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Ann Thorac Surg 2000;69:851-857
© 2000 The Society of Thoracic Surgeons
a Division of Cardiovascular-Thoracic Surgery, Childrens Memorial Hospital and Department of Surgery, Northwestern University Medical School, Chicago, Illinois, USA
Address reprint requests to Dr Mavroudis, Division of Cardiovascular-Thoracic Surgery, Childrens Memorial Hospital, 2300 Childrens Plaza, M/C 22, Chicago, IL 60614-3394
e-mail: c-mavroudis{at}nwu.edu
Presented at the Forty-sixth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, Puerto Rico, Nov 46, 1999.
| Abstract |
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Methods. Between 1984 and 1999, 11 patients underwent pulmonary artery band (PAB) to prepare the left ventricle for ASO conversion. One additional patient had subpulmonic stenosis and was naturally prepared. Mean age at the initial PAB was 12.2 ± 7 years (range, 1.9 to 23 years). Four patients underwent reoperation to tighten the PAB before ASO. Mean interval from PAB to ASO was 1.3 ± 0.9 years.
Results. There was no mortality from PAB. Six patients had ASO conversion and 2 died. Recent surgical modifications at the time of ASO were used to prevent neoaortic valve insufficiency and to cryoablate atrial reentry tachycardia. Four patients developed biventricular failure after PAB and had orthotopic cardiac transplantation (OCT) 14 ± 10 months after PAB. The other 2 patients are still with PAB: 1 is awaiting ASO conversion and the other has insufficient left ventricular hypertrophy necessary for ASO conversion despite two preparatory PABs.
Conclusions. A select group of patients with right ventricular failure after atrial baffle operations can undergo staged conversion to ASO with the opportunity for excellent long-term outcome. Surgical modifications at the time of ASO can address the problems of neoaortic insufficiency and persistent atrial arrhythmias. PAB may be a therapeutic endpoint in some patients not responding with adequate left ventricular hypertrophy. Those patients who develop biventricular failure after PAB will require cardiac transplantation.
| Introduction |
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A few centers have documented the clinical results of such a program [58] and identified accompanying complications, which can include ineffective induction of LV hypertrophy, neoaortic insufficiency, persistent troubling atrial arrhythmias, and biventricular failure that can lead to cardiac transplantation. The purpose of this article is to report our results with TGA patients with failed atrial baffle procedures who underwent PAB with the intention to treat by ASO conversion after induction of LV hypertrophy.
| Material and methods |
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Two recent patients had preparatory PAB and are presently being evaluated for ASO conversion based on LV posterior wall thickness, LV pressure, and LV function.
LV evaluation before ASO
Assessment of an adequately prepared LV after PAB was made by echocardiography and cardiac catheterization. Measurements included assessment of biventricular function, LV posterior wall thickness, and LV systolic pressure. In general, patients were referred for ASO conversion when the LV diastolic posterior wall measurement was more than 8 mm thick and when the LV systolic pressure was more than 80% of the RV (systemic) pressure with a well-functioning LV.
Clinical evaluation before cardiac transplantation
Patients became candidates for cardiac transplantation if they did not respond favorably to the preparatory PAB. They were deemed to have end-stage congenital heart disease based on poor systemic ventricular function, deteriorating functional class, and an estimated life expectancy of less than 6 months. None of these patients developed an increase in their LV posterior wall thickness. All of these patients were hospitalized for inotropic support before cardiac transplantation. Follow-up was complete in all patients. Results are expressed as mean ± standard deviation (SD).
| Results |
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| Comment |
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Preparatory PAB was successful in inducing the necessary LV hypertrophy and LV pressure for ASO conversion in some but not all of our patients. There seems to be an age-dependent time when preparatory PAB has a smaller chance of resulting in successful anatomic correction. Although all of our successful ASO patients were less than 16 years of age, 2 of our PAB patients who required OCT were 6 and 9 years of age. Our 1 patient who died because of an inadequately prepared LV was 17 years old. There seems to be little trouble in inducing LV hypertrophy in infants with unoperated TGA who have aged beyond the neonatal period by PAB and systemic-to-pulmonary artery shunt [13, 14]. Why this is not true in older children may be related to two factors. First, the neonatal heart, unlike the older childs heart, has the ability to undergo myocyte hyperplasia for several months, which favors myocardial mass development [15]. Second, the childs heart with a failed atrial baffle operation often has some degree of biventricular failure, which may respond unfavorably to PAB and LV retraining. In our series the mean age at PAB was 12.2 years, the mean age at ASO was 11.5 years, and the mean age at OCT was 13.5 years. In the review by Prieto and colleagues [8], older age was a significant risk factor for mortality: mean ages for survivors and nonsurvivors were 11.0 ± 4.8 vs 15.8 ± 5.1 years, respectively. However, Cetta and associates [16] reported successful ASO conversion in a 36-year-old patient. In general, we would conclude from our data and clinical review that the older the patient, especially older than 16 years of age, the less likely ASO conversion will be.
