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Eur J Cardiothorac Surg 2001;20:82-88
© 2001 Elsevier Science NL
a Children's Heart Center, Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands
b Center of Biostatistics, University of Utrecht, Utrecht, The Netherlands
Received 9 October 2000; received in revised form 21 March 2001; accepted 6 April 2001.
Corresponding author. Tel.: +31-30-2504002; fax: +31-30-2505347
e-mail: p.hutter{at}wkz.azu.nl
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Abstract |
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 Top Abstract 1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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Key Words: Arterial switch operation • Transposition of the great arteries • Congenital heart disease • Aortic valve • Aortic root
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1. Introduction |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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2. Patients and methods |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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The follow-up of the remaining 144 patients is 8.65 years (0.1–22.5 years). Ninety-seven patients had TGA with intact ventricular septum and 47 had TGA with ventricular septal defect (VSD), of whom 16 patients had double outlet right ventricle with sub-pulmonary VSD (Taussig–Bing anomaly). Eight patients had coarctation of the aorta, one had interrupted aortic arch and one had TGA with atrioventricular septal defect and cor triatriatum. The arterial switch was the first surgical procedure in 122 patients, 22 had a staged procedure, 21 after a prior pulmonary band and one after an aorto-pulmonary shunt in a patient with hypoplastic pulmonary artery branches. Median age at the arterial switch was 8 days (1–1878 days).
The aortic anastomosis was sutured with continuous 7.0 Prolene. The coronary arteries were implanted in trapdoor incisions, and also sutured with continuous 7.0 Prolene. Analysis of the coronary development of the same group of patients has previously been published in this journal [2].
Detailed echocardiography was performed yearly including Doppler interrogation of the flow-velocity in ascending and descending aorta. Since 1992, the diameter of the aorta was measured at four levels (Fig. 1) . After Lecompte's manoeuvre, the pulmonary bifurcation is anterior to the ascending aorta. At this level it is not possible to distinguish between aortic and pulmonary wall. Therefore, we preferred to measure the internal diameter at all levels. Measurements were performed at the time of the investigation, using 2D cineloop just prior to opening of the aortic valve. The resulting 608 measurements were compared to published normal values [3,4]. Body surface area (BSA) was calculated from length and weight using Mosteller's formula [5].
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2. The analysis was performed using commercially available software [9].
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3. Results |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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Fig. 3 demonstrates the development of the aortic valve diameter, expressed as z-score, in relation to age. No progressive valve dilatation could be demonstrated: the coefficient of aortic valve z-score growth was not significantly different from 0. At the last visit, the aortic valve z-score was above 2 in 51 patients, between -2 and 2 in 72 and less than -2 in six patients, none of whom had a flow velocity above 2 m/s.
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Fig. 5 demonstrates development of the sinu-tubular junction, the site of the aorto-pulmonary anastomosis. When a linear description is chosen, the anastomosis is less than 1 standard deviation larger than normal, but this is still significant (P=0.0001) and the anastomosis is dilating with age, increasing by almost 0.1 standard deviation per year (P<0.0001). On further analysis, this increase is mostly limited to the first 1–2 years of life. Because of this non-linearity, a polynomial was used in the figure.
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The ratio ascendens/valve is 0.92, without significant in- or decrease with time. The observed mean ratio was smaller than the normal ratio (1.0±0.1, P<0.01).
On further analysis the z-scores of the aortic valve, sinus as well as the anastomosis show a rapid increase in the first year of life, followed by a decrease of the z-score of the valve and the sinus. The z-score of the anastomosis increases further, but more slowly, beyond the first year of life. This is demonstrated in Table 1.
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At the latest follow-up, aortic flow velocity was less than 2 m/s in 128 patients, 2–3 m/s in eight patients and one patient had a velocity of 3.2 m/s. No patient developed stenosis of the aortic valve or of the aortic anastomosis leading to LV hypertrophy on ECG or echo.
