size of the aorta could be responsible. The presence of disproportionate valve rings in the cases with VSD and Taussig-Bing might also be one of the promoting mechanisms of aortic root dilation and subsequent development of AI. In addition, Mohammadi et al. [23] showed that VSD closure through the pulmonary valve increased the risk of developing AI in the long-term. In the present study we did not analyse if the transpulmonary, or the transatrial approach to VSD closure had any influence on the development of AI. It may be speculated that transpulmonary VSD closure could potentially damage the pulmonary valve, which then functions in the systemic circulation, thus promoting AI in the long-term [23]. The risk factors for the development of AI after ASO revealed in the present investigation correspond nicely with the findings by Losay et al. [17] in a study on 1156 survivors after the ASO. These authors also found the presence of a VSD as one strong predictor, which encompasses the other factors such as PAB, pulmonary-to-aortic size discrepancy and older age at operation.

In addition to the presence of a VSD, the reimplantation technique of the coronary buttons could lead to a potential distortion of the neo-aortic sinus and thus to late development of AI. A previous study revealed the ‘trap-door technique’ as an independent risk factor for the incidence of AI [20]. The authors explained this by a potential remodelling of the aortic root, caused by a greater enlargement of the aortic sinus by the ‘trap-door technique’ than by the ‘button technique’. Although more patients in our series had reimplantation of the coronary arteries with the ‘trap-door technique’, this technique was used only from 1990 on, and hence, follow-up time is shorter. The coronary anatomy itself did not turn up as a risk factor, although the coronary transfer in unusual cases may be more complicated and frequently requires the augmentation of the coronary ostia with patch material.

In the present study, the association of a LVOTO turned out to be an independent risk factor for the development of more than moderate AI in the long-term. This finding has also been described by Sharma et al. [25] in a cohort of 23 patients with LVOTO undergoing ASO. Nineteen percent of their patients developed AI at a follow-up time of up to 72 months, with 8% requiring subsequent AVR. As a potential explanation for the higher rate of AI in this subgroup of patients, the authors suggested that the pulmonary valve, which had been protected in a low-pressure zone up to the ASO, reacts to the sudden onset of arterial pressure by a dilatory response. Furthermore, subaortic resection may cause damage to the leaflets, equivalent to the findings correlated with transpulmonary VSD closure. Also, residual turbulent flow even in the absence of persistent LVOTO may promote neo-aortic regurgitation in the long-term [25].

Multivariate analysis revealed the presence of any AI at 1 year after the initial ASO to be an independent risk factor for the later occurrence of higher degree AI or AVR, while AI at discharge turned out as a risk factor by univariate analysis only. Other studies observed a certain degree of reduction in AI and aortic root dimensions in the early period after ASO [17,20]. However, in the study by Losay et al. [17] on 1156 patients after ASO, AI at discharge was also found to be predictive for the later development of AI. Hence, if AI persists at 1 year, this should be considered as a prognostic rather than a pathophysiologic risk factor and parents may be advised that their child is in the increased risk group for the later development of AI, making close follow-up even more important.

In conclusion, there is a steady time-dependent increase in the occurrence of AI after the ASO. So far, the incidence of late severe AI is low and the need for AVR is still rare. However, as the development of AI is progressive, we might just see the beginning of what could become a major problem in the next decade. This development of AI over time and its progression may have been underestimated in the past. Therefore, awareness of this late complication should be emphasised and patients should be referred to AVR before LV function is on the decline. Although we could identify specific risk factors for the development of AI, the cause of it remains multifactorial, with the presence of a VSD being the centre of attention. Patients who exhibit AI at discharge or at 1 year after the ASO should undergo close survey during follow-up, because they are at an increased risk for the later development of significant AI.

4.1 Study limitations
This is a retrospective study over a long period of time. Changes in surgical and postoperative management might have influenced the results and cannot be ruled out. The echocardiographic assessments were done by different examiners and at different centres, so that there might be some measurement variability. Especially trivial AI might have been over- or underestimated, depending on the examiner.


