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Ann Thorac Surg 1999;67:177-181
© 1999 The Society of Thoracic Surgeons

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Original Articles

Does left ventricular outflow tract obstruction influence outcome of interrupted aortic arch repair?

^a Cardiac Surgical Unit, Royal Children’s Hospital, Melbourne, Australia
^b Department of Cardiology, Royal Children’s Hospital, Melbourne, Australia

Accepted for publication July 7, 1998.

Address reprint requests to Dr Karl, Cardiac Surgical Unit, Royal Children’s Hospital, Flemington Rd, Parkville, 3052, Victoria, Australia

	Abstract

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Background. In previous studies left ventricular outflow tract obstruction (LVOTO) has been recognized as an important factor affecting survival and reoperation probability in patients having repair of an interrupted aortic arch (IAA).

Methods. All 72 patients who underwent operation for IAA from January 1, 1985 to June 30, 1997 were reviewed. The presence or absence of LVOTO was noted and the immediate and long-term results were analyzed.

Results. Type A IAA was found in 23 patients and type B IAA in 49 patients. Anomalous right subclavian artery was noted in 15 patients, all of whom had type B IAA. LVOTO was identified in 36 patients before arch repair and was associated with the presence of type B IAA and anomalous right subclavian artery (p = 0.02 and 0.007, respectively). There were 2 hospital deaths (within 30 days) for a mortality of 2.8% (confidence limit [CL] = 0% to 6.6%). There were 7 late deaths over 3,737 patient-months of follow-up (9.7%, CL = 2.9% to 16.6%). Actuarial survival for the whole cohort was 84.8% (CL = 73.2% to 94.4%) at 12 years. There was 87% 10-year survival (CL = 60% to 93%) for patients with LVOTO at presentation compared with 83% (CL = 62% to 92%) for patients without LVOTO (p = 0.85, hazard function 0.87). Twenty-eight patients have required at least one reoperation. The use of conduits to restore right ventricular to pulmonary artery continuity predicted the need for reoperation (p = 0.0001). Patients with presence of a nonseptatable heart were also more likely to need reoperation (p = 0.027) when compared to the rest of the cohort. Freedom from reoperation was 47.3% (CL = 30% to 62%) at 12 years. In patients with LVOTO, freedom from reoperation (55% at 10 years, CL = 33% to 72%) was not significantly different from those patients without LVOTO at presentation (29% at 10 years, CL = 7% to 56%; p = 0.97, hazard function 0.7). Actuarial freedom from recurrent arch obstruction requiring reintervention was 82.7% (CL = 66.7% to 98.7%) at 12 years.

Conclusions. Neonatal complete repair of patients with IAA is possible with low mortality. LVOTO was not a significant risk factor for hospital or late death in patients having complete repair of IAA during this period. The use of conduits for right ventricular to pulmonary artery continuity and the presence of a nonseptatable heart are important risk factors for further operation and will continue to provide added morbidity to these patients.

	Introduction

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Left ventricular outflow tract obstruction (LVOTO) complicates interrupted aortic arch (IAA) in up to 57% of patients [1]. There are multiple anatomic causes of this LVOTO. Most commonly LVOTO is the result of posterior deviation of the infundibular septum, but it also may result from hypertrophy of the anterolateral muscle bundle of the left ventricle, a small aortic valve annulus, or the presence of a bicuspid or dysplastic aortic valve [2, 3]. LVOTO may exist at more than one level in the same patient.

Several studies have emphasized the impact of LVOTO on operative mortality, late survival, and the probability of reoperation in patients with IAA [1, 3–8]. However, as operative mortality has fallen for repair of IAA in recent years, the effect of LVOTO on outcome has assumed greater importance. We analyzed all our patients undergoing IAA repair, with particular emphasis on LVOTO and associated cardiac lesions and their effect on morbidity and mortality.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Patients
Analysis was performed retrospectively by us using a comprehensive database. Confidence intervals for proportions are all expressed as 95%. Between January 1, 1985 and June 30, 1997, 72 patients underwent operation for IAA. The commencement date of the study coincides with the initiation of our policy of one stage neonatal repair of IAA and associated intracardiac defects whenever feasible. The age range was 1 to 180 days (median, 3 days), and the weight range was 0.96 to 4.52 kg (median, 3.04 kg). Operations were performed by us as well as former department members Drs Roger Mee, Ash Pawade, Shunji Sano, and William Brawn.

