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Ann Thorac Surg 2004;77:895-902
© 2004 The Society of Thoracic Surgeons
a Department of Surgery, Division of Cardiovascular Surgery, Hospital for Sick Children, University of Toronto Faculty of Medicine, Toronto, Ontario, Canada
b Department of Pediatrics, Division of Cardiology, Hospital for Sick Children, University of Toronto Faculty of Medicine, Toronto, Ontario, Canada
* Address reprint requests to Dr Van Arsdell, Division of Cardiovascular Surgery, Hospital for Sick Children, 555 University Ave, Toronto, ON, Canada M5G 1X8
e-mail: glen.vanarsdell{at}sickkids.ca
Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.
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Abstract |
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METHODS: Records of children undergoing AVSD repair between January 1995 and January 2002 were reviewed. Multivariable analysis defined risk factors for moderate or greater atrioventricular valve regurgitation (AVVR) and death/reoperation within 1 year of repair.
RESULTS: A total of 209 children (median age 5 months, median weight 5 kg) had defects whose repair included the possibility of bridging leaflet division. Bridging leaflets divided were both (n = 119, 58%), one (n = 30, 15%), or none (n = 55, 27%). Freedom from AVVR (moderate or greater) is 84%, 80%, and 78% at 1, 6, and 12 months. Risk factors include technical factors: number of bridging leaflets divided, longer cross-clamp time, and right-sided annuloplasty. Other risk factors include preoperative AVVR (moderate or greater), double-orifice or parachute left AV valve, and younger age. Freedom from death/reoperation for AVVR is 96%, 92%, and 90% at 1, 6, and 12 months. Risk factors are preoperative AVVR (moderate or greater) and parachute left AV valve. Findings at reoperation (n = 15, 7.2%) were cleft dehiscence or tear along cleft closure (n = 10), dehiscence of divided leaflet from septation patch (n = 1), or other (n = 4). Operative mortality (n = 6, 2.9%) included failed reoperations for AVVR (n = 4), dehiscence of divided leaflet from septation patch (n = 1), and sepsis (n = 1).
CONCLUSIONS: Division of bridging leaflets is a risk factor for AVVR (moderate or greater) during the first year after repair. Preservation of bridging leaflet integrity may improve valve competency, decrease the need for future reoperation, and eliminate some causes of operative mortality.
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Introduction |
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Recent early reoperation and sudden death from bridging leaflet dehiscence in a few children prompted us to reevaluate our methods of repair and return to the techniques originally described by Trusler and colleagues [1]. Herein we analyze our current experience since adopting a more liberal philosophy of dividing the bridging leaflets followed by a shift back to the Trusler sandwich repair.
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Patients and methods |
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Data collection
Data were collected through the first year after repair. Operative notes, echocardiography reports, perfusion records, and hospital cardiology charts were reviewed. AV valve morphology data were obtained from operative notes and preoperative echocardiograms. AV valve function data were obtained from echocardiograms performed before repair (n = 209, 100%), immediately after repair or before hospital discharge (n = 202, 97%), and within one year of repair (n = 128, 61%). Reoperations and mortality during the first year after repair were identified by the Congenital Cardiovascular Surgery Database and confirmed by operative notes and hospital cardiology charts. Additional follow-up was obtained by phone contact with referring physicians as needed. Follow-up was complete at 30 days for 206 (99%), 6 months for 197 (94%), and one year for 183 children (88%). Approval for this study was obtained from the Hospital for Sick Children Research Ethics Board.
Definitions
Atrioventricular valve regurgitation (AVVR) is defined as moderate or worse regurgitation by echocardiography. Catastrophic AV valve failure is defined as hemodynamic instability or collapse as a result of sudden development of AVVR. Operative mortality is defined as mortality within 30 days of repair or during the same admission. All cause mortality is used for analysis of risk factors for mortality. Reoperation for AVVR is defined as any reoperation where repair of an AV valve was the primary objective of the procedure.
