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Ann Thorac Surg 2001;72:1621-1629
© 2001 The Society of Thoracic Surgeons
a Department of Surgery, Medical University of South Carolina, Charleston, South Carolina, USA
* Address reprint requests to Dr Crawford, Department of Surgery, Medical University of South Carolina, 96 Jonathan Lucas St, Suite 409, Charleston, South Carolina 29425, USA
e-mail: crawfrdf{at}musc.edu
Presented at the Thirty-seventh Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 29–31, 2001.
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Abstract |
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Methods. One hundred seventy-two consecutive patients with atrioventricular septal defect were operated on by a single surgeon using a consistent operative technique (single patch; "cleft" closure). The patients’ age range was from 5 weeks to 9 years (mean, 10.8 ± 1.2 months).
Results. Overall operative mortality was 15 of 172 (8.7%) and this decreased significantly from 12 of 73 (16.4%) in the first decade to 3 of 99 (3.0%) in the second decade (p = 0.0021) with no operative deaths in the last 51 patients. Operative mortality was related to decade of operation (p = 0.0021) and to use of crystalloid cardioplegia (p = 0.0047) by univariate analysis, and to decade of operation (p = 0.0016) and postoperative time on ventilator (p = 0.0023) by multivariate analysis. Actuarial long-term survival including operative deaths was 79.0% ± 3.8% at 15 years. Ten of 157 (6.4%) operative survivors have undergone reoperation for late mitral regurgitation (9 mitral valve repair, 1 mitral valve replacement) with one death. Four of 8 patients surviving late mitral valve replacement have subsequently required mitral valve repair. Freedom from late reoperation for severe mitral regurgitation was 89.9% ± 3.1% at 15 years. Freedom from late reoperation for mitral regurgitation did not decrease in the second decade (84.2% ± 6.6% at 10 years) versus the first decade (94.5% ± 3.1%) (p = 0.0679).
Conclusions. Although operative mortality for repair of atrioventricular septal defect has decreased dramatically during the past decade, the incidence of late reoperation for mitral regurgitation has not improved, and better techniques to eliminate late mitral regurgitation are needed.
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Introduction |
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Material and methods |
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From January 1, 1981, through December 31, 2000, 172 infants and children with complete atrioventricular septal defect have been repaired at Medical University of South Carolina. This series of patients is limited to include only those with the complete form of the defect (common atrioventricular valve and nonrestrictive ventricular septal defect). Patients who were excluded included those with "partial" (ostium primum atrial septal defect) and "transitional" forms of the defect, complex forms of the defect such as associated tetralogy of Fallot, and unbalanced forms of the defect in which the patient went on to single ventricle type of repair. Ten (5.8%) children were initially palliated by pulmonary artery banding and then underwent subsequent correction. No patient has undergone palliative pulmonary artery banding at Medical University of South Carolina since 1995. One hundred sixty-two (94.2%) children underwent primary complete repair. This series of 172 complete atrioventricular septal defects represents 4.6% of all children (n = 3,749) undergoing correction of congenital heart defects at Medical University of South Carolina during this interval.
Demographic data are listed in Table 1. Age, weight, and body surface area were significantly less in the second decade compared to the first. One hundred thirty-eight (80.2%) patients underwent repair at less than 1 year of age, and 70 (40.7%) at less than 6 months of age. One hundred thirty-five (78.5%) patients had associated congenital cardiovascular anomalies (Table 2). In the first decade (1981 to 1989), all (73 of 73) patients were evaluated preoperatively by cardiac catheterization as well as by echocardiography and occasionally by magnetic resonance imaging. In the second decade (1990 to 2000), the majority (75 of 99, 75.8%) were evaluated by echocardiography alone with catheterization increasingly reserved for unusual circumstances such as the suspicion of severe or fixed elevation of pulmonary vascular resistance. Our current goals are to evaluate patients with complete atrioventricular septal defect preoperatively by careful echocardiography alone and to carry out elective primary repair between 3 and 6 months of age.