Type A IAA was diagnosed in 23 patients and type B IAA in 49 patients. Associated cardiac lesions (72 patients) noted are as follows: ventricular septal defect, 44; transposition of the great arteries and ventricular septal defect, 2; truncus arteriosus, 9; double inlet left ventricle with transposition of the great arteries, 6; aortopulmonary window, 3; anteroposterior window and ventricular septal defect, 1; double outlet right ventricle, 6; and none, 1 patient. Anomalous right subclavian artery was noted in 15 patients, all of whom had type B IAA.

The diagnosis of LVOTO was made using echocardiography in all 72 patients. In 10 patients, cardiac catheterization was required to characterize complex anatomic features and to augment the echocardiographic findings. The dimensions of the subaortic area, the aortic annulus, the ascending aorta, and the descending thoracic aorta beyond the level of the ductal insertion and at the level of the diaphragm were measured echocardiographically. The criteria for the presence of LVOTO used in this study were the following, isolated or in association: (1) dimensions of the LVOT smaller than the mean value minus 1 standard deviation (indexed to body surface area); (2) presence of a gradient of >10 mm Hg across the LVOT measured by Doppler echocardiography or at cardiac catheterization; (3) posterior deviation of the conal septum into the LVOT; and (4) presence of obstructing tissue in the subaortic area. In more recent years the Z-value determinations for the LVOT dimensions and the ratio of the subaortic area to the descending thoracic aorta have been used more consistently.

Di George syndrome was diagnosed in 20 patients, partial in 12, and complete in 8. Type B IAA was found in 18 of the 20 patients with Di George syndrome and type A IAA in the remaining 2 (p = 0.01). Criteria for diagnosing Di George were absent or hypoplastic thymus, reduced peripheral blood T-lymphocyte count, facial dysmorphism, and hypocalcemia. Partial Di George syndrome was diagnosed if all criteria existed, with the exception of a reduced peripheral blood T-lymphocyte count. Since 1996, fluorescent in situ DNA hybridization studies have been done on all patients with IAA to identify 22q11 deletion.

All patients but 1 were in some degree of cardiac failure, with 10 in cardiogenic shock. Forty-seven patients required some degree of resuscitation, with 48 patients requiring intubation and ventilation preoperatively. Prostaglandin E₁ was used to maintain ductal patency in 64 patients, with inotrope administration in 44 and sodium bicarbonate infusion for reversal of metabolic acidosis in 33 patients. Patients underwent operation if, with resuscitation, there was evidence of adequate lower body perfusion, reversal of metabolic acidosis, and evidence of adequate pulmonary function. All patients but 1 could be stabilized before operation was performed. This latter patient continued to deteriorate despite adequate resuscitative measures, and had an arch repair while still in a poor metabolic and hemodynamic condition.

Operative technique
At initial arch repair, 62 patients were approached through a median sternotomy alone, 9 through a left posterolateral thoracotomy, and 1 patient through both a thoracotomy and sternotomy at the same operation. An initial thoracotomy approach was only used in patients who were not thought to be suitable for neonatal biventricular repair, were in poor clinical and metabolic condition despite resuscitation, and in 1 patient who had an intact ventricular septum. All 9 of the patients initially having arch repair using a lateral thoracotomy required subsequent transternal revision of their arch repair using deep hypothermia and circulatory arrest (DHCA).

