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Eur J Cardiothorac Surg 2002;22:167-173
© 2002 Elsevier Science NL

Long-term results after surgical correction of atrioventricular septal defects

^a Department of Cardiovascular Surgery, University Hospital, Arnold-Heller-Strasse 7, 24105 Kiel, Germany
^b Institute of Medical Informatics and Statistics, University Hospital, Kiel, Germany
^c Department of Pediatric Cardiology, University Hospital, Kiel, Germany

Received 14 September 2001; received in revised form 24 April 2002; accepted 1 May 2002.

* Corresponding author. Tel.: +49-431-597-4400; fax: +49-431-597-4402
e-mail: aboening{at}kielheart.uni-kiel.de

	Abstract

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion 5. Conclusions References

 
Objective: Review of the results of surgical correction of atrioventricular septal defects (AVSD), identification of risk factors for mortality and failure of left AV valve repair and determination of the impact of cleft closure on postoperative AV valve function. Methods: Between 1975 and 1995, 121 consecutive patients (55 males, 66 females) underwent surgery for biventricular correction of AVSD with a median age of 1.2 years and a median weight of 7.6 kg. Sixty-five patients had a complete AVSD, 17 patients an intermediate type, and 39 patients a partial AVSD. The left AV valve (MV) cleft was closed in 53 patients (43.8%). The mean follow-up time is 7.2±4.6 years. Results: Actuarial survival of the whole group after 1 year was 80%, after 10 and 20 years 78 and 65%, respectively. There were 18 early deaths (7-day mortality, 10.7%; 30-day mortality, 14.9%) and eight late deaths. In a univariate analysis, risk factors for early or late death were diagnosis of complete AVSD (P=0.006), no cleft closure (P=0.024), postoperative complications (P<0.0001), age <1.2 years (P=0.017), weight <7.6 kg (P=0.002), PA/Ao pressure ratio >0.7 (P<0.0001), and ECC time >110 min (P=0.002). In the multivariate analysis, postoperative complications (P=0.003) and PA/Ao pressure ratio >0.7 (P=0.001) had parallel effects on the postoperative risk for mortality. Moderate or severe MV regurgitation was present in six patients (6.0%) in the first evaluation after discharge and in 20 patients (20.4%) in the most recent postoperative control. There were 25 reoperations in 17 patients, of which 15 had to be performed for MV regurgitation and two for MV stenosis. Freedom from reoperation was 91% at 1 year, 79% at 10 years, and 76% at 15 and 20 years. We could not identify a statistically significant risk factor for reoperation. Conclusions: In patients with AVSD of various morphologies closure of the left AV valve cleft significantly improves outcome without affecting the need for reoperation. Risk factors for early and late death (multivariate analysis) were a pulmonary/aortic pressure ratio >0.7 and the occurrence of any complication after surgery. The concept of an early surgical AVSD correction before an increase in pulmonary vascular resistance and AV valve deformations occur would represent a better surgical option than a late correction as done in our series. Early correction allows for reduction of early mortality, superior long-term survival rates and a high freedom from subsequential valve degeneration.

Key Words: Atrioventricular septal defect • Atrial septal defect • Survival • Reoperation • Cleft closure

	1. Introduction

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion 5. Conclusions References

 
The spectrum of atrioventricular septal defects (AVSD) caused by a maldevelopment of endocardial cushions and the bulboventricular fold includes forms of complete, intermediate, and partial AV-canals. The common definition differs between complete AV-canals with one common AV valve for both ventricles and an interatrial and intraventricular communication, partial AV-canals – also referred to as primum type atrial septal defect (ASD I) – with a distinguishable right and left AV valve and lack of an interventricular communication. An intermediate form of an AV-canal contains an ASD I defect and a fibrous tissue closing the intraventricular defect combined with a more common AV valve than distinguishable mitral and tricuspid portions. It is frequently discussed that early and late outcome as well as the reoperation rate after first surgical correction of these defects depend partly on the left AV-valve function [1–5]. With this background, we reviewed the results of surgical correction of AV septal defects to identify risk factors for mortality and failure of left AV valve repair and to determine the impact of cleft closure on postoperative AV valve function.

