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Ann Thorac Surg 2001;71:1978-1984
© 2001 The Society of Thoracic Surgeons
a Section of Cardiothoracic Surgery, Riley Hospital for Children, and Indiana University School of Medicine, Indianapolis, Indiana, USA
Address reprint requests to Dr Brown, Section of Cardiothoracic Surgery, Indiana University School of Medicine, 545 Barnhill Dr, EH 215, Indianapolis, IN 46202
e-mail: jobrown{at}iupui.edu
Presented at the Thirty-sixth Annual Meeting of the Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31Feb 2, 2000.
| Abstract |
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Methods. From 1986 to 1999, 201 consecutive patients underwent an arterial switch operation for TGA or Taussig-Bing anomaly. Multivariate analysis of perioperative variables was performed for operative morbidity/mortality. Patients were separated into two groups. Phase 1 (n = 29) included patients before mid-1989 who underwent an open coronary reimplantation technique. Phase 2 (n = 172) included the patients undergoing a technique of reimplanting coronary buttons after neoaortic reconstruction.
Results. The patient population included TGA with intact ventricular septum (58.7%, 118 of 201), with ventricular septal defect (31.3%, 61 of 201), and Taussig-Bing anomaly (10.0%, 22 of 201). Overall, early mortality was 9.5% (19 of 201) and there were five late deaths (2.7%). One-month, 1-year, and 5-year actuarial survival rates were 90.4%, 87.9%, and 87.9%, respectively. Reoperation rate for late pulmonary stenosis was 2.7% (5 of 182). The freedom from reoperation at 3 and 5 years was 97.5% and 93.3%, respectively. In the analysis by time period, the operative mortality declined from 27.6% (8 of 29) to 6.4% (11 of 172) (p = 0.002). Risk factors for operative death were coronary artery patterns (usual vs retropulmonary left coronary artery, p = 0.009) in phase 1 and preoperative instability in phase 2 (p = 0.002).
Conclusions. The arterial switch operation for TGA and Taussig-Bing anomaly has early low and late mortality and reoperation rates. Technical modifications in coronary reimplantation have minimized coronary artery pattern-related risks.
| Introduction |
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| Material and methods |
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Surgical technique
The surgical technique is well outlined in several previous reports and our technique can be summarized by stating that the ASO at our institution is done with continuous full-flow bypass at 20°C. Myocardial protection is accomplished with intermittent dose of cold crystalloid cardioplegia given every 20 to 30 minutes at 15 to 20 cc/kg. Cardioplegia is given into the aortic root before the aorta is opened and directly into the coronaries while the neoaorta is reconstructed and coronary transfer is being accomplished.
The neoaorta and coronary anastomoses are carried out with 7-0 absorbable monofilament sutures in running fashion. In most patients, a second 7-0 running suture is used to close the adventitial layer over the initial full-thickness aortic layer. The reduction in needle and suture size from 6.0 to 7.0 and the addition of the second-layer neoaortic anastomosis seems to have greatly reduced the incidence of troublesome bleeding at the completion of the operation. Once the neoaortic anastomosis has been completed, the aortic cross-clamp is released allowing the neoaortic root to distend. The coronary artery buttons are excised from their respective sinuses taking most of the sinus tissue. The coronary buttons were mobilized for a distance of 4 to 6 mm and allowed to rotate to the location on the distended neoaortic root where they will reside without torsion or tension. The ideal location on the neoaortic root is marked with a sterile pen. A stab wound is made at that mark taking care not to injure the previously marked anterior neoaortic commissure. The aortic cross-clamp is reapplied while a 2.5-mm aortic punch is used to remove a tiny button of neoaortic sinus tissue (Fig 1). Through this tiny hole, the location of the neoaortic commissure is confirmed and the opening enlarged to accommodate the coronary buttons. The coronary buttons are sewn into place and the aortic root deaired before completion of each respective anastomosis. The cross-clamp is removed. The distended appearances of the surface coronary branches of that coronary plus the hyperemic color of the myocardium assure proper coronary alignment.
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Postbypass monitoring
All patients receive a left atrial, PA, and a right atrial oxymetric catheter for postbypass and postoperative monitoring. Inotropic support is rarely needed with the ASO unless the ischemic time is significantly longer than 60 minutes. Any potentially pulmonary vasoconstrictive agent (dopamine or epinephrine) is administered via the left atrial (LA) line to reduce the potential for further pulmonary vasoconstriction. If one encounters low cardiac output or pulmonary hypertension (PH) that shows no residual anatomic pathology, then ECMO is instituted presuming myocardial stunning or persistent PH. We generally utilized the same cannula used for the ASO repair and on occasion add an LA decompression catheter Yd into the venous line to decompress a dilated or poorly contracting LV. The sternum and skin are left open only when transsternal extracorporeal membrane oxygenation (ECMO) cannula are in place or when sternal or skin closure compromises cardiac function. Under these circumstances, a silastic patch is sewn to the skin edges.