   Appendix A
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 Appendix A
References
 
Conference discussion

Dr D. Sidi (Paris, France): I think you’ve looked at most of the things, especially what the causes are.

I would like to stress the geometry. You said you looked at the geometry and you found that there was no incidence of aortic regurgitation. What did you look at on the geometry?

Dr Lange: I said that we did not have a chance to look at the discrepancy between the valve sizes, although it can, of course, be assumed that the patients with the Taussig-Bing and the VSD have a large discrepancy between valve sizes, but we did not look especially at this factor.

Dr Sidi: There is something that is appearing. We have studied a lot of the geometry and the flow pattern in coarctation of the aorta and found that when there was a Gothic type of aorta, then there was a problem with the fluid into the aorta, and when you do MRI studies you find that during systole you have a regurgitation of blood into the Valsalva in the Gothic style, and one of the concerns we have with the LeCompte maneuver, which pushes the aorta backwards, is that you have this kind of Gothic arch from the beginning of the ascending aorta, and then it goes back; it's squeezed a little bit. We haven’t done a study on all the switches but just some of the cases, and it appears that there is this systolic rejection, and I wonder if on the fragile sinus, because of the surgery and the technique, if you had this mechanical regurgitation of systolic blood, that because of the geometry of the arch, it's not an aggravating factor. What do you think?

Dr Lange: The more I get into this field and read about it and read other studies, I’m more and more convinced that there is no one single explanation, of course. Some people say that the geometric discrepancy between the bulbus and the ascending aorta might be a problem, but if you look at the studies where this has been solved by augmenting the ascending aorta, for example in the Paris study, then they do not have any different incidence of the development of aortic insufficiency. Another explanation that sounded good to me is that maybe by the switch operation there is a distortion of the vasa vasorum around the neoaorta, which you also find in the Ross operation. So this might also be a possible explanation. However, if you compare, for example, the Ross operation, the switch operation, and also what we find in the Norwood operation where you always have a pulmonary valve in the systemic circulation, they all don’t have one simple explanation for why aortic insufficiency develops in the long-term.

Dr Sidi: But I think you can do a mathematical model by looking at the angle of the aorta and maybe do some MRI studies on flow and you may find one of the factors.

The last comment, if I can, are you worried about the dilatation of the Valsalva in terms of risk of dissection or something like that, and do you think in the cases with big dilatation of the Valsalva there is an indication for beta-blockers in these patients?

Dr Lange: We haven’t seen one single dissection. However, in two cases we had to replace the ascending aorta because of severe dilatation.

So in the long-term, when they get older, and the longest follow-up is now 24 years, maybe that's something you have to consider.

Dr Sidi: Basically in a simple transposition with a switch, when you get what I call Doppler disease of the aorta more than valvular disease, because with a very sophisticated echo machine you can see this little drop, what do you say to the parents? Do you worry them about that? Or to the kid when he gets to about 20, what do you do? I mean do you allow him to do anything?

Dr Lange: Yes. As a surgeon, I will always allow him to do everything. Our cardiologists are a little bit more cautious about that.

Dr R. Cesnjevar (Hamburg, Germany): I have a brief question about the technique. Did you close the VSD through the neoaortic valve? Second, is there any influence of a residual VSD on the aortic incompetence after the operation?

Dr Lange: Closure of the VSD through the neoaortic valve has been advocated as a risk factor, too, and we have looked at this and we have done either technique, transatrial or through the neoaorta, and we didn’t find any difference. We did not find any influence of a residual VSD.


   Acknowledgments
 
The authors wish to thank gratefully Mrs Raymonde Busch, statistician at the Institut für Medizinische Statistik und Epidemiologie, Technische Universität München, for her assistance and support regarding statistical issues.


