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Original Articles: Pediatric Cardiac

Results of Definitive Repair of Complete Atrioventricular Septal Defect in Neonates and Infants

^a Section of Cardiac Surgery, University of Michigan Medical School, Ann Arbor, Michigan
^b Division of Pediatric Cardiology, University of Michigan Medical School, Ann Arbor, Michigan

Accepted for publication February 11, 2008.

^_* Address correspondence to Dr Ohye, 144 CVC/SPC 5864, 1500 E Medical Center Dr, Ann Arbor, MI 48109-5864 (Email: ohye{at}umich.edu).

	Abstract

Top Abstract Introduction Patients and Methods Results Comment References

 
Background: Early surgical intervention for complete atrioventricular septal defect (AVSD) has contributed to a decline in postoperative mortality.

Methods: We retrospectively evaluated outcomes in 116 complete AVSD patients undergoing definitive repair from February 1997 through October 2002. Patients with an unbalanced AVSD not suitable for biventricular repair, tetralogy of Fallot, or double-outlet right ventricle were excluded.

Results: Median age at operation was 4.8 months (range, 9 days to 5.4 years); weight was 4.8 kg (range, 2.1 to 23 kg). Follow-up was 93% complete (mean, 27 months; range, 1 to 73 months). Early definitive repairs were performed in 98% (110 of 112) of patients initially presenting to our institution. Ninety-two patients (79%) underwent repair before 6 months of age, including 25 (22%) before 3 months. Actuarial survival at 1, 3, and 5 years was 98%, 95%, and 95%, respectively. Seventy-five patients (68%) had trivial to mild left AV valve regurgitation at discharge; moderate or severe left AV valve stenosis developed in 3 (3%). Actuarial freedom from reoperation for left AV valve dysfunction at 1, 3, and 5 years was 94%, 89%, and 89%, respectively. Actuarial freedom from reoperation for left ventricular outflow tract obstruction at 1, 3, and 5 years was 100%, 93%, and 90%, respectively.

Conclusions: Definitive repair for complete AVSD can be performed in early infancy with excellent results. The two-patch technique is a safe and reproducible surgical method that can achieve low mortality and good midterm outcomes even in very young infants.

	Introduction

Top Abstract Introduction Patients and Methods Results Comment References

 
Early surgical intervention for complete atrioventricular septal defect (AVSD) has become the treatment of choice at many centers. This trend has contributed to the recent decline in the postoperative mortality [1–5]. However, despite this decrease in mortality, residual left atrioventricular (AV) valve regurgitation and the need for reoperation related to left AV valve dysfunction or left ventricular outflow tract (LVOT) obstruction remain problematic. In addition, although many surgeons would agree that definitive surgical repair before age 6 months provides a better clinical outcome, others maintain that palliative interventions still play an important role in the management for infants who are very young or have a very low birth weight, primarily caused by concerns about the fragility of valve tissue and the technical difficulty of the operation. Yet despite these concerns, it is unknown whether earlier age at operation is related to an increase in postsurgical morbidity, such as left AV valve dysfunction.

Our policy has been to perform definitive surgical repairs for AVSD regardless of age at presentation, with few exceptions. Operations are electively planned at age 3 to 6 months, unless the patient's clinical condition warrants earlier intervention. The surgical strategy used was a two-patch technique with complete left AV valve cleft closure whenever possible. This study evaluated this surgical strategy and identified risk factors for postoperative mortality and morbidity.

	Patients and Methods

Top Abstract Introduction Patients and Methods Results Comment References

 
Subjects included 116 patients with a complete AVSD who underwent definitive surgical repair from February 1997 to October 2002 at C. S. Mott Children's Hospital, the University of Michigan Health System. Follow-up was based on last known contact, with a closeout date of 2006. The study excluded patients with an incomplete AVSD, transitional AVSD, unbalanced AVSD that was not suitable for biventricular repair and AVSD with conotruncal anomalies, including tetralogy of Fallot and double-outlet right ventricle. The study was approved with waiver of consent by the Institutional Review Boards of the University of Michigan Medical School.