A small subgroup of patients may be able to have successful ASO conversion without a preparatory PAB. We had 1 such patient in our series, a 12-year-old patient who had progressive subpulmonic obstruction and natural occurrence of LV hypertrophy. Several centers have reported successful "one-stage" arterial switch, often in the setting of pulmonary venous obstruction, which creates pulmonary hypertension and in effect prepares the LV serendipitously [1618].
The technical aspects of our series are interesting because we have addressed the problems of resultant neoaortic insufficiency and troubling atrial arrhythmias at the time of ASO. Five of our 6 patients who eventually had ASO had some kind of neoaortic valve reconstruction at the initial operation (n = 4) or aortic valve replacement later because of neoaortic regurgitation (n = 1). So far, neoaortic insufficiency has not occurred in the patients who had neoaortic reconstruction at the initial operation. Whether this will be maintained over time and whether this approach will compare favorably with those patients who did not have modified neoaortic reconstruction remain to be evaluated. Cochrane and colleagues [6] reported 2 of 16 patients having ASO conversion requiring aortic valve replacement (12%) and 5 other patients (31%) having mild aortic insufficiency under observation. Chang and coworkers [7] reported a high incidence of neoaortic insufficiency after anatomic correction, and 1 of their 5 patients required an aortic valve replacement 4 months after ASO.
There was hope during the initial evaluation of this strategy that once the ASO was performed, the atrial pressures would decrease and this would be accompanied by a resolution of atrial arrhythmias. This has proved not to be the case. As a result, we instituted a strategy to evaluate for atrial arrhythmias and to perform arrhythmia operations when appropriate. This strategy, which we have applied in other patients [11], has been successful in our 2 patients with nodal reentry tachycardia and atrial reentry tachycardia, respectively.
Four patients in this series required OCT after PAB because of biventricular failure. The mean age of these patients at OCT was 13.5 ± 7 years. One of those patients died 7 years posttransplant from chronic rejection. OCT has been reported in many patients with end-stage congenital heart disease, including those with failed atrial baffle procedures [7, 12]. In our series these patients tended to have had other prior procedurestricuspid valve replacement (2), pacemaker (2), superior vena cava obstruction (1)and were not as easy to obtain a reasonable LV pressure at the time of PAB.
There is a subset of failed atrial baffle procedure patients that undergoes preparatory PAB resulting in improved functional class without sufficient LV hypertrophy induction or LV pressure for ASO conversion. The patients in this subset may improve their hemodynamic status because of induction of LV hypertrophy and septal deviation toward the midline resulting in more favorable geometric conditions for tricuspid valve function and improved ventricular contractility. These findings have been reported previously [5, 6] and are consistent with our results. We have 1 patient who had two PABs over a 2.5-year period who did not develop sufficient LV pressure or hypertrophy to undergo ASO. She has, however, experienced increased functional class because of improved RV function and decreased tricuspid valve regurgitation. One has to consider whether PAB in a subset of these patients will represent a therapeutic endpoint. Unfortunately, the needed and resolving prospective trial is unlikely to be performed. In many ways this is a diminishing problem as the current standard of care for patients with TGA is neonatal arterial switch. However, the large number of patients with extant atrial baffle operations will require some attention in the future. This makes small series like this and others like it all the more important to document the results and discuss the options that are likely to present themselves.
A select group of patients with RV failure after atrial baffle operations can undergo staged conversion to ASO with the opportunity for excellent long-term cardiac function. Surgical modifications can address the problems of neoaortic insufficiency and persistent atrial arrhythmias. Some PAB patients will improve symptomatically but will not develop sufficient LV hypertrophy for ASO conversion. Whether PAB will represent a therapeutic endpoint in these patients remains to be seen. Those patients who develop biventricular failure after PAB will require cardiac transplantation.
| Footnotes |
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| References |
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