	2. Patients and methods

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion 5. Conclusions References

 
Between 1975 and 1995, 121 patients (55 males, 66 females) underwent surgery for biventricular correction of AV-canal. Sixty-five patients had a complete AV-canal, 17 patients an intermediate type, and 39 patients an incomplete AV-canal. Patients with severe dominance of one ventricle and patients who died between palliation and total correction were not included in the analysis. The demographic data of all patients are depicted in Table 1.

2.1. Surgical technique
The surgical procedure was performed in general anaesthesia on extracorporeal circulation with a mean temperature of 26°C using St. Thomas'I cardioplegia in most of the cases. Six different surgeons carried out 121 procedures (operative time 247±69 min, bypass time 108±43 min aortic clamping time 69±29 min) The mitral valve cleft was closed in 53 patients (43.8%). In patients with ASD I, closure of the atrial septal defect was done by autologuous pericardial patch. In patients with intermediate type AV-canal, a two-patch-technique was applied in six patients and a one-patch-technique served for repair in another 11 patients. In patients with complete AV-canal, the septal defects were closed in nine patients with the one-patch method and in 57 patients with the two-patch method using different patch materials (autologous or heterologous pericardium, Dacron or PTFE). Table 1 comprises basic data of the patients regarding anatomy, demographics and procedures.

Postoperative mean ventilation time in the intensive care unit (ICU) was 3.9±6.6 days (median 1 day) and length of hospital stay amounted to 15.2±8.6 days.

2.2. Statistics
Statistical analyses were carried out using either the chi-squared test or Fisher's exact test for analysis of differences in frequencies from nominal scaled data, the Mann–Whitney test for analysis of not normally distributed quantitative data (ECC time, aortic clamping time) and the Kaplan–Meier survival analysis for evaluation of time dependent events in survival and reoperation. Risk factors for mortality and reoperation were sought to identify in a first step by univariate analysis. Simultaneous influence of risk factors was evaluated by a stepwise forward logistic regression procedure. All these analyses were carried out aided by the SPSS computer software. A ‘P-value’ <0.05 was considered as statistically significant. Data are presented as mean value±standard deviation or as median, where indicated.

	3. Results

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion 5. Conclusions References

 
3.1. Survival
During the follow-up period, 26 patients (21.5%) died; there were 18 early deaths (7-day mortality, 10.7%; 30-day mortality, 14.9%) and eight late deaths (late mortality, 7.7%). Two of these 25 patients died from pulmonary reasons, three from unknown reasons. Twenty patients died from cardiac causes, mainly in the early postoperative period because of low cardiac output after the first or a second surgical procedure. The early and late mortality of ASD I patients (5.1%) was significantly (P<0.0001) lower than that of intermediate type patients (23.5%) and complete AV-canal patients (29.2%) (Table 2).

View larger version (18K): [in this window] [in a new window]   Fig. 1. The long-term survival of patients with complete AV-canal is significantly reduced compared to patients with ASD I.

View larger version (15K): [in this window] [in a new window]   Fig. 2. The long-term survival of patients with all forms of AV septal defect shows that the perioperative mortality accounts for most of survival reduction.

In the whole group, we could not identify a risk factor for reoperation. Looking at the complete AVSD group alone, not having Down's syndrome was a risk factor (Fisher's exact test, P=0.067) of borderline statistical significance.

Of the 17 patients with reoperations, four patients died, three of them intraoperatively during the second surgical procedure and one patient 4 years after the second operation due to cardiac failure.

No correlation could be proven between reoperation and pre- or postoperative MV regurgitation, cleft closure, one-or two-patch method, age or weight.

Freedom from reoperation was 91% at 1 year, 87.6% at 5 years, 78.6% at 10 years, and 75.3% at 15 and 20 years (Fig. 3 ).

View larger version (17K): [in this window] [in a new window]   Fig. 3. The freedom from reoperation in patients with AV septal defects amounts to 75% after 15 years.

The occurrence of complications turned out to be a significant risk factor in the univariate (P<0.0001) as well as in the multivariate (P=0.003) analysis.

3.4. Rhythm disturbances
Major rhythm disturbances in the early postoperative period were absent in 85 patients (70.2%). Two patients (1.7%) had AV-dissociation and nine patients (7.4%) complete AV-block after the surgical correction. One patient received a pacemaker 14 days, one 8 weeks after the procedure; the remaining two pacemakers were implanted 9 months and 6 years after surgery because of bradyarrythmia. Five patients recovered and had sinus rhythm at the last control. Of the remaining five patients with postoperative AV-block, three died within the first 4 postoperative days, one died 2 months after surgery while still being in the ICU from MOF, and one died 8 years after surgery from non-cardiac causes.

