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Eur J Cardiothorac Surg 2001;20:816-823
© 2001 Elsevier Science NL

Transposition of the great arteries associated with ventricular septal defect: surgical results and long-term outcome

Department of Pediatric Cardiac Surgery, Deutsches Kinderherzzentrum, 53757 Sankt Augustin, Germany

Received 17 October 2000; received in revised form 8 June 2001; accepted 11 July 2001.

Corresponding author. Tel.: +49-2241-249601; fax: +49-2241-249602
e-mail: andreas.e.urban.md{at}t-online.de

	Abstract

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion Appendix A. Conference... References

 
Objectives: To identify potential risk factors influencing early and late outcome following the arterial switch operation (ASO) for transposition of the great arteries associated with ventricular septal defect including double-outlet right or left ventricle. Methods: All patients who underwent ASO in our department until August 2000 (n=105) were included in this study. There were 77 transpositions of the great arteries with ventricular septal defect, 22 Taussig–Bing hearts and six patients with double-outlet morphology. The median age at operation was 24 days. Aortic arch obstruction was present in 25 patients; in 13 of these patients, a repair with aortic arch reconstruction was done before ASO. The usual coronary artery pattern was present in 59% of the patients. In six patients, we found an intramural course of at least one coronary artery. The ventricular septal defect was closed with a patch through the right atrium (n=35), the aorta (n=25), the pulmonary artery (n=25) or the right ventricle (n=3); in 17 patients a combined approach was necessary. Results: There were five hospital deaths (4.7%, 95% confidence limit 2–11%). The median duration of follow-up was 72 months. Fourteen patients underwent 15 reoperations 33 months after repair (median), eight for right ventricular outflow tract obstruction or neopulmonary stenosis. Four late deaths occurred, two due to complications related to coronary artery anomalies. Statistical analysis revealed no significant risk factor whatsoever correlating with death or need for reoperation. Survival after 12 years was 91.6%, and freedom from reoperation was 82.6%. Latest follow-up data showed that 13% of patients were in NYHA class II and/or required medical treatment; 87% were in NYHA class I. Conclusions: ASO associated with patch closure of ventricular septal defect can be performed early in life with a low risk of mortality (<5%), low incidence of reintervention (<15%) and promising long-term outcome.

Key Words: Heart defects • Congenital • Transposition of great arteries • Arterial switch operation

	1. Introduction

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion Appendix A. Conference... References

 
The arterial switch operation (ASO) was first attempted in patients with transposition of great arteries (TGA) and ventricular septal defect (VSD), believed to be the only condition suitable for a primary anatomical repair [1–3]. However, this procedure was successfully extended to patients with TGA and intact ventricular septum and, since the early 1980s, the ASO had rapidly become the standard surgical procedure for this anomaly. With increasing experience, numerous surgical series were published in which patients presenting with the association of a VSD with TGA had a higher rate of mortality [4,5]. The latter was not confirmed in our series. This report details our total institutional experience with the ASO for TGA with VSD including double-outlet right ventricle (DORV) or double-outlet left ventricle (DOLV) with particular emphasis on the surgical anatomy and techniques influencing early and late outcome.

	2. Patients and methods

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion Appendix A. Conference... References

 
Between June 1984 and August 2000, in our institution, 105 patients underwent an ASO associated with patch closure of a hemodynamically significant VSD. At the beginning of the study period, three additional patients presenting with TGA with VSD underwent Mustard-type atrial switch repair and VSD closure with no early or late mortality. One surgeon performed 103 of 105 operations. The series included 22 patients with DORV and subpulmonary VSD, mainly with Taussig–Bing heart (21%) [6,7]. Double-outlet ventricle was diagnosed when we found a pulmonary-mitral discontinuity. In five other patients, double-outlet infundibular morphology with perimembraneous inlet or inlet VSD and in one other patient the presence of both of the great arteries mainly arising from the left ventricle were intraoperatively observed. For description of coronary artery anatomy the Leiden convention was used (Table 1) [8]. The aorta was anterior-right or strictly anterior to the pulmonary artery in the majority of cases (n=73, 70%). Side-by-side great arteries were observed in 18 patients (17%) and in 14 patients the great artery relationship was that of L-malposition (13%). Associated aortic arch obstruction was observed in 25 patients (24%): 24 coarctations and one interrupted aortic arch. Eight patients underwent coarctation repair prior to ASO. In six patients, palliation with pulmonary artery banding (PAB) had been performed prior to ASO. In five of these patients, PAB was performed together with coarctation repair. One other patient with restrictive VSD and cyanosis in which the left ventricle was judged ‘unprepared’ underwent a rapid two-stage procedure [9]. At repair, the median age was 24 days (range 4–690 days) and the median weight was 3.6 kg (range 1.9–9.7 kg).