Aortic arch reconstruction was performed with DHCA in 63 patients at the first operation. Our technique for initiating cardiopulmonary bypass and DHCA for arch repair has been described in detail [8]. During cooling to a core temperature of 18°C, the upper descending aorta was mobilized as far distally as possible, well beyond the ductus insertion. With a clamp on the descending aorta and the head vessels occluded, all ductal tissue was excised, and then the arch was reconstructed using a 7-0 or 8-0 polypropylene suture. After completion of the arch repair, the intracardiac defects were repaired while rewarming on cardiopulmonary bypass.

At initial arch repair, 66 patients had a direct end-to-side anastomosis, 1 each had homograft arch augmentation, subclavian flap repair, both subclavian flap and homograft arch augmentation, left common carotid turndown, and a polytetrafluoroethylene interposition graft. One patient had a palliative Van Praagh operation [2].

It is important in our repair technique to keep the ventricular septal defect patch relatively small to prevent bulging of the infundibular septum into the outflow tract and the development of LVOTO. In patients with the diagnosis of LVOTO made before operation, transaortic inspection of the LVOT, aortic valve, and subaortic area was performed as required. In the presence of clearly obstructing muscle or valvular tissue, resection or valvotomy, or a combination of both, was done at this time.

Pulmonary artery banding was necessary in 10 patients at initial operation, 5 of whom had a staged repair of their arch. Indications for banding were nonseptatable hearts (univentricular, hypoplastic ventricle, or multiple ventricular septal defects) (n = 4), complex double outlet right ventricle (n = 3), multiple ventricular septal defects (n = 2), and very poor medical condition despite resuscitation (n = 1).

The mean cardiopulmonary bypass time was 96.5 minutes (confidence limit [CL] = 87.1 to 105.8 minutes), DHCA time 45.6 minutes (CL = 40.4 to 50.9 minutes), and ischemic time 62.1 minutes (CL = 56.4 to 67.8 minutes). Isolated myocardial perfusion was used in 11 patients [9]. Of the 63 patients having repair through a median sternotomy, delayed sternal closure was required in 16.

	Results

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Left ventricular outflow tract obstruction
The LVOTO was found in 36 patients, 29 patients with subaortic stenosis and 7 with isolated aortic stenosis. Of the 49 patients with IAA type B, 29 had LVOTO and 12 of the 15 patients with anomalous right subclavian artery had LVOTO. Therefore, the LVOTO was found to be associated with both IAA type B and anomalous right subclavian artery (p = 0.02 and 0.007, respectively).

The LVOTO was regarded as severe enough to require surgical treatment in 15 (42%) of the 36 patients. Subaortic stenosis was dealt with at the first operation by resection of obstructing muscle tissue through the pulmonary artery in 2 patients, the right ventricle in 3, and the right atrium in 3 patients. Four patients with LVOTO had an arterial switch operation and 3 had a Damus connection in the presence of LVOTO. Only 1 patient, who also had subaortic muscle resection, required an aortic valvotomy. In the remaining 21 patients with LVOTO, arch repair with correction of the intracardiac defect was sufficient.

Survival
There were two hospital deaths (2.8%; CL 0% to 6.6%). One occurred in a patient with a IAA type B who had responded poorly to resuscitation. The patient had an 8-mm graft placed between the main pulmonary artery and the descending thoracic aorta with distal main pulmonary artery banding. The second hospital death occurred in a patient with IAA type A without LVOTO who had irreversible pulmonary hypertension after repair and could not be weaned from ventilator support.

There were seven late deaths during 3,737 patient-months follow-up (mean, 52 months). Four patients were lost to follow-up. Three deaths occurred in premature infants with bronchopulmonary dysplasia, who were ventilator dependent at the time of initial operation. All three died 2 to 4 months after arch repair from complications of their respiratory condition. Another patient, who had a gradient of 70 mm Hg across the aortic valve 3 months after operation, died after unsuccessful balloon valvuloplasty. This patient had a subaortic resection, but the aortic valve had not seemed obstructive at the time of arch repair. A patient with double outlet right ventricle and a noncommitted ventricular septal defect died during elective diagnostic catheterization from sustained ventricular fibrillation, a complication of the procedure. Another patient with double outlet right ventricle and a noncommitted ventricular septal defect, who had an initial neonatal arch repair with pulmonary artery banding, died at age 16 months after conversion to a bidirectional cavopulmonary shunt, from hypoxemia and low cardiac output. One patient died suddenly at home 4 years after arch repair. This child had had two operations subsequent to arch repair (removal of a pulmonary artery band with closure of a ventricular septal defect, and repair of a regurgitant tricuspid valve with residual ventricular septal defect closure).