In the first control after surgery, 109 patients (90.2%) were in sinus rhythm without any other rhythm disturbances. There was neither a correlation between rhythm disturbances and any demographic factor nor between rhythm disturbances and any surgical variable.

3.5. AV-valve defects
Before surgery, 39 patients (32.2%) had preexisting mitral valve regurgitation (MR). The first control after surgery revealed moderate (n=4) or severe (n=2) MI in six of 99 patients (6.0%). Along with the most recent control follow-up MR was assessed as moderate (n=18) or severe (n=2) in 18 of 98 patients (20.4%, Table 6). During the follow-up time, MR decreased in 14 patients, but increased in 38 patients. As already mentioned, 12 patients had to be reoperated because of an AV-valve defect.

3.6. Influence of the surgeon
Three out of nine surgeons performed 101 (83.5%) of 121 procedures with one surgeon operating mainly in 1975–1985, another surgeon mainly in 1986–1995 and a third surgeon throughout the whole time period. There was no correlation between the surgeon and survival or occurrence of postoperative mitral valve insufficiency. We found no significant differences regarding the surgical approach, intraoperative times or methods and regarding the reoperation rate among the three main surgeons.

	4. Discussion

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion 5. Conclusions References

 
4.1. Mortality: risk factors
While there were several risk factors for mortality after AVSD repair identifiable in the univariate analysis, only two of them remained statistically significant in the multivariate analysis (Table 4). These two risk factors are first, the preoperative ratio between systolic pulmonary and aortic pressure defining the degree of pulmonary hypertension and second, the occurrence of any complication during the early postoperative period.

Preoperative pulmonary hypertension occurred most frequently in the group with complete AVSD. Early surgical correction is currently preferred [2,6], as delayed timing of surgery rather results in further elevation of pulmonary vessel resistance and fixed pulmonary hypertension [6,7]. As in the 1970s and 1980s, patients were operated on later than nowadays; more patients died during this time period due to untreatable pulmonary hypertension in the early postoperative time. Accordingly, there are different reports [3,4,11], assessing that postoperative pulmonary hypertension or a high PA/Aortic pressure ratio is associated with increased mortality.

The occurrence of complications is a significant risk factor in the univariate (P<0.0001) as well as in the multivariate (P=0.003) analysis, revealing a 6.2-fold higher mortality risk for the patients with any complication (Table 4).

The specific risk factors for mortality in the univariate analysis (Table 3) were: diagnosis of a complete AVSD, age at repair <1.2 years, weight at repair <7.6 kg, ECC time >110 min, two-patch technique and omittance of cleft closure. The connection between these risk factors is formed by the diagnosis ‘complete AVSD’. This connection is confirmed by the results of the subgroup analysis of complete AVSD patients (Table 3), showing that in this group the only significant risk factors were the occurrence of complications and of moderate or severe MV regurgitation. Even though patients with the complete form of AVSD seem to be at a higher mortality risk per se [8], the subset of risk factors include lower age and weight at repair as well as longer ECC times due to the more difficult repair than in the ASD I group. Similarly, Rizzoli et al. [9] and Günther et al. [10] could also assess a correlation between age of the patients and operative mortality. In contrast to our results, this may be explained by the technical difficulties when operating on infants in the early 80s. Besides this, the surgical strategy of applying PA banding in more than 40% of their very young patients [9,10] may have been disadvantageous.

Conclusively, it could be expected that ASD I corrections in contrast to more complex procedures which require longer ECC times [1] and aortic clamping times [11] have a more favourable early outcome. Surprisingly, in the report of Alexi-Meshkivili et al. [3], procedural times were no risk factor for perioperative mortality possibly because this study covers only patients with complete AV-canal.

As the surgical procedure in cases of ASD I consists naturally of a one-patch repair, the patients with a two-patch repair belong to the complete or intermediate group. This explains the higher risk of a two-patch technique in our analysis.

The early mortality of the whole group (14.9%) is comparable to the rates of 16% reported by Studer et al. [8] and Michielon et al. [2], but worse than the rates between 5.7 and 10% reported by others [3,4,5,11,14].

Long-term survival of complete AVSD patients after surgery is reported to be 88% at 5 years [8], 82% [11] or 91.3% [4] at 10 years, and 75.9% at 15 years [2]. Because of our higher early mortality, our long-term survival of complete AVSD patients is 74% after 5, 10 and 15 years. For partial AVSD patients, El-Najdawi et al. [12] reported a survival of 93% at years and 87% at 20 years. This is comparable to our results with a survival of partial AVSD patients of 93% after 10 and 15 years.

4.2. Reoperation
Reoperations were necessary in 14% of our patients (see Fig. 3): In two cases, mitral valve stenosis and in 12 cases, mitral valve insufficiency was the indication for redo surgery. In most of these patients reoperated on for MV problems, a repair could be performed. Only five patients received a MV replacement. One left ventricular outflow tract stenosis occurred and was treated surgically. No patient has been reoperated because of a residual VSD. Our reoperation rate (all forms of AVSD) of 78.6% at 10 years is comparable to the rates reported by McGrath and Gonzalez-Lavin [11] with 85% for partial and 68% for complete AVSD and to the rate reported by Pozzi et al. [7] with 84.2%.

4.3. Cleft closure
The closure of the left sided AV valve was performed in 53 of 121 patients, more often in the ASD I group (66.7%) than in the complete AVSD (35.4%) or in the intermediate (29.4%) group. The fact that two-thirds of complete or intermediate AVSD patients did not have the cleft closed may explain the inferior survival in these groups. Likewise, significant improvement of the outcome after correction of partial [12] and complete AVSD [1] by cleft closure has been already described. This observation was not confirmed by Bando et al. [4], Günther et al. [10], Alexi-Meshkivili et al. [3] and Hanley et al. [5], but these authors had a cleft closure rate near 100% and thus could not compare to patients without cleft closure.

The reason for not closing the cleft in all AVSD patients was the individual preference of some of the 11 surgeons over this 20 years period. Until the 1980s, the understanding of the left sided AV valve was either that of a two- or a three-leaflet valve, which led some surgeons to leave the cleft open [1]. Since the beginning of the 1990s, the concept of a two-leaflet AV-valve in AVSD patients and the consequent closure of the cleft (or ‘Zone of apposition’, [1]) was increasingly accepted with improved surgical results [9,12].

However, besides reducing mortality cleft closure did neither decrease the reoperation rate nor the rate of postoperative moderate and severe mitral valve regurgitation in our analysis.

4.4. AV valve function
AV-valve defects in patients with AVSD are common before as well as after the surgical correction. In our patient group, 39 patients had preexisting AV valve regurgitation. In contrast to Pozzi et al. [7] and Studer et al. [8], we were unable to identify preoperative AV valve insufficiency as risk factor.

In the first control after surgery, 93 of our patients (93.9%) had absent or mild MV insufficiency, in the last control during the follow-up period, 90 patients (91.8%) had absent or mild MV insufficiency. This is better than that reported by Weintraub et al. [13] and Wetter et al. [1] (84 and 78%, respectively, absent and mild MV regurgitation after surgery) and comparable with the data reported by Bando et al. [4] and Agny and Cobanoglu [14] (94 and 100%, respectively, absent and mild MV regurgitation). During the postoperative course, 14 patients (12.9%) developed an improvement and 38 patients (34.8%) a deterioration of the MV insufficiency, mainly (but not statistically significant) in patients without cleft closure. Similarly, Wetter et al. [1] reported an increase in the degree of valve regurgitation postoperatively in 15%, also predominantly in patients without cleft closure.

As also observed by Weintraub et al. [13], there was no correlationship between the existence of a preoperative AV valve regurgitation and the amount of MV regurgitation in the early postoperative period or at most recent follow-up. In the complete AVSD group, the presence of a moderate or severe MV regurgitation in the most recent follow-up turned out to be a risk factor for mortality. A low degree of postoperative MV regurgitation as positive factor for patients' outcome is also described in the studies of Studer et al. [8], Bando et al. [4] and Rizzoli et al. [9]. A severely dysplastic valve or an AV-valve with double orifice of the future mitral valve proved to be a perioperative risk factor [3–5,8].

4.5. Limitations
The advantage of this study is the examination of the whole spectrum of AVSDs over a long time period, giving us the opportunity to examine different methods of surgical repair, for example, one- or two-patch-technique, cleft closure or not. Inherently, this obvious advantage gives rise to some limitations, as in 20 years, a certain number of surgeons influence the results in a way that the surgeon's own learning curve and style rather than only patient's factors affect some of the results. Also improvements of ECC technique over time and the possibility to control the operative results in the operating room by transesophageal echocardiography influence the results of surgery in an unforeseeable way.