One patient had transposition with sub-pulmonary VSD and LV outflow-tract stenosis. Pre-operative it was estimated that this stenosis was largely caused by bulging of the septum because of the pressure difference between the ventricles and would resolve when the pressures would be reversed. After the arterial switch at 4 months of age, the stenosis persisted and worsened, requiring re-operation 6 months later.
The patient with interrupted aortic arch developed severe stenosis at the site of aortic cannulation, requiring re-operation within the first post-operative week. A third patient required re-operation for pulmonary stenosis, this patient had, in addition, an aortic flow of 3 m/s and an invasive pressure gradient of 20 mmHg. Despite the mild gradient and the absence of left ventricular hypertrophy on echocardiography and ECG, it was decided to perform angioplasty of the ascending aorta, rather than risking worsening of the stenosis necessitating a second re-intervention later in life. This patient developed moderate aortic insufficiency (grade 3/4) later.
3.3. Flow in the aortic arch, coarctation and re-coarctation
The flow in the aortic isthmus, when eliminating patients operated for coarctation, was 1.41+0.01*age. The increase with time, though clinically irrelevant, was statistically significant (P=0.013).
Transposition was associated with coarctation of the aorta in eight patients. Of these patients, two had an intact ventricular septum, three had coarctation in the setting of Taussig–Bing anomaly and the remaining three had muscular VSDs.
One additional patient had transposition, muscular VSD and interrupted aortic arch. Re-coarctation developed in two patients and were treated with balloon-angioplasty 6 and 7 years after initial surgery. The patient with interrupted arch developed re-stenosis at the anastomosis between ascending and descending aorta, initially balloon-angioplasty was performed, but 3 years later the stenosis recurred and the patient was treated with patch-angioplasty.
3.4. Influence of associated cardiac malformations
3.4.1. VSD
Patients with VSD have an aortic valve z-score 0.75 higher than patients without VSD (P=0.027). Development over time was not significantly different between patients with or without VSD (P=0.80). This is demonstrated in Fig. 6A.
No significant influence of VSD on the sinus z-score at birth or during growth was encountered.
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3.5. Coarctation
Aortic valve z-score of patients with coarctation was 2.5 above patients without coarctation (P<0.001). During somatic growth, z-score did not change significantly in either group (Fig. 6C). The sinus is larger in patients with coarctation than in patients without coarctation (2.25 vs. 1.36, P=0.011) and doesn't change with increasing age in either group. All coarctations were present before the arterial switch operation.
The initial size and the development of the anastomosis were not significantly different in patients with or without VSD, Taussig–Bing anomaly or coarctation.
3.6. Influence of banding and age at arterial switch
3.6.1. Banding
Second stage arterial switch after pulmonary artery banding did not influence the aortic valve z-score (P=0.7) and the anastomosis (P=0.3), but did have a significant influence on the size of the sinus.
After banding the sinus is 2.8 z-scores larger (P=0.014). During the arterial switch, the band was opened, and the pulmonary artery was transected at the level of the band. This resulted in sufficient size. No additional surgical procedures, such as patch implantation, were necessary to relieve residual stenosis.
3.6.2. Age at arterial switch
For every day the patient was older at the time of arterial switch, the aortic valve z-score increased by 0.013 (P=0.008). There was no significant influence on the sinus (P=0.16) or the anastomosis (P=0.66).
3.7. Aortic insufficiency
Aortic insufficiency was absent in 100, trivial in 39, grade 2/4 in three and grade 3/4 in one. One patient required valve replacement for grade 4/4 insufficiency. This patient's post-operative course was complicated by left ventricular dysfunction and arrhythmia. Patients with no or trivial aortic insufficiency had valve z-scores of 1.5±2.3. The patients with insufficiency grade 2/4 or above had mean z-score 4.6±2.6 (P=0.004). Three of these patients had Taussig–Bing anomaly (P=0.01) and one had pulmonary artery banding and second stage arterial switch (P=0.55).