Patient characteristics
Two hundred nine children (116 female, 56%) underwent complete repair at a median age of 5.0 months (range, 6 days to 15 years) and a median weight of 5.0 kg (range, 1.9 to 37 kg). 132 children (63%) were repaired at less than age 6 months (our current practice). Down's syndrome was identified in 167 children (80%). A small ventricle (unbalanced defect) was noted by echocardiography or the operating surgeon at the time of repair in 30 children (14%, 25 small right, 5 small left) but was not hypoplastic enough to preclude a two-ventricle repair.
Associated cardiac malformations in addition to patent ductus arteriosus and secundum atrial septal defects were identified in 49 children (23%). The associated defects include tetralogy of Fallot (n = 12, 5.7%), aortic arch hypoplasia (n = 8, 3.8%, with left ventricular outflow tract obstruction in 1), heterotaxy syndrome (n = 6, 2.9%), coarctation (n = 6, 2.9%, with heterotaxy syndrome in 1), pulmonary artery or valvar stenosis (n = 4, 1.9%), subaortic membrane (n = 3, 1.4%), double outlet right ventricle with or without right ventricular outflow tract obstruction (n = 3, 1.4%), multiple ventricular septal defects (n = 2, 1%), and other (n = 6, 2.9%).
Previous palliative procedures were performed in 17 children (8.1%). Thirteen children (6.2%) had pulmonary artery banding including 6 with unbalanced ventricles, 6 with aortic coarctation repairs (associated with unbalanced ventricles in 2), 1 with complex left ventricular outflow tract obstruction due to anomalous position of an anterolateral papillary muscle, and 2 for unclear reasons (referred from outside hospitals). Tetralogy of Fallot was initially treated with modified Blalock-Taussig Shunts in 4 children (1.6%).
Atrioventricular valve morphology and function
Rastelli's classification of bridging leaflet morphology (182 children) is type A in 112 children (62%), B in 10 children (5.5%), and C in 60 children (33%). Fourteen have a parachute left AV valve. Nine have a double orifice left AV valve. Preoperative left AVVR (184 children) was absent in 31 (17%), trace to mild in 146 (79%), and moderate to severe in 7 (3.8%). Preoperative right AVVR (178 children) was absent in 13 children (7.3%), trace to mild in 159 children (89%), and moderate to severe in 6 children (3.4%).
Surgical technique
Moderate hypothermia was used in 187 children (89%), including 4 with selective cerebral perfusion and brief periods of intermittent circulatory arrest (8 to 22 minutes' duration) for repair of aortic arch hypoplasia or coarctation. Profound hypothermia was used in 22 children (11%) combined with circulatory arrest for arch reconstruction (n = 1) or intracardiac repair (n = 21). Since 1996 profound hypothermia and circulatory arrest for intracardiac repair was used in only one child due to small size (2.2 kg). Cold blood cardioplegia was used in all children. Aortic cross-clamp times averaged 96 ± 29 minutes (n = 209). Circulatory arrest times for intracardiac repairs averaged 67 ± 6.0 minutes (n = 21). Total cardiopulmonary bypass times, including periods of circulatory arrest, averaged 139 ± 43 minutes (n = 209). Details of the surgical technique are summarized in Table 1. Patch material used for closure of ventricular septal defects (VSD) included Gore-Tex (W. L. Gore & Assoc, Flagstaff, AZ), Dacron (C. R. Bard, Haverhill, PA), or glutaraldehyde-treated autologous pericardium. Atrial septal defects (ASD) were closed with autologous pericardial patches (either treated or untreated). Most VSD and ASD patches were secured using running suture. Interrupted horizontal mattress sutures were commonly used to resuspend bridging leaflets or sandwich them between the two septation patches. Techniques for treatment of subaortic stenosis associated with AVSD have been previously described [3].