As this study is retrospective, not in every patient a complete follow-up could be obtained because of documentation problems in the 1970s and because not every patient could be traced over time. However, a follow-up completeness of 94.8% seems to be sufficiently high for a reasonable and conclusive analysis.

	5. Conclusions

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion 5. Conclusions References

 
Our results confirm that all types of AV canal defects can be operated on with satisfying short- and good long-term results. In a multivariate analysis, preoperative pulmonary hypertension and the occurrence of postoperative complications proved to be risk factors with simultaneous influence on mortality. The concept of an early surgical AVSD correction before an increase in pulmonary vascular resistance and AV valve deformations occur would represent a better surgical option than a late correction as done in our series. Early correction allows for reduction of early mortality, superior long-term survival rates and a high freedom from subsequential valve degeneration.

	Footnotes

 
Presented at the joint 15th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 9th Annual Meeting of the European Society of Thoracic Surgeons, Lisbon, Portugal, September 16–19, 2001.

	References

Top Abstract 1. Introduction 2. Patients and methods 3. Results 4. Discussion 5. Conclusions References

 

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2. Michielon G., Stellin G., Rizzoli G., Milanesi O., Rubino M., Moreolo G.S., Casarotto D. Left atrioventricular valve incompetence after repair of common atrioventricular canal defects. Ann Thorac Surg 1995;60:S604-S609.
3. Alexi-Meshkivili V., Ishino K., Dähnert I., Uhlemann F., Weng Y., Lange P.E., Hetzer R. 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]
4. Bando K., Turrentine M.W., Sun K., Sharp T.G., Ensing G.J., Miller A.P., Kesler K.A., Binford R.S., Carlos G.N., Hurwitz R.A., Caldwell R.L., Darragh R.K., Hubbard J., Cordes T.M., Girod D.A., King H., Brown J.W. Surgical management of complete atrioventricular septal defects. J Thorac Cardiovasc Surg 1995;110:1543-1554.[Abstract/Free Full Text]
5. Hanley F.L., Fenton K.N., Jonas R.A., Mayer J.E., Cook N.R., Wernovsky G., Castaneda A.R. Surgical repair of complete atrioventricular canal defects in infancy. J Thorac Cardiovasc Surg 1993;106:387-397.[Abstract]
6. Yasui H., Nakamura Y., Kado H., Yonenaga K., Shiokawa Y., Fusazaki N., Sunagawa H., Tokunaga K. Primary repair for complete atrioventricular canal: recommendation for early primary repair. J Cardiovasc Surg 1990;31:498-504.[Medline]
7. Pozzi M., Remig J., Fimmers R., Urban A.E. Atrioventricular septal defects – analysis of short- and medium term results. J Thorac Cardiovasc Surg 1991;101:138-142.[Abstract]
8. Studer M., Blackstone E.H., Kirklin J.W., Pacifico A.D., Soto B., Chung G.K.T., Kirklin J.K., Bargeron L.M. Determinants of early and late results of repair of atrioventricular septal (canal) defects. J Thorac Cardiovasc Surg 1982;84:523-542.[Abstract]
9. Rizzoli G., Mazzucco A., Brumana T., Valfre T., Rubino M., Rocco F., Daliento L., Frescura C., Gallucchi V. Operative risk of correction of atrioventricular septal defects. Br Heart J 1984;52:258-265.[Abstract/Free Full Text]
10. Günther T., Mazzitelli D., Haehnel C.J., Holper K., Sebening F., Meisner H. Long-term results after repair of complete atrioventricular septal defects: analysis of risk factors. Ann Thorac Surg 1998;65:754-760.[Abstract/Free Full Text]
11. Mc Grath L.B., Gonzalez-Lavin G. Actuarial survival, freedom from reoperation, and other events after repair of atrioventricular septal defects. J Thorac Cardiovasc Surg 1987;94:582-590.[Abstract]
12. El-Najdawi E.K., Driscoll D.J., Puga F.J., Dearani J.A., Spotts B.E., Mahoney D.W., Danielson G.K. Operation for partial atrioventricular septal defect: a forty-year review. J Thorac Cardiovasc Surg 2000;119:880-890.[Abstract/Free Full Text]
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