Data collection and analysis
Variables including demographics, previous palliative procedures, morphology, coronary artery pattern, and operative procedure-related variables were assessed by means of univariate analysis utilizing
2 test and multivariate logistic regression analysis. Intraoperative data collection forms, hospital charts, and echocardiographic and catheterization reports were reviewed. In the analysis of risk factors for early death, variables with significance levels of 0.1 in univariate analysis were admitted to a multivariate logistic regression model. Factors with p values of less than 0.05 were considered significantly related to early death. Kaplan-Meier analysis was used for the actuarial survival rates and freedom from reoperation rate. Differences in survival curves were assessed by log-rank test.
Early mortality was defined as death during initial hospitalization or within 30 days of operation. Any deaths later than that were defined as late mortality. In our series, all the early deaths occurred during the initial hospitalization and all the late deaths occurred after discharge from the initial hospitalization.
| Results |
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Late complications
Late complications were seen in 23 (12.6%) survivors of ASO and are shown in Table 7. Seven patients (3.8%) developed a pulmonary gradient of more than 30 mm Hg and 4 (2.2%) developed mild pulmonary regurgitation. Mild aortic stenosis (AS) gradient less than 20 mm Hg has developed in 3 patients (1.6%) and 6 (3.3%) developed mild aortic valve regurgitation (AR). No patient with AS or AR has required reoperation and only 5 of 11 patients with pulmonary valve stenosis required reintervention. One patient each has required a permanent pacemaker and revision of a previous coarctation repair. Actuarial freedom from reoperation at 3 and 5 years was 97.5 and 93.3%, respectively. Actuarial survival and freedom from reoperation are given in Figures 2 to 5.
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| Comment |
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PH as a risk factor for early death has been mentioned frequently in most series but was the second most common cause of early death in this series (Table 6). PH was manifested by a high left ventricular/right ventricular pressure ratio and very low arterial oxygen saturation preoperatively in spite of prostaglandin E1 administration and a satisfactory balloon atrial septostomy. Several of our patients with preoperative PH required ECMO support after a technically satisfactory ASO. Our ability to diagnose and medically manage PH is made possible by our postbypass monitoring of RA, PA, and LA pressures as well as mixed venous oxygen saturation. Alpha blockers (Thorazine and Minipress) as well as nitric oxide were introduced late during phase 2 of our ASO experience for both preoperative and postoperative management of PH. We are hopeful that these drugs will decrease or eliminate PH as a risk factor for early death.
The availability of ECMO to support infants after ASO who have myocardial stunting or persistent PH has improved survival in phase 2. Long-term survival in 8 of 15 patients (53%) who required ECMO support pre- or postoperatively was observed. As expected, bleeding was a problem when ECMO was introduced immediately after coming off bypass, and multiple organ failure was seen when ECMO was initiated too late and end organ failure had ensued.
A risk factor, which we cannot explain and which has not been noted in other series, is female gender. Female gender was a significant risk factor for adverse outcome in univariant analysis (p = 0.019) and multivariate analysis (p = 0.009). The reason for this finding is still unclear.
The 29 patients (14%) who required preoperative mechanical ventilation in addition to significant inotropic support were considered "unstable" preoperatively and had a higher postoperative mortality (27.6%) (p = 0.01). Three unstable patients underwent ECMO support preoperatively. PH was the most important risk factor in most infants in this preoperatively unstable group. Nitric oxide and alpha-adrenergic blockers are being used to reduce PH, however, it is early to know if these modalities make a significant difference.
Our low incidence of late complications and reoperation (3.7%) compares favorably with other reports [10, 13, 18]. The most common problem requiring reoperation is pulmonary stenosis (PS), and is reported in up to 7% in some series [20]. Our incidence of PS (gradient over 30 mm Hg) is 3.7% and the need for reoperation for PS is 2.2%. We attribute our low incidence of PS to extensive mobilization of the branch pulmonary arteries to reduce anastomotic tension and the use of an oversized pantaloon patch of fresh pericardium, as advocated by others [14, 20, 21].