Data were obtained from hospital records and from referring pediatric cardiologists. Doppler echocardiography was used to ascertain the severity of AV valve regurgitation, which was graded none, trace, 1+ (mild), 2+ (mild-to-moderate), 3+ (moderate-to-severe), or 4+ (severe) [6].

The technique of definitive repair had been consistent over the study period. All patients underwent bicaval and aortic cannulation and were perfused with moderate hypothermia, except in the setting of an associated coarctation of the aorta. In such circumstances, the coarctation was repaired using deep hypothermic circulatory arrest (3 patients). Cardiac arrest was achieved by intermittent infusion of cold blood cardioplegic solution. Surgical management of AVSD was performed solely through the right atrium. A two-patch technique was used for closure of septal defects in 98 patients (84.5%). Polytetrafluoroethylene patches were used for the ventricular component and glutaraldehyde-treated autologous pericardium for the atrial defect. The modified single-patch technique, similar to that described by Nunn and colleagues [7], was used in the other 18 patients (15.5%) who had a shallow ventricular component. Clefts of the newly created left AV valve were approximated by interrupted suture.

Complete closure was attempted in all patients at the surgeon's discretion, depending on individual valve anatomy. Additional commissuroplasty or commissural annuloplasty, or both, were performed in 35 patients (30.2%) to increase the degree of coaptation of the leaflets. All associated cardiovascular anomalies were simultaneously repaired, except for insignificant additional ventricular septal defects and trivial LVOT obstruction.

Intraoperative transesophageal echocardiography was routinely performed to ascertain the severity of residual left AV valve dysfunction after the repair. If more than moderate, further valve repair was attempted.

Statistical analysis was performed with StatView software (SAS Institute Inc. Cary, NC). Normal data are expressed as the mean ± the standard deviation. Nonnormal data are expressed as medians and ranges. An unpaired t test was used to determine differences between the groups. Categoric variables were analyzed by use of ² analysis or the Fisher exact test. The Kaplan-Meier and Cox proportional hazards models were used for actuarial analysis. A complete list of the variables analyzed is reported in the Appendix. The multiple logistic regression model was used to identify independent contributions to potential risk factors for postoperative left AV valve dysfunction. Factors that were statistically significant on bivariate analysis (p 0.1) were entered into multivariate analysis.

	Results

Top Abstract Introduction Patients and Methods Results Comment References

 
Of the 116 study patients, current follow-up information was available in 107 of 114 surviving patients (94%). The mean follow-up was 27 months (range, 1 to 73 months). Median age at operation was 4.8 months (range, 9 days to 5.4 years), and weight was 4.8 kg (range, 2.1 to 23 kg). Operations occurred at between 3 and 6 months in 67 patients (57%) and before age 3 months in 25 (22%), including 5 (4%) in the neonatal period. The indication in all 25 patients who were operated on before the age of 3 months was intractable heart failure. In 13 of the 24 patients older than 6 months, the definitive repairs could be postponed due to a restrictive shunt. Forty-six patients (39.7%) were boys, 80 (68.9%) had Down syndrome, and 4 patients (3.4%) had heterotaxy. Associated cardiac anomalies are summarized in Table 1. Five patients had major cardiovascular anomalies, including coarctation of the aorta, aortopulmonary septal defect, and interrupted aortic arch (IAA). For data analysis, these patients were subgrouped as having "complex AVSD." Additional anomalies that required surgical intervention are summarized in Table 2.

A significantly unbalanced AV valve was noted in 14 patients (12%), including imbalance to the right in 8 and to the left in 6. Imbalance was defined subjectively by echocardiography using a subcostal view between coronal and sagittal angles, to obtain the valve en face at the level of the leaflet tips, in combination with intraoperative surgical confirmation. An imaginary line is drawn at the level of the septum, and the areas of the left and right side of the valve are compared.