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Analyses were performed to determine the prevalence of and risk factors for two primary outcomes: (1) death or reoperation and (2) development of moderate or worse AVVR. Nonrisk-adjusted estimates of freedom from each outcome were calculated using Kaplan-Meier methods. Modeling the hazard function, searching for various phases of risk, and determining the characteristic equation of each phase allowed calculation of parametric estimates of time-related freedom from each outcome [4].
Demographic, morphologic, and surgical factors associated with each outcome after AVSD repair were sought by multivariable regression of the parametric hazard models with criterion of p less than 0.15 for variable entry and p less than 0.10 for retention. The analysis for development of AVVR was further explored to determine risk factors separately for left and right AVVR. In the case of missing data missing value indicator variables were created and the mean value of available information imputed noninformatively. In the multivariable analyses significant missing value indicators were carried to adjust for the possibility that children with a given missing value differ with respect to outcome from those in whom the value is not missing.
Reported variable estimates represent the contribution of a variable to the overall model. Variable increment and mathematical transformation affect interpretation of the contribution and are specified where applicable. The multivariable models were solved for single or combination of risk factors to demonstrate the magnitude of effect of these factors on outcomes.
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Results |
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Reoperations for AVVR
Reoperation for AVVR (14 left sided, 2 right sided) was required in 15 children (7.2%). The most common finding at reoperation was cleft dehiscence or adjacent tear (n = 10, 4.8%) involving distal portion (n = 7), basal portion (n = 2), or entire length (n = 1) of cleft. Associated findings with cleft dehiscence were leaflet tear along cleft (n = 3), residual VSD (n = 2), dilated left AV valve annulus (n = 1), double orifice left AV valve (n = 1), right AVVR (n = 1), and bridging leaflet tears at previous repair sites (n = 1). Left-sided bridging leaflet dehiscence from the VSD patch with associated residual VSD at the crest of the ventricular septum was found in 1 child. Ruptured primary chordae to the left superior leaflet after resection of accessory valve tissue at the initial operation were found in 1 child. A prolapsed mural leaflet with residual VSD was found in 1 child. A severely dysplastic left AV valve associated with left inferior pulmonary vein stenosis (left atrial endocardial fibrosis) and a residual VSD at the infundibular septum was found in 1 child. Poor coaptation of right-sided bridging leaftlets in association with atrial septal patch dehiscence was found in 1 child. In total residual ventricular septal defects were repaired in 5 children at time of AV valve reoperation.
Reoperation techniques for atrioventricular valve regurgitation
Valve repair (n = 14) was attempted in all children except 1 with a severely dysplastic left AV valve. Cleft reclosure and leaflet repair techniques frequently utilized autologous pericardium for pledgets and patches. Annuloplasty or commussuroplasty sutures were used in the majority of redo repairs. Mechanical valve replacement after reoperation was performed in 4 children at 3, 13, 306, and 311 days after reoperation. A total of 6 children (2.9%) in this series had mechanical valve replacement during the first year.
Mortality
Operative mortality was 2.9% (n = 6, within 30 days or the same hospital admission) with an additional 3 deaths during the first year (total 1-year mortality 4.3%, n = 9). Catastrophic left-sided AV valve failure accounts for 5 of the 6 operative mortalities (83%). Both superior and inferior bridging leaflets were divided in 4 of 5 children with catastrophic left-sided AV valve failure. One child (4.4 months of age) presented to the emergency room in cardiac arrest within 24 hours of discharge. At autopsy he had leaflet dehiscence of previously divided bridging leaflets from the septation patch. Two children with division of both bridging leaflets were resuscitated with extracorporeal membrane oxygenation (3 and 7 days after repair), underwent emergency reoperation for ruptured chordae or cleft dehiscence, and both died. Two additional children underwent unsuccessful reoperations for either cleft dehiscence or leaflet tear along cleft closure (1 of the 2 had division of both bridging leaflets). Two children died of infectious complications (Staphylococcus organism sepsis or fulminant hepatitis). Two children died outside of the hospital more than 5 months after repair for unknown reasons. One or more bridging leaflets were divided in 6 of 9 children who died during the first year after repair.