Hypothermic (25°C), low hematocrit (8%)–high flow CPB was performed. Fifty percent of the operations (n=52) were partially done under deep hypothermia (18°C) and total circulatory arrest (median 35 min, maximum 62 min) in order to obtain optimal exposure for transatrial VSD closure. The Median CPB time was 204 min (range 120–1554 min), and the median aortic cross-clamp time was 115 min (range 78–244 min). Since 1992, modified ultrafiltration (500 ml) has been routinely performed at the end of CPB. The serum lactate levels were monitored during the CPB [12].

2.3. Operative technique
Standard surgical techniques were used. The following details were considered. A single initial infusion of crystalloide (St. Thomas II solution) cardioplegia was used for the majority of the series with a dose of 20 ml/kg for the majority of the series. Each coronary ostium was harvested with a generous U-shaped aortic cuff and dissected away from the sinus of Valsalva. In cases where the coronary orifice showed severe excentricity or where an intramural course of a coronary artery was present, the affected commissure was dissected from the aortic wall and later resuspended onto the wall of the repaired vessel. The Lecompte manoeuvre was always used with the exception of one extraordinary case. In this case with side-to-side relation of the great arteries, an extra-anatomical anastomosis of the reconstructed pulmonary artery into the right pulmonary artery was performed to avoid both coronary artery compression and pulmonary artery branch stenosis which seemed to be inevitable without this procedure. The coronary buttons were reimplanted in trap-door incisions at the adjacent pulmonary sinuses [13]. The pulmonary artery reconstruction was routinely performed with a single pantalon-shaped autologous pericardial patch which had been exposed to glutaraldehyde for fixation. The VSD was closed in all patients by means of a dacron or goretex (n=88) or autologous pericardial patch (n=17). According to the location and the type of the defect, several different approaches were used. Closure through the right atrium was always attempted. This was generally sufficient (n=35) for defects without severe malalignment. However, this approach necessitated the removal of the right atrial cannula thus causing a period of total circulatory arrest. The transarterial approaches constituted the alternative approaches for VSD closure (transaortic, n=25; transpulmonary, n=25). Right ventriculotomy was used in three patients, and in 17 patients combined approaches were necessary. Separate pledgetted polyester U sutures (transatrial, transaortic closure) or continuous prolene sutures were used (transpulmonary closure).

In 12 patients (11 coarctation and one interrupted aortic arch), the surgical procedure included concomitant aortic arch obstruction repair. This was performed on CPB but without myocardial ischemia and total circulatory arrest in six patients and during a period of total circulatory arrest in the other six patients. The technique was end-to-end (or end-to-side) direct anastomosis in 11 patients and homograft patch enlargement in one patient.

After transection of the great arteries and closure of the VSD, resection of obstructive myocardium or fibrous tissue (LVOT) was systematically performed either through the aorta or pulmonary artery and/or transatrially in patients for which the preoperative investigations demonstrated that the ventricular outflow tract was more than 2 mm narrower than normal values for right and left ventricular outflow tracts in matching individuals. The same procedure was chosen when severe septal malalignment was observed. According to this principle, 45 patients required right and 11 patients left ventricular outflow tract enlargement.

2.4. Postoperative care
Sedation was routinely used for at least 12 h after operation. Monitoring included surface electrocardiogram, pulse oxymetry, arterial line, central venous line, transthoracically placed left atrial line and central as well as peripheral temperature probes. Temporary atrial and ventricular wires were routinely placed. Inotropic support was given as 6 µg/kg per min of dopamine through the left atrial line. Norepinephrine (0.05–0.4 µg/kg per min) was added when necessary. Afterload reduction was obtained with phentolamine (2–8 µg/kg per min); more recently, milrinone (0.5–1 µg/kg per min) has become our second-line drug to provide the combination of inotropic support and afterload reduction. The strategy of the postoperative management and the inotropic support was based on hemodynamic parameters as well as regularly performed echocardiographic examinations.

2.5. Data analysis
Perioperative data were collected on a retrospective basis. Medical records, echocardiographic and cardiac catheterization data as well as operative notes were all taken into consideration. Early survivors were defined as patients who were discharged from the hospital and who survived for at least 30 days from the time of repair. During follow-up, every patient was seen by his or her cardiologist who collected the pertaining clinical and echocardiographic data. To identify the risk factors for mortality and reoperation, univariate analysis with ² or Fisher's exact test was initially used for each variable including preoperative patient-related variables, surgical anatomy and technique of repair. Ninety-five percent confidence limits (CL) were stated. Survival and freedom from reoperation probabilities were estimated by the Kaplan–Meier method and their values are expressed as the mean±SEM.

	3. Results

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion Appendix A. Conference... References

 
3.1. Early results
There were five hospital deaths (4.7%, 95% CL 2–11%). All five patients had undergone primary anatomical repair. Their features are listed in Table 3. Twenty-six patients (25%) required delayed sternal closure. In ten patients, postoperative peritoneal dialysis was necessary. The median postoperative mechanical ventilation time was 72 h (range 24–1456 h). Two patients required reoperation during the early postoperative period. One patient underwent reoperation on the ninth postoperative day because of residual aortic arch obstruction (see Table 3 for details of patient no. 5). A patch enlargement of the aortic arch was performed. Another Taussig–Bing patient with previous coarctation repair and PAB performed elsewhere required reoperation for pulmonary stenosis at the twenty-eighth postoperative day and received an additional right ventricle to pulmonary artery conduit. The right coronary artery was crossing the hypoplastic native aortic valve annulus anteriorly, thus prohibiting transannular patch insertion. Two patients developed postoperative complete atrio-ventricular block and required permanent pace-maker implantation.

3.3. Reoperations
Including the two patients who underwent an early reoperation, 14 patients (14%, 95% CL 8–22%) underwent 15 reoperations 33 months after ASO (median). Indications for reoperation are listed in Table 4. Six out of eight patients who underwent reoperation for pulmonary stenosis required a transannular patch insertion. A pulmonary vein stenosis in one patient resulted in a left pneumonectomy. The univariate analysis revealed the presence of a side-by-side great artery relationship as a risk factor for subsequent reoperation for pulmonary stenosis (P=0.03).

View larger version (21K): [in this window] [in a new window]   Fig. 1. Kaplan–Meier estimate of survival for 105 patients. Error bars show ±1 SEM.

View larger version (25K): [in this window] [in a new window]   Fig. 2. Kaplan–Meier estimate of freedom from reoperation for 105 patients. Error bars show ±1 SEM.

	4. Discussion

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion Appendix A. Conference... References

Anatomical repair is performed in early infancy, more likely within the first 3 weeks after birth. The usual approach of delaying complete repair until the patient is older and the anatomical structures are larger under the assumption that it improves the safety of the procedure without running the risk that the left ventricle may become adapted to the lower pressures of the normal pulmonary circulation carries significant hazards that are related to severe congestive heart failure and early development of pulmonary vascular obstructive disease, both of which occur commonly in patients with TGA and VSD. Occasionally, the VSD may spontaneously diminish in size, resulting in subsystemic left ventricular pressure by the time anatomical repair is planned. Our current policy is to perform ASO as soon as the diagnosis has been established, if possible during the same hospital stay.

The preoperative management policy with beginning of anesthesia and mechanical ventilation 12–24 h before the procedure and placement of arterial and central venous lines in the ICU was followed whenever possible. We believe strongly that this type of management minimizes the risk of exposure of the patient to perioperative stress during the procedure when the patient is especially sensitive to hemodynamic instability.

VSD closure was performed through the right atrium in about 50% of the patients, including the patients with a combined approach. In our experience, this technique had the advantage of a high degree of safety while an adequate exposure of the VSD could be achieved when removing the right atrial cannula. This approach, however, implies a period of time under total circulatory arrest to close the VSD. Therefore, if the VSD is a perimembranous VSD or an inlet VSD, we nowadays tend to cannulate both caval veins in order to avoid total circulatory arrest.

If the conal septum is anteriorly deviated, or if the surgeon has to place the superior border sutures through the sinus of Valsalva, VSD closure through the pulmonary artery should probably be avoided. Closure of the VSD through the pulmonary artery was a risk factor for postoperative neo-aortic valve incompetence and its increase with time [5,15].

Associated aortic arch obstruction was present in approximately 25% of our series. This was probably due to an institutional referral pattern which distorts the usual case mix [13,16]. The presence of an associated coarctation, independently from the management strategy, was not a significant risk factor for both mortality and reoperation. Several centers reported the feasibility of a single-stage surgical repair with a lower risk [17,18]. Our current procedure of choice is to perform one-stage total repair in this complex subgroup of patients. The employed surgical technique for associated coarctation repair through an anterior approach was resection and end-to-end (or end-to-side) anastomosis in 11/12 of the patients. The choice of the aortic arch repair technique should be adapted to the anatomy of the arch as well as the presence and the severity of arch hypoplasia. The technique of end-to-end anastomosis presented the advantage of avoiding total circulatory arrest and additional myocardial ischemia in six of the patients. The presence of severe arch hypoplasia indicates an increased likelihood of the need to perform a patch enlargement.

The presence of complex coronary artery anatomy including intramural course was not found to be a significant risk factor for mortality. The cause of two of the early deaths and the two cardiac-related late deaths (4/7) was suboptimal coronary artery transfer and/or intramural course, respectively, resulting in myocardial ischemia. With increasing experience, the complexity of coronary artery anatomy is no longer acceptable as a contraindication for ASO. Nevertheless, it can be assumed that the principle cause of mortality after ASO still remains to be inadequate coronary artery relocation.

RVOTO remains the most frequent cause of reoperation following ASO [19,20]. In previously published series the pulmonary stenosis had, in the majority of the cases, a supravalvular location and was mostly described after ASO in simple TGA. In the present series, in six of the eight patients who underwent reoperation for pulmonary artery stenosis, the level of obstruction was subvalvular and/or valvular. Thus, the technique of the reconstruction of the pulmonary bifurcation was confirmed. No significant anatomical (including Taussig–Bing and coarctation) or procedural risk factor for postoperative pulmonary stenosis was observed. Akiba et al. [21] reported a rate of 5% of subpulmonary obstruction and speculated that the subtle degrees of mismatch in size between the proximal aorta and the pulmonary trunk, although considered irrelevant at the time of repair, may set off a process of increasing adaptive infundibular hypertrophy.

In patients for whom the preoperative investigations demonstrated that the ventricular outflow tract was more than 2 mm narrower than normal values for right and left ventricular outflow tracts in matching individuals and where severe septal malalignment was observed, we systematically performed the resection of potentially obstructive myocardial tissue through the pulmonary artery and/or transatrially [22]. It seems that preventive right ventricular outflow tract enlargement which was performed in 43% of patients did in fact decrease the rate of reoperation for RVOTO.

We conclude that ASO in association with VSD closure can be performed in early life (<3 weeks) with a low mortality (<5%), a low risk of reintervention (<15%) and promising long-term outcome. The risk of reoperation for pulmonary stenosis is relatively high in a subgroup of patients presenting with complex infundibular anatomy, including patients with Taussig–Bing heart. The single-stage management constitutes the procedure of choice when an associated aortic arch obstruction is present. The VSD closure through the native pulmonary artery should be avoided as a routine but can be performed in selected cases.

	Footnotes

 
Presented at the 14th Annual Meeting of the European Association for Cardio-thoracic Surgery, Frankfurt, Germany, October 7–11, 2000.