   Footnotes
 
{star} Presented at the 21st Annual Meeting of the European Association for Cardio-thoracic Surgery, Geneva, Switzerland, September 16–19, 2007.

1 Both authors contributed equally to the manuscript. Back


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 Appendix A
 References
 

  1. Kirklin J, Blackstone E, Tschervenkov C, Castaneda A, for the Congenital Heart Surgeons Society Clinical outcomes after the arterial switch operation for transposition: patient, support, procedural and institutional risk factors. Circulation 1992;86:1501-1515.[Abstract/Free Full Text]
  2. Losay J, Touchot A, Serraf A, Litvinova A, Lambert V, Piot JD, Lacour-Gayet F, Capredou A, Planché C. Late outcome after arterial switch operation for transposition of the great arteries. Circulation 2001;104(Suppl. I):121-126.
  3. Prêtre R, Tamisier D, Bonhoeffer P, Mauriat P, Pouard P, Sidi D, Vouhé P. Results of the arterial switch operation in neonates with transposed great arteries. Lancet 2001;357:1826-1830.[CrossRef][Medline]
  4. Williams WG, McCrindle BW, Ashburn DA, Jonas RA, Mavroudis C, Blackstone EH, the members of the Congenital Heart Surgeon's Society Outcomes of 829 neonates with complete transposition of the great arteries 12–17 years after repair. Eur J Cardiothorac Surg 2003;24:1-10.[Abstract/Free Full Text]
  5. Haas F, Wottke M, Poppert H, Meisner H. Long-term survival and functional follow-up in patients after the arterial switch operation. Ann Thorac Surg 1999;68:1692-1697.[Abstract/Free Full Text]
  6. Brown JW, Hyung JP, Turrentine MW. Arterial switch operation: factors impacting survival in the current era. Ann Thorac Surg 2001;71:1978-1984.[Abstract/Free Full Text]
  7. Serraf A, Roux D, Lacour-Gayet F, Touchot A, Bruniaux J, Sousa-Uva M, Planche C. Reoperation after the arterial switch operation for transposition of the great arteries. J Thorac Cardiovasc Surg 1995;110:892-899.[Abstract/Free Full Text]
  8. Prifti E, Crucean A, Bonacchi M, Bernabei M, Murzi B, Luisi SV, Vanini V. Early and late outcome of the arterial switch operation for transposition of the great arteries: predictors and functional evaluation. Eur J Cardiothorac Surg 2002;22:864-873.[Abstract/Free Full Text]
  9. von Bernuth GV. 25 years after the first arterial switch operation: mid-term results. Thorac Cardiovasc Surg 2000;48:228-232.[CrossRef][Medline]
  10. Imamura M, Drummond-Webb JJ, McCarthy JF, Mee RB. Aortic valve repair after arterial switch operation. Ann Thorac Surg 2000;69:607-608.[Abstract/Free Full Text]
  11. Alexi-Meskishvili V, Photiadis J, Nürnberg JH. Replacement of the aortic valve after the arterial switch operation. Cardiol Young 2003;13(2):191-193.[CrossRef][Medline]
  12. Quaegebeur JM, Rohmer J, Ottenkamp J, Buis T, Kirklin JW, Blackstone EH, Brom AG. The arterial switch operation. An eight-year experience. J Thorac Cardiovasc Surg 1986;92:361-384.[Abstract]
  13. Zarauza J, Ares M, Vilchez FG, Hernando JP, Gutiérrez B, Figueroa A, Vázquez de Prada JA, Durán RM. An integrated approach to the quantification of aortic regurgitation by Doppler echocardiography. Am Heart J 1998;136:1030-1041.[CrossRef][Medline]
  14. 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;69:1880-1886.[Abstract/Free Full Text]
  15. Schwartz ML, Gauvreau K, del Nido P, Mayer JE, Colan SD. Long-term predictors of aortic root dilation and aortic regurgitation after arterial switch operation. Circulation 2004;110(Suppl. I)II-128–II-32.[Medline]