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Comment |
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Risk of dividing bridging leaflets
For the first time we have been able to identify the number of bridging leaflets divided during repair of AVSD as an incremental risk factor for postoperative AVVR by multivariable analysis. Bogers and associates [5] found a negative effect of division of the inferior bridging leaflet on reoperation. Others have reported no significant influence [6, 7]. Bridging leaflet division and resuspention may cause distortion of leaflet tissue [8]. Loss of leaflet tissue necessary for reattachment of divided bridging leaflets may result in subtle, complex geometric changes that increase tension on the cleft closure and increase the risk of cleft dehiscence (the most common site of dehiscence at reoperation in this series, and others) [9, 10]. Greater loss of valve tissue by division of both bridging leaflets may explain why division of two leaflets is a stronger risk factor than division of only one leaflet.
Competent AV valves before repair suggest the presence of adequate leaflet tissue capable of sufficient coaptation and should remain competent in the immediate postoperative period after an adequate repair. The incidence of immediate postoperative AVVR compared with preoperative AVVR is greater however after repair with division of both bridging leaflets (17.9% after repair compared with 4.2% preoperatively). Preservation of bridging leaflet integrity may be most likely to maintain valve competency.
Atrioventricular valve regurgitation
The strongest risk factor for postoperative AVVR in this series is preoperative AVVR. When division of both bridging leaflets is added to preoperative AVVR the outcome is dismal with 25% freedom from AV valve regurgitation at 12 months. Preoperative AVVR suggests an intrinsically pathologic valve where even minor distortion, changes in leaflet tension, or loss of leaflet tissue may worsen regurgitation. Children identified as being at high risk for postoperative AVVR due to the presence of preoperative AVVR may benefit most from preservation of bridging leaflet integrity (increase from 25% to 63% freedom from AVVR at 12 months). Right AV valve annuloplasty as a risk factor for postoperative AVVR may indicate leaflet tissue deficiency. Younger age at repair has less effect on postoperative AVVR but its significance as a risk factor suggests caution in managing leaflets. Rastelli type is not a risk factor for postoperative AVVR, suggesting a lack of correlation between Rastelli type and bridging leaflet division. The Rastelli classification system does not take into account either the location or extent of naturally occurring divisions of the bridging leaflets that may preclude surgical division of a leaflet.
Catastrophic AVVR
Preserving bridging leaflet integrity may also protect against catastrophic AVVR. Suture disruption at the atrioventricular septal patch junction is more likely to cause shunting than sudden regurgitation (as would occur with division and resuspension of bridging leaflets). Two children in this series had leaflet dehiscence from a septation patch after bridging leaflet division and died despite extracorporeal membrane oxygenation resuscitation in 1. These 2 children may have been preventable deaths.
Residual VSD after preservation of bridging leaflets
Decreased visibility of the VSD may be a disadvantage of bridging leaflet preservation in comparison with bridging leaflet division [2]. Reoperation for residual VSDs in our previous series (69% bridging leaflet preservation) occurred in 2.5% of children (n = 9, 2 in association with left AV valve repair). In the current series (27% bridging leaflet preservation) reoperations for residual VSDs occurred in 2.9% of children (n = 6, 4 with small residual defects closed at time of left AV valve repair). The incidence of residual VSDs is nearly identical in both series. Only 1 child in the current series with bridging leaflet preservation had a residual VSD. (The remaining 5 children had division of both bridging leaflets.) With meticulous and somewhat time-consuming techniques bridging leaflets may be preserved without an increased incidence of residual ventricular septal defects.
Operative mortality
Operative mortality for repair of AVSDs has declined over the past several decades to between 2.8% and 6% in recent reports [2, 5, 7, 8, 11–13]. Several factors account for improved survival including better understanding of anatomy, improved myocardial protection, improved surgical techniques, and better postoperative care based on early repair [11].