	Appendix A. Conference discussion

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion Appendix A. Conference... References

 
Dr W. Daenen (Leuven, Belgium): I presume that you gave up closure of the VSD through the pulmonary artery because another reason for not doing this is the high incidence of surgical block. Did you have some surgical blocks in this subset of patients where you closed the VSD through the pulmonary artery?

Dr Urban: We didn't give it up. I think we identified the reason. The reason was that we fixed the patch too high beneath the neoaortic valve, sometimes into the sinus, and I presume by growing, the patch pulled down the valve. We had two cases of block in this series but none by closure of the VSD through the pulmonary artery; both blocks occurred in patients who had straddling valve morphology.

Dr F. Haas (Munich, Germany): What do you think are the main reasons for the higher mortality in patients with TGA and VSD in comparison with simple TGA? The second question is, have you seen any coronary stenosis in your late follow-up after the switch operation?

Dr Urban: The first question I cannot answer. I do not know. Its probably due to experience because the death of the patients were all quite back in the history of our switch operation. The second question, we had only 20 coronary angiograms postoperatively, except for that patient who died after reoperation, and on those 20 there was no stenosis.

Dr M. Metras (Marseilles, France): I would like you to clarify something. If I am right, it looks like you had preoperatively 40 patients who had right ventricular outflow tract obstruction. Can you clarify this population? That seems extremely important in a subset of transposition and VSD. It was subaortic, I guess.

Dr Urban: Yes, subaortic right ventricular outflow tract obstruction, and we have a big number of those patients, and this is probably due to our approach to the problem. We very carefully measure the diameter of the right ventricular outflow tract and relate it to the normal values of age-matched patients. We go then in the operation and measure with Hegars the size of the right ventricular outflow tract, and if its diameter is not appropriate, we do resect, although I'm aware that in most of the patients there are no preoperative gradients. So we are rather aggressive about the right ventricular outflow tract and do surgery there and we think this is good. You may not agree, but that is our approach.

Dr Metras: Its an obstruction without gradient, is that what you mean?

Dr Urban: Well, a VSD in this setting always makes a gradient disappear, so you really don't know, and that was the reason why we measured diameter by echo preoperatively and by Hegar dilators at operation.

Dr M. Elliott (London, UK): I would like to pursue this discussion about the incidence of heart block. We have been very alarmed by a number of patients, particularly with Taussig–Bing anomaly, who develop heart block in the confirmed presence of a muscular VSD, a muscular rim around the margin of the ventricular septal defect. I know that Marc and I have had a number of patients with that exact anatomy who have developed heart block. I am a little bit concerned that the descriptions of the anatomy in Taussig–Bing and the location of the bundle may not be complete, because you see this even though it fulfills all the basic criteria of a muscular VSD, and yet heart block follows. Have you seen that or have others seen that, or are we doing something completely wrong? This is through a ventriculotomy rather than through the pulmonary artery.

Dr Urban: Well, there are publications about the course of the bundle in Taussig–Bing and it is not quite the same as in the normal heart with VSD. I think this is probably a clue to the problem. We have not had complete heart block in all our Taussig–Bings operated upon.

	References

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion Appendix A. Conference... References

 