  16. McMahon CJ, Ravekes WJ, Smith EO, Denfield SW, Pignatelli RH, Altman CA, Ayres NA. Risk factors for neo-aortic root enlargement and aortic regurgitation following arterial switch operation. Pediatr Cardiol 2004;25(4):329-335.[Medline]
  17. Losay J, Touchot A, Capderou A, Piot JD, Belli E, Planche C, Serraf A. Aortic valve regurgitation after arterial switch operation for transposition of the great arteries: incidence, risk factors, and outcome. J Am Coll Cardiol 2006;47(10):2057-2062.[Abstract/Free Full Text]
  18. Hutter PA, Thomeer BJM, Jansen P, Hitchcock JF, Faber JAJ, Mejboom EJ, Bennink GBWE. Fate of the aortic root after the arterial switch operation. Eur J Cardiothorac Surg 2001;20:82-88.[Abstract/Free Full Text]
  19. Marino BS, Wernovsky G, McElhinney DB, Jawad A, Kreb DL, Mantel SF, van der Woerd WL, Robbers-Visser D, Novello R, Gaynor JW, Spray TL, Cohen MS. Neo-aortic valvar function after the arterial switch. Cardiol Young 2006;16(5):481-489.[CrossRef][Medline]
  20. Formigari R, Toscano A, Giardini A, Gargiulo G, Di Donato R, Picchio FM, Pasquini L. Prevalence and predictors of neoaortic regurgitation after the arterial switch operation for transposition of the great arteries. J Thorac Cardiovasc Surg 2003;126:1753-1759.[Abstract/Free Full Text]
  21. Lalezari S, Hazekamp MG, Bartelings MM, Schoof PH, Gittenberger-de Groot AC. Pulmonary artery remodeling in transposition of the great arteries: relevance for neoaortic root dilatation. J Thorac Cardiovasc Surg 2003;126(4):1053-1060.[Abstract/Free Full Text]
  22. Murakami T, Nakazawa M, Momma K, Imai Y. Impaired distensibility of neoaorta after arterial switch procedure. Ann Thorac Surg 2000;70(6):1907-1910.[Abstract/Free Full Text]
  23. Mohammadi S, Serraf A, Belli E, Aupecle B, Capderou A, Lacour-Gayet F, Martinovic I, Piot D, Touchot A, Losay J, Planche C. Left-sided lesions after anatomic repair of transposition of the great arteries, ventricular septal defect, and coarctation: surgical factors. J Thorac Cardiovasc Surg 2004;128(1):44-52.[Abstract/Free Full Text]
  24. Hwang HY, Kim WH, Kwak JG, Lee JR, Kim YJ, Rho JR, Bae EJ, Noh CI. Mid-term follow-up of neoaortic regurgitation after the arterial switch operation for transposition of the great arteries. Eur J Cardiothorac Surg 2006;29(2):162-167.[Abstract/Free Full Text]
  25. Sharma R, Choudhary SK, Bhan A, Kumar RP, Juneja R, Kothari SS, Saxena A, Venugopal P. Late outcome after arterial switch operation for complete transposition of the great arteries with left ventricular outflow tract obstruction. Ann Thorac Surg 2002;74:1986-1991.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 CirculationHome page
S. M. Emani, R. Beroukhim, D. Zurakowski, F. A. Pigula, J. E. Mayer, P. J. del Nido, T. Geva, and E. A. Bacha
Outcomes After Anatomic Repair for D-Transposition of the Great Arteries With Left Ventricular Outflow Tract Obstruction
Circulation, September 15, 2009; 120(11_suppl_1): S53 - S58.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Julie Cleuziou
Klaus Holper
Christian Schreiber
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lange, R.
Right arrow Articles by Schreiber, C.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Lange, R.
Right arrow Articles by Schreiber, C.
Related Collections
Right arrow Congenital - acyanotic
Right arrow Great vessels

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS