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Ann Thorac Surg 1998;66:829-835
© 1998 The Society of Thoracic Surgeons

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Original articles: Cardiovascular

Primum atrial septal defect in children: early results, risk factors, and freedom from reoperation

^a Division of Cardiovascular Surgery, Department of Surgery, and Division of Paediatric Cardiology, Department of Paediatrics, The Hospital of Sick Children, University of Toronto, Faculty of Medicine, Toronto, Ontario, Canada

Address reprint requests to Dr Williams, Division of Cardiovascular Surgery, The Hospital of Sick Children, 555 University Ave, Toronto, ON M5G 1X8, Canada

Presented at the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.

	Abstract

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Background. Repair of primum atrial septal defect in children usually is associated with a low operative mortality, except for a subgroup of children with congestive heart failure. To determine the early mortality and incidence of reoperation in children with primum atrial septal defect, we analyzed retrospectively the results of patients who underwent repair of this defect.

Methods. Between July 1982 and December 1996, 180 children underwent repair of primum atrial septal defect. The mean age at repair was 4.6 years (median, 3.6 years; range, 1 month to 16.4 years); of the 180 children, 23 were infants less than 1 year of age. Absent or mild symptoms were present in 145 (80%), whereas 34 (20%) of children presented with severe symptoms or congestive heart failure.

Results. Early mortality occurred in 3 (1.6%); 2 were less than 1 year of age. Follow-up ranged from 2 months to 14.5 years (mean, 6 ± 4.2 years). Actuarial survival is 98% at 10 years with no late deaths. Age less than 1 year is a predictor of death. During follow-up, 17 (9%) of the 180 patients underwent reoperation, 5 of whom were in the infant group. Five underwent reoperation for subaortic obstruction, and 12 for left atrioventricular valve regurgitation of whom 11 were repaired; and 1 required valve replacement. Age and preoperative moderate-to-severe left atrioventricular valve regurgitation were predictors of reoperation.

Conclusions. Results of the repair of primum atrial septal defect during childhood are favorable. Infants have a higher risk for death and reoperation. Left atrioventricular valve insufficiency and subaortic stenosis are important late complications and can be repaired safely at reoperation.

	Introduction

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Primum atrial septal defect (ASD-I), also referred to as partial atrioventricular septal defect, is part of the spectrum of atrioventricular septal defects. Children with ASD-I, as described by Anderson [1] and Penkoske [2] and their colleagues have an interatrial communication and an atrioventricular valve consisting of five leaflets guarding a separate left and right ventricular inlets, and an essentially intact inlet ventricular septum. These children present with a variable clinical picture, often with an asymptomatic murmur.

Since the initial report of a successful repair of ASD-I by Lillehei and colleagues [3] in 1955, results of the repair continue to improve because of a better understanding of the morphology of the lesion, refinements in surgical technique, improvement in preoperative and operative care, including better myocardial protection. In published reports multiple risk factors for early death were identified, among them severe preoperative congestive heart failure [4, 5], earlier age at repair [6], moderate-to-severe left atrioventricular valve (LAVV) regurgitation [4, 5, 7], and morphologic lesions of the LAVV [8, 9]. The reported mortality ranges from 3% to 36% [5, 6] depending on the group. Children who require repair at an earlier age because of severe failure to thrive or congestive heart failure are identified in the literature as having "unique features" and a worse outcome [6, 9]. Risk factors predicting late reoperation after initial repair include severe prerepair LAVV regurgitation [10] and abnormalities of the left subvalvular apparatus [8].

We undertook this review to examine the trends in the early outcome of children undergoing ASD-I repair. We will elucidate whether the previously reported risk factors continue to be predictors of outcome given our current understanding of the morphology of atrioventricular valves and improved surgical results.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Between July 1982, when our computerized database was established, and December 1996, 180 consecutive children underwent repair of ASD-I at The Hospital for Sick Children, Toronto, Canada.

Children with unrestrictive inlet ventricular septal defect, unbalanced defects with severe hypoplasia of either of the ventricles requiring univentricular repair, and atrioventricular or ventriculoarterial discordance were excluded from this analysis. Follow-up information was available for 171 of the 177 (97%) surviving children. Mean follow-up was 6 ± 4.2 years (range, 2 months to 14.5 years).

Data acquisition
Details of hospital records including clinical presentation, operative reports, pre- and postoperative investigations, reoperations, and echocardiographic follow-up were analyzed. Follow-up data were obtained by reevaluation of the child in the outpatient clinic, by telephone, or by contact with their referring physicians.

Patient characteristics
There are 97 girls and 83 boys in the series. The mean age at operation was 4.6 ± 3.59 years (median, 3.6 years; range, 1 month to 16.4 years). The children’s characteristics are summarized in Table 1. The diagnosis of an ASD-I was established by echocardiography in all 180 children. In addition 60 (33%) had preoperative cardiac catheterization. Associated anomalies were present in 102 children (Table 2). Three children had the morphology of normally developed mitral and tricuspid valves with no clefts.

View larger version (12K): [in this window] [in a new window]   Fig 1. Age distribution of the entire cohort sorted by age groups in years.

Our approach to management of the cleft in the LAVV was individualized for each child. After opening the right atrium, the competency of the LAVV was assessed under cardioplegic arrest by filling the left ventricle with cold saline. The LAVV was inspected and the apex and base of the cleft were identified. Stay sutures were inserted in the free edge of the cleft at its junction with the major chordae. This allows assessment of the cleft length, alignment and the effective orifice of the LAVV. Interrupted braided sutures are used to close the cleft using the rolled edge thereby avoiding the opposing surfaces of the leaflet. The orifice of the LAVV was measured and maintained within one standard deviation of normal diameter for age.

In children with a parachute LAVV, complete closure of the cleft may predispose the valve to stenosis because of the peculiar subvalvular anatomy; the outlet of blood from the left atrium is through the space between the converging chordae. Approximating the bridging leaflets completely in parachute valves decreases the effective orifice excessively.

In children with a double-orifice LAVV, the cleft length is variable and the degree of incompetence and the risk of causing stenosis determine closure of the cleft. The accessory orifice is not closed; neither is it opened to create a common orifice. The subvalvular apparatus may cause or aggravate stenosis.

In this series, the cleft in the LAVV was closed completely in 107 (59%) of the 180 children, and partially in 52 (29%); no cleft closure was done in 21 (12%) children.

Autologous pericardium was used to patch the atrial defect in 171 (95%) and Dacron in 9 (5%). The patch was initially secured rightward to the junction of the inferior bridging leaflets of the atrioventricular valve with a fine monofilament continuous suture. This continuous suture line is placed along the annulus of the LAVV to avoid the conduction system and to leave the coronary sinus draining physiologically to the systemic venous side. This approach avoids complex baffling in the 13 children (7%) who have an anomalous left superior vena cava draining to right atrium.

Recently, intraoperative transesophageal echocardiography is used routinely after weaning from cardiopulmonary bypass to examine the adequacy of LAVV repair and to rule out the presence of a subaortic gradient or residual atrial shunt. In addition, caval and pulmonary oxygen saturations are obtained. Moderate residual LAVV regurgitation or a residual atrial shunt are indications to reinstitute cardiopulmonary bypass to correct the residual defects.

Associated procedures
Associated procedures were done in 25 children and are as follows: muscular ventricular septal defect closure, 7 patients; subaortic resection for left ventricular outflow obstruction, 6; repair of partial anomalous pulmonary venous drainage, 5; bidirectional cavopulmonary shunt, 2; lung biopsy, 2; patch fenestration, 2; pacemaker implant, 1; division of posterolateral tract (Wolf Parkinson White syndrome), 1; and coarctation repair, 1 patient. The associated ventricular septal defects were restrictive muscular and remote from the inlet septum, which differentiates them from the ventricular septal defects of the complete form of atrioventricular septal defect.

Subaortic fibromuscular obstruction was approached through the aortic valve in children with subaortic gradient. Six children underwent concomitant repair of ASD-I and subaortic resection. In children with borderline ventricular size (70% of predicted normal volume) deemed suitable for a biventricular repair, an associated bidirectional cavopulmonary shunt (n = 2) or an atrial patch fenestration (n = 2) is done as an adjunct to the repair to offload the ventricle. In children presenting with coarctation of the aorta and ASD-I, an initial repair of the coarctation, usually in the first few months of life, is undertaken, followed by complete intracardiac repair at age 3 to 4 years of life. Only 1 child in this series underwent a concomitant repair.

Data analysis
Data were analyzed with SPSS statistical software (release 6, SPSS, Inc, Chicago, IL). Continuous variables are expressed as mean ± standard deviation (range). The ² test was used to test the difference in proportions. The cohort was divided into two groups, infants equal or less than age 1 year and older children. Univariate and multivariate stepwise Cox regression analysis was done to identify the risk factors associated with mortality, reoperation, and the incidence of late LAVV regurgitation. Age was entered in the models as a dichotomous variable with 1 year being the dividing age. Variables entered as continuous were weight, body surface area, preoperative mean pulmonary artery pressure, total cardiopulmonary bypass time, myocardial ischemic time, and follow-up time. Variables entered as categorical data, in addition to age, were gender, presenting symptom, Down’s syndrome, presence of other anomalies, grade of pre- and postoperative LAVV regurgitation, type of patch, closure of LAVV cleft, concomitant procedure, complication, death, and reoperation. Highly correlated variables were removed from the statistical model. Kaplan-Meier curves were constructed to determine estimates of survival and freedom from reoperation.

	Results

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Early mortality
In-hospital mortality occurred in 3 (1.6%) of 180 children. Two of the deaths occurred in infants less than 1 year old. These infants had severe congestive heart failure and died in the postoperative period of myocardial failure. Their death occurred in the early part of this series (before 1986). In the last 141 operations there was 1 (0.7%) early death (p = 0.05). The third child who died was referred at age 14 years with a diagnosis of ASD-I associated with subaortic obstruction. He underwent closure of the defect with autologous pericardial augmentation of the superior leaflet of the LAVV. The postoperative period was complicated by sepsis. Echocardiography showed dehiscence of the patch in the LAVV. The child underwent a second operation to repair the dehiscence, but he died 14 days after the operation of low cardiac output and multiorgan failure.

The 10-year survival is 98% (95% confidence interval, 0.95 to 0.99). All children are in New York Heart Association functional class I or II at recent follow-up and there were no late deaths. The only significant predictors of deaths in univariate and multivariate analysis is age less than 1 year (p = 0.023). The presence of severe symptoms, which was associated with young age, approached statistical significance (p = 0.06).

Of the 23 children who underwent operation at less than 1 year of age (Table 3), 2 died (early in the series) and 6 required reoperation. In comparison with the older group (n = 157), both the difference of mortality risk (2 of 23 versus 1 of 157; p = 0.05) and reoperation rate (6 of 23 versus 11 of 157; p = 0.01) are statistically significant.

Morbidity
Early morbidity occurred in 46 children (Table 4 ). Atrial arrhythmia (3%) and all incidences of atrioventricular block (1.6%) in the early postoperative period were transient and did not require placement of a permanent pacemaker. One child had a pacemaker inserted during the initial repair. This was a child with ASD-I, dextrocardia, left atrial isomerism, interrupted inferior vena cava, bilateral superior vena cavae, partial anomalous pulmonary venous connection, and sick sinus syndrome. Another child who underwent repair at 10 years of age required permanent pacemaker insertion 6 years after the initial repair for development of late-onset complete atrioventricular block.

Reoperation for LAVV valve regurgitation occurred in 12 children at a mean interval of 2.4 ± 2.2 years (range, 0.3 to 7.6 years). Freedom from reoperation for LAVV valve regurgitation at 10 years is 89% (95% confidence interval, 0.85 to 0.93; Fig 2 ). At reoperation, LAVV repair was performed in 11 children and a 9-year-old child required a valve replacement with a mechanical valve (27-mm Bjork-Shiley). During reoperation a residual LAVV cleft was found in 9 children, disrupted previously closed cleft in 2, obvious annular dilatation in 3, and small residual ASD in 2 patients. Reparative techniques used included a combination of completion of cleft closure in 11 patients, commissuroplasty in 6, DeVega-type annuoloplasty in 2, shortening of chordae in 2, patch repair of LAVV in 1, and mechanical valve in 1 patient. Except for 1 child who required only closure of residual LAVV cleft, all other children required more than one component of repair.

View larger version (10K): [in this window] [in a new window]   Fig 2. Freedom from reoperation for left atrioventricular valve (LAVV) regurgitation.

Univariate risk factor analysis revealed age less than 1 year (p = 0.02), and moderate-to-severe preoperative LAVV regurgitation (p = 0.008) predicted reoperation for LAVV regurgitation. These two risk factors proved significant in the multivariate model as well (p = 0.01 and 0.006, respectively). Other variables entered into the statistical model were not predictive of reoperation.

Reoperation for subaortic stenosis occurred in 5 children at a mean interval of 5.7 ± 3.6 years (range, 2.7 to 11.7 years) after initial repair. Only 1 of these children had subaortic resection in the primary repair. Freedom from reoperation for subaortic stenosis at 10 years is 90% (95% confidence interval, 0.87 to 0.95; Fig 3 ). The mechanism of subaortic stenosis and its repair has been previously reported [11]. Repair included subaortic resection of the fibromuscular tissue through the aortic valve in all children and an additional infundibular patch (septoplasty) [12] to enlarge the left ventricular outflow tract in 1 child.

View larger version (9K): [in this window] [in a new window]   Fig 3. Freedom from reoperation for subaortic stenosis (SAS).

	Comment

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Surgical repair of uncomplicated ASD-I, for the most part, is simple and yields generally good results, except in specific situations. Infants who present with severe congestive heart failure and require surgical repair have been identified as a higher risk group of death [6, 9]. The reported mortality for this group is 25% to 36% [6, 9]. In our series the mortality was 8.6% for infants and 0.6% for older children (p = 0.05). Infants have been reported to have a higher incidence of left-sided anomalies, abnormal LAVV, subaortic stenosis, pulmonary hypertension, and a lower incidence of Down’s syndrome [6, 8]. Our series confirms the higher incidence of severe symptoms, mildly hypoplastic ventricles, pulmonary hypertension, death, and reoperation in the infant group. However, we found no statistical difference in the incidence of Down’s syndrome and associated anomalies including LAVV anomalies.

Our series demonstrates the improved results in the repair of children with ASD-I in the current era. We speculate that previously reported risk factors on mortality has diminished in the recent years. This is in part attributable to the better understanding of the morphology of the LAVV and the disposition of the conduction system in this type of defect. In our series the early mortality of 1.6% improved in the recent era (after 1986) to 0.7%.

The atrioventricular valves in children with ASD-I are not synonymous with mitral and tricuspid valves [13]. The concept of a trileaflet LAVV, introduced by Carpentier [14], has become the accepted description of the LAVV morphology. As he described it, the cleft is a functional commissure between the two bridging leaflets, although lacking commissural support [13, 14]. This concept has been accepted and promoted by Anderson [1] and Penkoske [2] and their colleagues. The phenotypic feature of atrioventricular septal defects is a common atrioventricular junction in which the left ventricular component is guarded by a valve with three discrete leaflets [15]. In our series 3 children had the morphology of a mitral and tricuspid valves with no clefts. This finding has been reported previously by Pillai and associates [13], and may represent a forme fruste of ASD-I. On the other hand, a cleft in an otherwise normal mitral valve is not an atrioventricular septal defect [16]. We adopted an individualized approach to closing the cleft in the LAVV, depending on the amount of regurgitation. We prefer to close the defect completely provided the closure does not cause stenosis, or distortion, even in the absence of any leakage through the valve.