During late follow-up, mild neoaortic insufficiency has developed in 6 patients (3.3%) and does not appear to be progressive. Arterial switch for Taussig-Bing DORV where the VSD is closed through the PA resulted in a higher incidence of mild AR. In some series, mild AR is seen in up to 30% of patients after a mean follow-up of 6 years [16]. Aortic regurgitation has rarely been an indication for reoperation in any series and has not been an indication for reoperation in our series (Table 7). Further careful long-term echo follow-up of AR is needed to see if the severity of regurgitation progresses.
Late outcomes after ASO have been quite favorable to the reported results for atrial switch procedures. At last follow-up, 96.7% of our late survivors of ASO are in New York Heart Association class I and 3.3% in class II. Freedom from reoperation of 99.3% at 3 years and 97.5% at 5 and 10 years was observed in our series.
Preoperative aortic arch obstruction was seen in 12 patients in our series and was seen only in patients with TGA-VSD or Taussig-Bing DORV. In all but 1 patient, the obstruction was repaired before the ASO. This two-stage approach was not an independent risk factor for mortality in this series (p = 0.644) (Tables 4 and 5). One patient has required reoperation for a recurrent coarctation during long-term follow-up.
In conclusion, the ASO continues to produce excellent early and late results for TGA-IVS, TGA-VSD, and Taussig-Bing DORV. Continued technical refinements have eliminated coronary anatomy as an independent risk factor for early death. The late mortality and complications related to anatomic factors continue to decrease. The only important risk factors in the current era are preoperative hemodynamic instability and female gender. Preoperative and postoperative nitric oxide and alpha-blockers along with ECMO support should continue to decrease mortality and improve long-term survival.
| Footnotes |
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| Discussion |
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The first area is the issue of the operative technique of coronary transfer. In your presentation and in the manuscript, you have identified what you have termed the open technique as a risk factor for coronary transfer and mortality for this arterial switch operation. Use of this technique, however, was also part of the phase I of your study. In Boston, we have used the open technique for essentially all of the over 800 arterial switch operations that we have done, and the only difference in the technique from what you have described is that before going on bypass we actually mark on the neoaorta with little marking sutures where we think the coronaries should go. Using this technique we have achieved mortality rates of less than 3% for transposition with intact ventricular septum and 5% to 6% for transposition with ventricular septal defect. Similar to your results, in a recent review of our last 5 years experience, coronary artery anatomic pattern no longer is a risk factor as it had been when we first reviewed the first 300 operations that we had done. With this background, I would like you to address the question of whether you really believe it is the technique of coronary transfer or simply more experience with coronary transfer by any technique that was associated with improved results.
The second area I would like you to address is the management of pulmonary hypertension, which you have identified as a significant risk factor for these patients. It has been my own philosophy that it is better to manage the perinatal pulmonary hypertension by medical measures, including mechanical ventilation, insurance of a more than adequate balloon atrial septostomy, sedation, and, now, nitric oxide before bringing the patient to the operating room so that one can let the pulmonary hypertension associated with perinatal events completely resolve. I would like you to comment on your current approach to the preoperative management of pulmonary hypertension in this group of patients and on how you decide the timing for your arterial switch operation.
Thank you for the opportunity to review the manuscript and to discuss this paper.
DR BROWN: Thank you, John. Those are pertinent questions. First of all, to address the coronary artery reimplantation technique, I do not think it makes a difference if you have the usual coronary artery pattern about which technique to use, but with those complex retropulmonary arteries, left coronary arteries, we found that even though marking what we thought was going to be the ideal location of the coronaries utilizing the open technique that in these difficult coronary patterns we still had problems: they were either stretched or twisted or not quite right. In the arterial switch operation with these complex coronary patterns, it seemed to us that allowing the aorta to fill and distend and then select the precise location for reimplantation once the coronary arteries had actually been mobilized, because the coronary arteries may be sort of held down by their adventitial attachments early on, but then after mobilizing them and having the aortic arch distended, one could better locate the precise location where the coronaries should go.
It is very difficult, however, to argue with your experience, because it has absolutely been superb, and many other centers around the world have used the open technique. But it seems to us, for at least the surgeon beginning and with less experience with the arterial switch operation, that doing the aortic anastomosis first and then selecting the site for the coronary would be better. Your second question had to do with pulmonary hypertension. I think early in our experience we were forced by our cardiology group to intervene in patients who were quite unstable, and most of this was due to pulmonary hypertension of the newborn. Our current technique is not to rush into the operating room with these patients but to place these patients on nitric oxide or other alpha-blockers, and even, if necessary, to place them on ECMO to let their neonatal pulmonary hypertension subside before taking them to the operating room and performing an elective arterial switch operation.
Again, I would like to thank the Society for the privilege of presenting this paper.
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