Actuarial survival for the cohort was 84.8% (CL = 73.2% to 94.4%) at 46 months with no further death to 12 years of follow-up. Actuarial survival curves for patients with and without LVOTO are shown in Figure 1. There was 87% 10-year survival probability (CL = 60% to 93%) for patients with LVOTO at presentation compared with 83% (CL = 62% to 92%) for patients without LVOTO. Comparison of the two survival curves (Mantel-Haenszel method) yielded p = 0.85 and hazard function 0.87.

View larger version (12K): [in this window] [in a new window]   Fig 1. Actuarial survival curves for patients with and without left ventricular outflow tract obstruction (LVOTO), with standard error for each group.

Reoperation
Twenty-eight patients required at least one reoperation for indications listed in Table 2 , 6 for LVOTO. One of the 8 patients who had resection of subaortic muscle required repeat resection. Three patients, who had LVOTO but had no resection at the time of their arch repair, required a second operation for relief of their LVOTO. Another 2 patients developed new subaortic stenosis after repair. One patient eventually required a Konno operation after three attempts at resection. This patient had a 4.5-m aortic annulus with an unobstructed subaortic area, and a weight of 1.85 kg at the time of arch repair. Simple resection of the obstructing subaortic muscle tissue in the other patient was curative.

View larger version (12K): [in this window] [in a new window]   Fig 2. Actuarial freedom from reoperation for patients with and without left ventricular outflow tract obstruction (LVOTO) with standard error for each group.

As one would expect, the use of conduits to restore right ventricular to pulmonary artery continuity predicted the need for reoperation (p < 0.001). Likewise, patients who had nonseptatable hearts at initial operation were more likely to need reoperation (p = 0.027) as compared to the rest of the patient cohort.

Recurrent arch obstruction was diagnosed by a peak gradient of >30 mm Hg at rest or degree of symptoms related to lower limb ischemia with any stenosis of the anastomotic site. Eleven patients developed recurrent arch obstruction. Three had successful initial balloon angioplasty but 2 of the 3 eventually needed surgical revision. Of the remaining 8 patients, 6 have had surgical revision of their arch repair site. Five of them initially had a direct anastomosis and 1 had a polytetrafluoroethylene graft. Another 2 patients who had polytetrafluoroethylene grafts await replacement, as the grafts have become gradually obstructed over 10 years. Actuarial freedom from recurrent arch obstruction requiring reintervention was 82.7% (CL = 66.7% to 98.7%) at 12 years.

	Comment

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
The first successful direct correction of IAA with repair of the associated intracardiac defect was reported by Trusler and Izukawa in 1975 [10]. Early experience with this policy resulted in mortality of up to 65%, particularly in the presence of LVOTO [7]. Fortunately, mortality for patients having repair of IAA has decreased in parallel with improvements in results of neonatal repair of other complex heart lesions over the past 15 years [11, 12]. The focus has thus moved from early outcome to medium and long-term results [4].