As with complete atrioventricular septal defects [17], LAVV regurgitation is the most common cause of late reoperation after primary repair. Incidence of reoperation for LAVV regurgitation in published series ranges from 7% to 22% [5, 10], and in our series the incidence was 7%, and an 89% freedom from reoperation at 10 years. Although we found residual cleft in the majority of children reoperated for LAVV regurgitation (9 of 12), almost all children (11 of 12) required some form of reduction annuoloplasty or commissuroplasty or other reparative technique in addition to cleft closure to improve valve function. This finding suggests that although a residual cleft has been consistently blamed for residual regurgitation, other morphologic changes may also be equally important, such as annular dilatation or chordal elongation. We speculate changes in chordal length, annular dilatation, leaflet prolapse, and disrupted cleft sutures in the interval between the initial operation and the reoperation may change the look of a previously "completely" closed cleft. On the other hand, it is equally possible that regurgitation through the cleft produces annular dilatation or chordal elongation.

The association of subaortic stenosis with complete or partial atrioventricular septal defect has been previously described [17, 18]. There is a higher association of subaortic stenosis with partial atrioventricular septal defect. At our institution, the overall incidence of subaortic obstruction in complete atrioventricular defects is 1.3%, and freedom from reoperation for subaortic stenosis is 95% at 10 years [17], compared with an incidence of 3% in this series with a 90% freedom at 10 years. There are three causes for subaortic stenosis in atrioventricular defects: discrete fibromuscular ring, tunnellike obstruction, and left valvular and subvalvular tissue attached to the outflow tract [19]. Management of subaortic stenosis should be tailored to the cause: subaortic fibromuscular resection, septoplasty or modified Konno [12], or LAVV leaflet augmentation [19], respectively. Our approach in the presence of a significant gradient across the left ventricular outflow tract (ie, >40 mm Hg) is a concomitant subaortic resection through the aortic valve and repair of the ASD-I. Unfortunately because of the unique morphology of the left ventricular outflow tract in atrioventricular septal defect, these children are predisposed to the late development of subaortic obstruction. In addition it is previously reported [16, 20] to be higher in Rastelli type A complete atrioventricular septal defect and ASD-I defects because of the attachment of the superior bridging leaflet to the scooped ventricular septum. On the basis of this observation it has been suggested that the superior bridging leaflet be detached from the ventricular septum, essentially converting it to a complete form, then the leaflet is elevated by inserting a patch of autologous pericardium [20]. This approach may provide a good solution for the problem, although the recent publication by Wilcox and colleagues [21] in which they described attaching the bridging leaflets of a complete atrioventricular septal defect to the crest of the ventricular septum, essentially reverting it to a primum defect, with good early results, is of interest in this context. During reoperations for subaortic obstruction we did a transaortic resection in 6 children in this series; in 1 child we inserted a patch in the infundibular septum.

In this series none of the children had development of early permanent complete atrioventricular block, which compares favorably with other series [5]. Only 1 child required insertion of a pacemaker, and this occurred late (6 years after operation). Reports of long-term follow-up in adults indicate a similar trend of late development of complete atrioventricular block [22, 23].

In conclusion, repair of ASD-I in children can be done with low operative mortality. Young age (<1 year) increases the operative risk. Preoperative moderate-to-severe LAVV regurgitation are predictors of reoperation for LAVV regurgitation. Incomplete closure of the cleft is predictive of the development of moderate-to-severe LAVV regurgitation postoperatively. Reoperation for LAVV regurgitation and subaortic stenosis are important complications, leading to 11% and 10% chance of reoperation, respectively, within 10 years of initial repair.

	Acknowledgments

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
We acknowledge Drs George A. Trusler, Ivan M. Rebeyka, Michael D. Black, and Glen S. Van Arsdell who did primum atrial septal defect repair on some of the children in this series.

	References

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 

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