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4. Discussion |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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After the Ross operation, it has been demonstrated that the graft does increase in size and that the pattern of this increase is suggestive of early passive dilation followed by normal active growth [12]. The Ross operation however, is a free transplant, with the pulmonary root anastomosed both distally and proximally with re-implantation of the coronaries. This disturbs the anatomy at the sinu-tubular junction, the sinus, and at the ventriculo-aortic junction. During the arterial switch, the infringement on the neo-aorta occurs only at the sinus and the sinu-tubular junction, not at the ventriculo-aortic junction. However, a similar pattern of dilatation followed by growth is encountered in our study. This longitudinal study with up to eight measurement moments per patient allows us to postulate that in the development of the neo-aorta three factors may play a dominating role: (1) the larger initial pre-operative size of the aorta, (2) the immediate post-operative dilating phase and (3) the final normal growth of the vessel.
The larger initial size of the aorta finds its origin in the fetal circulatory physiology, where 60% of the combined cardiac output passes the right ventricle. Despite the fact that the pulmonary artery originates from the left ventricle, a larger size of the pulmonary artery in comparison to the aorta, is reported [13,14]. The immediate post-operative dilating phase in the Ross procedure has been described in recent publications by Solymar et al. [15] and to a lesser extent by Solowiejczek et al. [11] and attributed to passive dilatation [16] due to the higher systemic blood pressure and the implantation technique employed. In transposition, the annulus is not involved in the surgical technique, however, we find a similar rapid initial dilatation of the valve. The thinner pulmonary wall, as reported by Schoof [10], is likely to distend under systemic pressures. In the third phase, gradual neo-aortic growth occurs. The size regresses to more normal values over a period of 6–10 years, although the mean remains 1 standard deviation above normal, possibly representing a balance between a structurally thinner pulmonary (neo-aortic) wall and the systemic blood pressure it is exposed to. The valve, sinus and ascending aorta all show a similar pattern of initial dilatation and slowly regress towards the normal values over a period of more than 10 years. Unlike the report by Solowiejczek et al. [11] where surgical technique during the Ross procedure prevents dilatation of the semilunar valve, the arterial switch technique allows dilatation at all levels. We deliberately compared the neo-aortic values to the values of normal aortas and not pulmonary arteries since pulmonary normal values are less reliable and obtained from different echocardiographic views and are therefore incomparable.
The fact that six patients have an aortic valve below -2 SD represents the normal statistical spread and not pathology, as evidenced by their normal flow velocities. The explanation of the ongoing increase in z-score of the anastomosis is unclear. Real aneurysmatic dilatation caused by turbulence at the mismatched anastomosis as postulated by Blume and Wernovsky [14] seems unlikely. On angiography performed at the end of follow-up in 61/144 patients, the anastomosis is most often not even recognizable [2].
The effects of associated cardiac malformations on the development of the neo-aorta have not yet been included in previous studies. We addressed the influence of associated cardiac malformations and long-term consequences of disproportionate valves after the arterial switch in VSD, Taussig–Bing anomaly and coarctation of the aorta. In transposition with subpulmonary VSD the outlet septum is variably malaligned, eventually encroaching on the right ventricular outflow tract. The diminished fetal flow to the aorta and compensatory increased flow to the pulmonary artery results in a more pronounced mismatch. After the arterial switch growth is normal and shows a trend towards normal (0.009*age). A less pronounced mismatch is present in patients with other types of VSD, in whom a small difference in valve z-scores remains, throughout the study period. Statistical analysis failed to find a trend towards normalization in these patients. Patients with coarctation have larger valves, but their numbers are small, and again no trend toward normalization could be proven. Age at arterial switch did influence valve size; the size of the sinus or anastomosis was not affected. There is no reason to believe that the pulmonary root dilates prior to the arterial switch, while it is not submitted to exceedingly high flow or pressure. We therefore believe that this is not a direct effect, but some interaction with other factors: patients who were operated early in our experience were operated older, especially when the patient had a VSD, in addition more of these patients were banded as a method to delay arterial switch. However, banding did not influence the valve, nor the anastomosis, but did influence the sinus. This dilatation of the sinus, without dilatation of the valve, can not be explained by surgical enlargement, as none of the patients required patch-plasty to overcome narrowing caused by the band.