The LVOTO had been recognized as an important predictor of nonsurvival and reoperation in patients with IAA in other studies. However, we could not find a strong association of survival or reoperation probability with LVOTO. We have assumed that the diagnosis of LVOTO was uniform throughout the study period but the precision with which LVOTO was diagnosed has become more precise in more recent years. Initially, cardiac catheterization was used more frequently to diagnose LVOTO. It has been pointed out by several investigators that even in the presence of a narrow LVOT, there may be no measurable gradient because of the relatively small volume of blood flowing across it [13, 14]. This volume is further reduced in patients with type B IAA and those with anomalous right subclavian artery. The echocardiographic criteria used to diagnose LVOTO are now standardized, but were not uniformly applied in the earlier years of this study, therefore the precision of the diagnosis is uncertain [12, 14]. The 2 patients who were thought not to have LVOTO at initial arch repair and developed LVOTO were both noted to have small aortic annuli, but adequate normalized outflow tract dimensions. These LVOT did not grow as expected and became obstructive over time. It appears that although patients may have LVOTO of varying degrees of severity, a small proportion will require actual surgical intervention. The remainder may be improved by restoration of normal intracardiac anatomy and pressure differential between the left and right ventricles [3, 6]. One may speculate that provided that the ventricular septal defect patch is not too large, it appears to pull the infundibular septum out of the LVOT after repair, preventing progression of LVOTO. Although we have not used it, the concept of placing the patch on the left side of the conal septum is also attractive [4, 12].

From our analysis, it appears that there will be patients who will develop recurrent or new LVOTO and will require reoperation, but this will not affect 10-year survival. These patients are a small proportion of all patients having LVOTO. Although we expressed concern about the ongoing recurrence of LVOTO in the past, it appears that this will be of less importance than initially thought [8].

In patients with a diminutive annulus, a Ross-Konno type operation has been used by Reddy and Starnes and their colleagues [15, 16] with good results. With the evidence for growth of the pulmonary autograft, it can be presumed that recurrent LVOTO will become even less frequent [15, 17]. Some researchers still advocate repair of the arch and the intracardiac defect, even in the presence of a small annulus. The subsequent growth of the annulus can be satisfactory without further intervention [6, 11]. Those patients whose left ventricular to aorta complexes do not grow can then have a Ross-Konno type repair later in childhood.

Although multiple variables were reported in the Congenital Heart Surgeons Society Study as risk factors for death, we could find no similar predictors. However, total circulatory arrest time correlated with death at any time during follow-up. The deaths in these patients did not appear to be related to their prematurity or to any neurologic condition, and the increased duration of circulatory arrest more likely pointed to technically difficult arch repairs in small infants.

It is clear that the potential for long-term survival is excellent, with a low incidence of recurrent arch obstruction. The potential for growth of the aortic arch after repair is well documented and this reinforces our policy of direct anastomosis wherever feasible [8, 18, 19]. However, the need for reoperation remains a concern in the patient population as a whole and is not influenced by the presence of LVOTO. The use of conduits for arch repair or right ventricular to pulmonary artery continuity negatively influences freedom from reoperation, as all will require replacement at some stage in childhood. Early homograft and porcine valve degeneration is well described in childhood [20]. A more durable conduit for the pediatric population is unavailable, and this will continue to provide indications for reoperations. Patients who are candidates for single ventricle repairs will all need multiple reoperations before they have their Fontan circulation completed. These reoperations are planned and unavoidable and do not appear to affect survival.

In conclusion, complete repair of IAA in the neonatal period is possible in the present surgical era with low mortality. LVOTO as a risk factor for both operative and late mortality, and as well as for reoperation, has been neutralized to a large extent. The use of conduits increases the risk of reoperation, as does single ventricle anatomy, without an increased risk for death. There is a small risk of recurrent arch obstruction that can be dealt with by angioplasty or operation with low risk [21]. In the future, the morbidity related to patients with IAA will assume increasing importance, in particular neurologic development and the ongoing need for conduit replacement.

	Acknowledgments

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Dr. Mas’ work was partially supported by a grant from the Caja Costarricense de Seguro Social, Costa Rica.

	References

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): James O. Fulton Christian P.R. Brizard Andrew D. Cochrane Tom R. Karl Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fulton, J. O. Articles by Karl, T. R. Search for Related Content PubMed PubMed Citation Articles by Fulton, J. O. Articles by Karl, T. R.