1. Jatene A.D., Fontes V.F., Souza L.C.B., Paulista P.P., Abdulmassih Neto C., Sousa J.E.M.R. Anatomic correction of transposition of the great arteries. J Thorac Cardiovasc Surg 1982;83:20-26.[Medline]
2. Yacoub M.H. The case for anatomic correction of transposition of the great arteries. J Thorac Cardiovasc Surg 1979;78:3-6.[Medline]
3. Pacifico A.D., Stewart R.W., Bargeron L.M., Jr. Repair of transposition of the great arteries with ventricular septal defect by an arterial switch operation. Circulation 1983;68(Suppl II):49-55.
4. Wernovsky G., Mayer J.E., Jonas R.A., Hanley F.L., Blackstone E.H., Kirklin J.W., Castaneda A.R. Factors influencing early and late outcome of the arterial switch operation for transposition of the great arteries. J Thorac Cardiovasc Surg 1995;109:289-302.[Abstract/Free Full Text]
5. Planché C., Lacour-Gayet F., Serraf A. Arterial switch. Pediatr Cardiol 1998;19:297-307.[Medline]
6. Taussig H.B., Bing R.J. Complete transposition of the aorta and a levoposition of the pulmonary artery. Am Heart J 1949;37:551.[Medline]
7. Van Praagh R. What is the Taussig–Bing malformation? (editorial). Circulation 1968;38:445-449.[Free Full Text]
8. Gittenberger-de Groot A.C., Sauer U., Oppenheimer-Dekker A., Qauegebeur J.M. Coronary arterial anatomy in complete transposition of the great arteries: a morphologic study. Pediatr Cardiol 1983;4(Suppl I):15-23.
9. Jonas R.A., Giglia T.M., Sanders S.P., Wernovsky G., Nadal-Ginard B., Mayer J.E., Castaneda A.R. Rapid, two-stage arterial switch for transposition of the great arteries and intact ventricular septum beyond the neonatal period. Circulation 1989;80(Suppl I):203-208.
10. Soto B., Becker A.E., Moulaert A.J., Lie J.T., Anderson R.H. Classification of ventricular septal defects. Br Heart J 1980;43:332-343.[Abstract/Free Full Text]
11. Hoyer M.H., Zuberbuhler J.R., Anderson R.H., del Nido P. Morphology of ventricular septal defects in complete transposition. J Thorac Cardiovasc Surg 1992;104:1203-1211.[Abstract]
12. Cheifetz I.M., Kern F.H., Scholman S.R., Greeley W.J., Ungerleider R.M., Meliones J.N. Serum lactates correlate with mortality after operations for complex congenital heart disease. Ann Thorac Surg 1997;64:735-738.[Abstract/Free Full Text]
13. Brawn W.J., Mee R.B.B. Early results for anatomic correction of transposition of the great arteries and for double-outlet right ventricle with subpulmonary ventricular septal defect. J Thorac Cardiovasc Surg 1988;95:230-238.[Abstract]
14. 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]
15. Di Donato R.M., Wernovsky G., Walsh E.P., Colan S.D., Lang P., Wessel D.L., Jonas R.A., Mayer J.E., Castaneda A.R. Results of the arterial switch operation for transposition of the great arteries with ventricular septal defect. Surgical considerations and midterm follow-up data. Circulation 1989;80:1689-1705.[Abstract/Free Full Text]
16. Daebritz S.H., Nollert G., Sachweg J.S., Engelhardt W., von Bernuth G., Messmer B. Anatomical risk factors for mortality and cardiac morbidity after arterial switch operation. Ann Thorac Surg 2000;69:1880-1886.[Abstract/Free Full Text]
17. Planché C., Serraf A., Comas J.V., Lacour-Gayet F., Bruniauy J., Touchot A. Anatomic repair of transposition of great arteries with ventricular septal defect and aortic arch obstruction. One-stage versus two-stage. J Thorac Cardiovasc Surg 1993;105:925-933.[Abstract]
18. Blume E.D., Altmann K., Mayer J.E., Colan S.D., Gauvreau K., Geva T. Evolution of risk factors influencing early mortality of the arterial switch operation. J Am Coll Cardiol 1999;33:1702-1709.[Abstract/Free Full Text]
19. Serraf A., Roux D., Lacour-Gayet F., Touchot A., Bruniaux J., Sousa-Uva M., Planché 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]
20. Williams W., Quaegebeur J.M., Blackstone E.H., The Congenital Heart Surgeons Society. Outflow obstruction after the arterial switch operation: a multiinstitutional study. J Thorac Cardiovasc Surg 1997;114:975-990.[Abstract/Free Full Text]
21. Akiba T., Neirotti R., Becker A.E. Is there an anatomic basis for subvalvular right ventricular outflow tract obstruction after an arterial switch repair for complete transposition? A morphometric study and review. J Thorac Cardiovasc Surg 1993;105:142-146.[Abstract]
22. Urban A.E., Brecher A.M. The arterial switch repair and the obstructive right ventricular outflow tract: does it matter?. Thorac Cardiovasc Surg 1991;39(Suppl):170-175.

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