Definitive repairs were preceded by palliative operations in 6 patients (5%), including placement of pulmonary artery band in 4, a combined repair of coarctation of the aorta and pulmonary artery banding in 1, and a combined repair of IAA and pulmonary artery banding in 1. These palliative procedures had occurred at other hospitals in 4 patients. In the remaining patients, who were twins, pulmonary artery banding had been performed at 4 months of age at our hospital for intractable congestive heart failure because their parents' religious beliefs precluded the use of blood products during the repair. Preoperative cardiac catheterization was used in 8 patients (6.9%). Indications included evaluation for pulmonary artery pressure and pulmonary vascular resistance in 6 patients, further delineation of branch pulmonary artery anatomy in 1 patient, and assessment of ventricular size for biventricular repair in 1 patient with an unbalanced AVSD.

Complete closure of the cleft of newly created left AV valve was feasible in 103 patients (89%). Partial closure was performed to prevent a restrictive valve orifice in 10 patients. In 2 patients, the clefts were left unrepaired for either an unbalanced to the right AV valve with a double orifice left AV valve or a severely deficient left lateral leaflet. The remaining patient with severe left AV valve leaflet dysplasia required prosthetic valve placement at the initial repair. Significant regurgitation on intraoperative transesophageal echocardiography compelled 3 patients to return to bypass for successful valve revision.

Significant postoperative morbidity occurred in 3 patients. Two patients required extracorporeal membrane oxygenation for pulmonary hypertensive crisis and respiratory failure related to respiratory syncytial virus, respectively. Mediastinitis developed in the remaining patient.

Hospital survival was 98.3% (114 of 116). One hospital death occurred in a patient who had undergone IAA repair combined with pulmonary artery banding at another hospital. He died of progressive ventricular failure after AVSD repair and interval left AV valve replacement due to severe residual regurgitation. The other patient, who required left AV valve replacement at the initial repair, died from ventricular failure and right AV valve stenosis. Two late deaths occurred. One patient died of ventricular failure after a left AV valve replacement for postoperative stenosis, and the other death, which was not cardiac related, occurred in a patient who died of Crohn disease.

Actuarial survival rates at 1, 3, and 5, years were 98%, 95%, and 95%, respectively (Fig 1). Potential risk factors associated with death subject to multivariate analysis are summarized in Table 3. Bivariate analysis revealed the presence of additional major cardiovascular anomalies, a deficient left lateral leaflet, heterotaxy syndrome, staged operation, and the need for left AV valve replacement were significant factors for poor outcome. On multivariate analysis, no risk factor for mortality could be shown to reach significance.

View larger version (10K): [in this window] [in a new window]   Fig 1. Actuarial patient survival, including early mortality.

Excluding the 4 patients who required reoperation for residual left AV valve regurgitation before discharge and 1 patient who died in-hospital, 75 of the remaining 111 hospital survivors (68%) available for analysis showed negligible (1+) left AV valve regurgitation at discharge. When the age groups were compared, 87% of patients undergoing repair after 3 months of age showed negligible left AV valve regurgitation, whereas 48% of those undergoing repair before 3 months of age showed negligible left AV valve regurgitation. Assessment for risk factors of significant (3+) residual left AV valve regurgitation is summarized in Table 4. Although bivariate analysis revealed age younger than 3 months as a significant predictor, only the presence of a deficient left lateral leaflet (odds ratio [OR], 10.47; p = 0.0134) and leaflet dysplasia (OR, 9.75; p = 0.0324), were risks for significant postoperative left AV valve regurgitation on multivariate analysis. There was a trend toward increasing postoperative AV valve regurgitation for non-Down syndrome patients (OR, 6.42; p = 0.0526) on multivariate analysis, which approached significance.

Overall, 9 of 107 patients (8%) available for follow-up required reoperations for left AV valve dysfunction, including left AV valve regurgitation in 7 and left AV valve stenosis in 2. Reoperations were performed at a median interval of 3.5 months after the initial repair (range, 2 days to 33 months), and three reoperations were performed within 30 days. Reclosure of the clefts or additional annuloplasty for residual regurgitation, or both, was feasible in 4 patients. Prosthetic valve replacement was required in the remaining 5 patients, including 3 with regurgitation and 2 with stenosis. Two patients died of progressive ventricular dysfunction.

Actuarial freedom from reoperation for left AV valve dysfunction at 1, 3, and 5 years after the initial repair was 94%, 89%, and 89%, respectively (Fig 2). Analysis for potential risk factors associated with the need for reoperation for left AV valve dysfunction is summarized in Table 5. Dysplastic valve leaflet (OR, 5.99; p = 0.0358) and a deficient lateral leaflet (OR, 5.1; p = 0.0468) were incremental risk factors identified by multivariate analysis. Younger age at definitive repair was not shown to be a risk factor.

View larger version (13K): [in this window] [in a new window]   Fig 2. Actuarial freedom from reoperation for left atrioventricular valve dysfunction after repair of complete atrioventricular septal defect.

Reoperations were performed at a median interval of 21 months (range, 15 to 42 months) after the initial repair. Bivariate and multivariate analyses for potential risk factors associated with reoperations for LVOT obstruction are summarized in Table 6. Association of aortic arch obstruction was the single independent risk factor (OR, 11.23; p = 0.0485). Actuarial freedom from reoperation for LVOT obstruction after the initial repair at 1, 3, and 5 years was 100%, 93%, and 90%, respectively (Fig 3).

View larger version (13K): [in this window] [in a new window]   Fig 3. Actuarial freedom from reoperation for left ventricular outflow tract obstruction after repair of complete atrioventricular septal defect.

	Comment

Top Abstract Introduction Patients and Methods Results Comment References

 
In the last 2 decades, improved understanding of the natural history and morphology of complete AVSD, in addition to advances in surgical techniques, have steadily decreased postoperative mortality for this condition [1–5]. Advances in preoperative diagnosis, intraoperative support, and postoperative management have all contributed to the improvement. Despite this remarkable decrease in postoperative mortality, postoperative morbidity remains significant, the most prevalent being short- and long-term AV valve dysfunction as well as late LVOT obstruction.

The trend towards earlier intervention has decreased the incidence of pulmonary hypertensive crises. Although earlier reports consistently described postoperative pulmonary hypertension as a major risk factor of death, recent long-term results demonstrate that early surgical intervention before the development of pulmonary vascular obstructive disease is the optimal approach [2, 5, 8, 9]. Our experience also supports this concept. Only 1 of the 116 patients had a significant postoperative pulmonary hypertensive crisis.

Other data suggest that early definitive surgical repair of an AVSD preserves AV valve function. Earlier definitive repair is theoretically advantageous because degenerative changes or annular dilation of the common AV valve, or both, may progress as the patient ages. Michielon and colleagues [3] demonstrated that annular dilatation is important in the development of left AV valve regurgitation and increases a risk for reoperations in older patients.

Although earlier surgical intervention has decreased the incidence of pulmonary vascular disease, left AV valve regurgitation remains a significant source of short- and long-term morbidity. Reoperations for AV valve regurgitation were required in 6.5% of our patients. This incidence is similar to that found in previous reports, which range between 3.9% and 11.6 % [2, 3, 5, 8–11]. A recent meta-analysis of 794 patients by Backer and Mavroudis [12] demonstrated and 8% need for reoperation for left AV valve regurgitation. Recent studies have shown that bifoliate reconstruction (cleft closure) may minimize the need for reoperation or the degree of residual regurgitation of the left AV valve, or both [9–11, 13], and we have used this strategy. Only the presence of dysplastic valve leaflets or a deficient lateral leaflet, or both, were found to be independent risk factors for significant left AV valve regurgitation by multivariate analysis.

In the current literature, the incidence of significant LVOT obstruction after AVSD repairs requiring reoperations is 2.7% to 5.6 % [10, 14]. Previously reported risk factors for postoperative LVOT obstruction include accessory valve tissue and abnormal structures such as secondary chordae associated with some degree of membranous or muscular subaortic obstruction, or both, or fixed secondary chordae in the LVOT [14–16]. In our series, the prevalence of reoperations for LVOT obstruction corresponded to those of the previous reports at 5%. Unlike the previous reports, our data found that associated aortic arch obstruction was the sole independent risk factor for reoperation for LVOT obstruction.

Whether a single-patch or two-patch technique is superior in repair of complete AVSD with a significant ventricular component is a technical issue of controversy. Recent reports have shown that regardless of technique, the incidence of reoperations for residual left AV valve incompetence does not differ [10, 12, 13]. We continue to prefer the two-patch technique because it avoids the need to divide and reattach the leaflets; this preserves valve tissue, which may be particularly important in small infants with a limited quantity of AV valve tissue. The modified single-patch technique [7] was used in a limited number of patients with small ventricular components to their AVSD in our series. The results were uniformly positive, but the study design and small numbers of patients undergoing this technique prevents comment on the applicability of the technique in all patients, regardless of VSD size.

Most surgeons currently prefer to perform definitive repair before age 6 months. Medical therapy or surgical palliation is still favored by many in very young or low-birth-weight babies, or both, because of technical concerns about the fragility of the AV valve tissue. Reddy and colleagues [10] propose that earlier definitive repairs do not result in an increase in the incidence of AV valve incompetence and recommend elective repair at age 2 to 3 months. By contrast, Prifti and colleagues [16] demonstrated that definitive repairs for small infants who weighed less than 5 kg resulted in an increased risk for late reoperations for residual left AV valve regurgitation. In their experience, suture separation at the cleft site or between the leaflets and the patch was commonly responsible for residual regurgitation in low-body-weight infants.

Our management strategy has entailed complete repair at any age when symptoms of congestive heart failure cannot be managed by medical therapy. As might be expected, patients requiring operation at age younger than 3 months had a much higher incidence of 3+ AV or greater valve regurgitation compared with the older cohort (16% vs 6%, respectively). Despite this higher incidence of preoperative regurgitation, age at the repair of younger than 3 months could not be shown as an increasing risk factor for postoperative residual regurgitation or reoperation for left AV valve dysfunction in our series. In these patients, our analysis suggested that the risk factor for late reoperation was related not to tissue fragility or patient size or age, but anatomic valve leaflet abnormality, such as the presence of dysplasia or deficiency, or both.

Our policy has been to perform elective repairs for AVSD at age 4 to 6 months. Although we would hesitate to take a position that all patients should undergo elective repair before age 3 months, as others have, we do support a policy of complete repair regardless of age or weight when symptoms intervene in the absence of mitigating circumstances. Even though patient numbers were small, previous palliative operation was shown to be a risk factor for death. However, additional procedures such as pulmonary artery angioplasty were often required at the definitive operation in those patients. Despite this downside, we continue to believe that in selected cases, palliation still holds an important role in the surgeon's armamentarium, as in the 2 low-birth-weight patients who were palliated in this series owing to parental religious beliefs. Patients in poor clinical condition with comorbidities such as respiratory syncytial virus infection may also benefit from initial palliation.

Overall, our institution's policy of primary repair for AVSD has resulted in low mortality and excellent midterm outcomes, even in small infants, neonates, and patients with complex forms of AVSD. Although limited to a sample size of 116 patients, hospital mortality, left AV valve regurgitation or stenosis, and the development of LVOT obstruction were not shown to relate to age at operation. However, the management of AV valve leaflet dysplasia and a deficient left lateral leaflet still remain as challenges to optimal short- and long-term outcomes.