Early repair has obviated pulmonary hypertensive crisis, but may have uncovered new technical problems. Operative mortality in this series (2.9%) is the result of technical problems in all but 1 child who died of overwhelming sepsis. The elimination of technical problems in this series would result in a theoretical operative mortality for repair of AVSDs of less than 1%. Leaflet tears, cleft disruption, ruptured chordae, and leaflet dehiscences suggest the need for further refinement in surgical technique. Bridging leaflets were divided in 5 of 6 children who died (although the numbers are too small to reach statistical significance). Technical problems after complete repair of AVSDs are universal [2, 5, 7–17]. Further reduction of operative mortality in the current era will require solutions to technical problems.
Weaknesses and limitations
Several weaknesses and limitations of this analysis are identified. The status of repair and AV valve function in 3 children who died after discharge is unknown. Death from all causes is used in the analysis to exclude this effect. No patients required reoperation for isolated AV valve stenosis. However we did not include the evaluation of AV valve stenosis in this analysis. Five surgeons performed operations with inherent differences in technique. Echocardiograms were not independently reviewed. Late echocardiogram follow-up is only 61%.
Conclusions
Division of bridging leaflets is a risk factor for development of moderate or worse AVVR during the first year after repair of AVSDs. Preoperative AVVR magnifies the risk of dividing bridging leaflets. Dehiscence of divided leaflets is a source of early reoperation and mortality. Surgical techniques emphasizing preservation of bridging leaflet integrity may improve valve competency, decrease the need for future reoperation, and eliminate the risk of divided leaflet dehiscence.
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Discussion |
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DR FORTUNA: There are series in the literature where bridging leaflets are divided without reports of increased regurgitation, reoperation, or mortality. Certainly those results are enviable. Our series is somewhat unique because it shows a shift in surgical technique at a single institution. We did find that when we changed our technique to dividing bridging leaflets we had more problems and have since shifted our technique back.
DR PEDRO J. DEL NIDO (Boston, MA): This is a very interesting presentation on a very difficult problem. One of the questions I had is your interpretation that the cause of the regurgitation when you divide a leaflet being purely on the basis of the fact that you take up more leaflet when you reattach it to the patch. Is it not fair to say that probably the single biggest factor that will affect coaptation of the leaflets is how much surface area actually overlaps, which will be governed by the width of your patch and to some degree by the distance from the crest of the septum to where the leaflets meet?
Another explanation for your findings, and I don't disagree with your findings, would be that in fact when you divide the leaflets it's too easy to make the patch a bit too wide. And that actually pulls the leaflets apart at the cleft because you're pulling the aortic end and the AV node end of the valve annulus apart. I notice that the regurgitation was through the cleft and not that the leaflets had dehisced. If you're pulling the superior and inferior leaflets apart, in fact at the cleft, your sutures are going to have to withstand the forces of systole with every heartbeat. It's going to let go eventually. So that another interpretation of your data would be that one needs to remember how to construct the patch particularly with respect to its width. I don't think it matters so much whether you have one patch or two.
DR FORTUNA: Yes, I would agree, there are multiple factors that go into creating a competent valve, including those which you have discussed. Unfortunately those concerning the patch are something that it would be very difficult, if not impossible, for us to take into account in this type of a study.
DR WINFIELD J. WELLS (Los Angeles, CA): One of the arguments for dividing the leaflets would be to reduce the incidence of residual VSD. So the question is, did you have a higher incidence of residual VSD in patients where the leaflets were not divided?
DR FORTUNA: The incidence of residual VSDs in this series is 2.9%. And as you know, in this series 73% of patients had divided leaflets. If I compare that historically to our previous series reported, where 31% of the leaflets were divided, the incidence of residual VSDs is 2.5%. So we don't see much of a difference in the incidence of residual VSDs between these two series.
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