Aortic stenosis leading to LV hypertrophy did not occur. The incidence of re-coarctation is not dissimilar to the series of native coarctation without transposition. Unlike Serraf, [17] we did not encounter any coarctation that developed after the arterial switch.
Finally, clinically significant insufficiency of the aortic valve is encountered in only five patients in our series. This group is too small for reliable statistical analysis. All patients with insufficiency have large valves, however, many patients with large valves have no insufficiency. Three out of five patients with insufficiency had Taussig–Bing anomaly. The lack of subvalvar support for the overriding semilunar valve in Taussig–Bing anomaly might form a possible explanation for the development of insufficiency. We did not find an influence of prior pulmonary artery banding as was reported by Blume [14] and by Martin et al. [18].
4.1. Limitations
This study is a retrospective study based on measurements obtained in a normal out-patient clinic setting without sedation of the patients. This means that not all observation could be performed at all moments and studies were performed by different echocardiographists. Inter- and intra-observer variability could not be assessed.
4.2. Conclusion
After the arterial switch, the neo-aortic valve and sinus are larger than normal. This, at least in part, represents the natural size difference in the prenatal situation. Patients with associated cardiac malformations, VSD, Taussig–Bing anomaly and coarctation, have a more pronounced difference in size. In the first year of life, there is rapid dilatation of the new aorta followed by active growth with tendency towards normalization of the valve and sinus size. Stenosis at the anastomosis was not observed. Aortic dilatation by itself is rarely associated with significant insufficiency.
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Footnotes |
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Appendix A. Conference discussion |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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Dr Bennink: I saw a recent article of Solowiejczyk and Quaegebeur from the New York group that compared the pulmonary valve in the Ross procedure with the pulmonary valve in the normal patients. One of the reasons that we went for the comparison with the aortic valve is that, according to my cardiologists, the pulmonary valve, it is more difficult to assess with less reliable measurements. That's why we went for the aortic valve. Another thing is that during the life it will behave like an aortic valve, and although your starting point is similar to the pulmonary valve, for the rest of the life we think you have to consider it as an aortic valve.
Dr F. Lacour-Gayet (LePlessis Robinson, France): The arterial switch is increasing the aortic root. The coronary button that are placed on the neo-aortic root enlarge the diameter. Therefore there is always a discrepancy in diameter between the proximal aorta and the distal aorta, and this is particularly true in transposition with VSD. I have been using for several hundred patients a technique that tries to cope with this problem. The technique is to use the top of the right coronary button to patch and to enlarge the distal ascending aorta. This is quite helpful, allows to place the right coronary in good position, and control the potential sinotubular problem. My question is, have you observed in patients with very large discrepancy a funny shape of the aortic control and more significant aortic insufficiency?
Dr Bennink: Actually we have used in the last 2 years the same technique that you described. We did not see, although there was a funny shape, any problems with tapering of that starting neoaortic root versus the native aorta. I'm pretty sure about this because last year we presented here a paper about the coronary problems after the arterial switch, and in 70 patients we did an angiography, and in none of those patients can you see any sign of stenosis. If you look at echocardiographic measurements at that level, out of those 144 patients, only in two patients was there a flow of more than 2 m/sec. I think it was up to 3 m/sec, but without any clinical significant effects.
Dr H. Uemura (Osaka, Japan): Have you included patients with a bicuspid pulmonary valve? In the setting of a bicuspid pulmonary valve, do you think its growth is normal?
Dr Bennink: I think in the whole series there were six patients with a bicuspid valve.
Dr Uemura: Its growth was normal in such patients?
Dr Bennink: The growth was normal in such patients.
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References |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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