	Appendix

 
Variables Analyzed for Correlation With Atrioventricular Valve Function, Postoperative Events, and Death
Demographic and Diagnostic

Age (continuous, < months, < 3 months, < 4 months, < 6 months)

Weight

Sex

Rastelli type

Trisomy 21

Unbalanced atrioventricular septal defect

Double-orifice left AV valve

Single papillary muscle

Dysplastic valve leaflet

Deficient left lateral leaflet

Additional ventricular septal defects

Complex atrioventricular septal defect, including any of the following:

• coarctation of the aorta,

• aortopulmonary septal defect, or

• interrupted aortic arch

Aortic arch obstruction

Heterotaxy syndrome

Other anomalies

Preoperative atrioventricular valve regurgitation (> 2+, > 3+)

Abnormal cords across left ventricular outflow tract

Operative

Cardiopulmonary bypass time

Aortic crossclamp time

Left atrioventricular valve replacement

Incomplete cleft closure

Return to bypass for valve revision

Additional commissuroplasty and/or commissural annuloplasty

Staged operation

Combined procedure

	References

Top Abstract Introduction Patients and Methods Results Comment References

 

1. Hanley FL, Fenton KN, Jonas RA, et al. Surgical repair of complete atrioventricular canal defects in infancy J Thorac Cardiovasc Surg 1993;106:387-397.[Abstract]
2. Bando K, Turrentine MW, Sun K, et al. Surgical management of complete atrioventricular septal defects. A twenty-year experience. J Thorac Cardiovasc Surg 1995;110:1543-1554.[Abstract/Free Full Text]
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6. Snider AR, Serwer GA, Ritter SB. Echocardiography in pediatric heart disease2nd ed.. St Louis, MO: Mosby-Year Book; 1997. pp. 186-189.
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8. Alexi-Meskishvili V, Ishino K, Dähnert I, et al. Correction of complete atrioventricular septal defects with the double-patch technique and cleft closure Ann Thorac Surg 1996;62:519-525.[Abstract/Free Full Text]
9. Wetter J, Sinzobahamvya N, Blaschczok C, et al. Closure of the zone of apposition at correction of complete atrioventricular septal defect improves outcome Eur J Cardiothorac Surg 2000;17:146-153.[Abstract/Free Full Text]
10. Reddy VM, McElhinney DB, Brook MM, Parry AJ, Hanley FL. Atrioventricular valve function after single patch repair of complete atrioventricular septal defect in infancy: how early should repair be attempted? J Thorac Cardiovasc Surg 1998;115:1032-1040.[Abstract/Free Full Text]
11. Boening A, Scheewe J, Heine K, et al. Long-term results after surgical correction of atrioventricular septal defects Eur J Cardiothorac Surg 2002;22:167-173.[Abstract/Free Full Text]
12. Backer CL, Mavroudis C. Atrioventricular canal defectsIn: Mavroudis C, Backer CL, editors. Pediatric cardiac surgery. 3rd ed.. Philadelphia,PA: Mosby; 2003. pp. 321-338.
13. Najm HK, Coles JG, Endo M, et al. Complete atrioventricular septal defects. Results of repair, risk factors, and freedom from reoperation. Circulation 1997;96(suppl II):II-311-II-315.
14. Sittiwangkul R, Ma RY, McCrindle BW, Coles JG, Smallhorn JF. Echocardiographic assessment of obstructive lesions in atrioventricular septal defects J Am Coll Cardiol 2001;38:253-261.[Abstract/Free Full Text]
15. McElhinney DB, Reddy VM, Silverman NH, Hanley FL. Accessory and anomalous atrioventricular valvar tissue causing outflow tract obstruction. Surgical implications of a heterogeneous and complex problem. J Am Coll Cardiol 1998;32:1741-1748.[Abstract/Free Full Text]
16. Prifti E, Bonacchi M, Bernabei M, et al. Repair of complete atrioventricular septal defects in patients weighing less than 5 kg Ann Thorac Surg 2004;77:1717-1726.[Abstract/Free Full Text]

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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): Takaaki Suzuki Edward L. Bove Eric J. Devaney Toru Ishizaka Jennifer C. Hirsch Richard G. Ohye Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Suzuki, T. Articles by Ohye, R. G. Search for Related Content PubMed PubMed Citation Articles by Suzuki, T. Articles by Ohye, R. G. Related Collections Congenital - cyanotic Related Article