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2 test as appropriate. Actuarial estimates were calculated to describe mortality and incidence of reoperation using the Kaplan-Meier technique and are reported with the standard error of the estimate [16]. Comparisons of Kaplan-Meier estimates between groups were performed using the Mantel-Cox (log rank) test [17]. Predictors of operative mortality were examined using logistic regression techniques [18]. Only those variables with at least marginal (p < 0.2000) association with operative mortality in univariate testing were included in the multivariate analysis. All analyses were conducted using NCSS 2000 (Kaysville, Utah).
Operative technique
The single patch technique essentially as described and illustrated by the Mayo Clinic group has been used exclusively [3, 19]. All patients were operated through a median sternotomy incision using bicaval cannulation and moderate (24°C to 26°C) hypothermia. Circulatory arrest was not used in any patient in this series. When present, a patent ductus arteriosus was ligated as cardiopulmonary bypass began. Initially, single and subsequently multidose antegrade 4°C crystalloid cardioplegia was used for myocardial protection, but since August, 1993, multidose 4°C blood cardioplegia has been used exclusively. In most patients subsequent administrations of cardioplegia at 20-minute to 25-minute intervals were given through a small retrograde cardioplegia cannula inserted directly into the coronary sinus. Mean total cardiopulmonary bypass time was 118.7 ± 2.1 minutes, and mean aortic cross-clamp time was 78.7 ± 1.4 minutes. Exposure through a right atriotomy was maintained with several stay sutures. The increasing confidence in myocardial protection provided by multidose blood cardioplegia permitted a detailed and unhurried assessment of the unique anatomy of each patient. This probably accounted for the increased cross-clamp and bypass time in recent years (Table 1). When small associated atrial septal defects or patent foramen ovales were identified, they were usually closed separately. When large atrial septal defects were separated from the atrioventricular septal defect by a bridge of tissue, this bridge was divided, and the entire atrial defect closed as one. The common atrioventricular valve leaflets were inspected carefully with the ventricles collapsed and after distending gently with saline. The common anterior and posterior leaflets were then carefully marked at points of apposition with stay sutures. These leaflets were then completely divided into "mitral" and "tricuspid" components parallel to the crest of the ventricular septum but with a tendency to be more generous to the mitral component. Chordal attachments to the crest of the ventricular septum were usually divided to improve exposure for placing sutures to anchor the ventricular component of the repair patch. Once leaflet division was completed, multiple interrupted sutures backed with felt pledgets were placed along the right ventricular aspect of the ventricular septum with particular attention paid to the posterior junction of the ventricular septum and the atrioventricular valve annulus to avoid injury to the conduction system. These sutures were then passed separately through the repair patch, initially Teflon felt, but in recent years bovine pericardium (Bio-Vascular, Inc, St. Paul, MN) and the sutures tied. The patch was made slightly smaller than the defect to avoid contributing to dilatation of the subsequent left atrioventricular valve orifice. The superior portion of the patch was then cut to the appropriate size for subsequent closure of the atrial septal defect. The previously divided valve leaflets were resuspended to the patch, usually 5 to 10 mm above its attachment to the septum, again using multiple 5-0 horizontal mattress sutures which first penetrated the left atrioventricular valve leaflet, then the patch, and then the corresponding portion of the right atrioventricular valve leaflet. Pledgets were not routinely used to support reattachment of the valve leaflets. The mitral and tricuspid valves were then carefully inspected for competence. The septal commissure ("cleft") was closed in 168 patients (97.7%) at the point of apposition with several simple interrupted 5-0 sutures. In 4 patients the cleft was not closed, but the reason was not recorded. Although careful attention was always paid to obtaining mitral valve competence, in recent years with increasing confidence in myocardial protection, considerable time was spent assuring competence of the mitral and tricuspid valves. Occasionally adding a suture to the commissural cleft closure or at other times removing a previously placed cleft suture may improve mobility and insure competence. In recent years we have frequently used annuloplasty sutures as described by Capouya and colleagues [7]. Narrowing the valve orifice so much as to produce obstruction was carefully avoided by visual inspection and by assessment with intraoperative transesophageal echo. Once the two valves were judged to be optimally repaired, the atrial component of the defect was closed by suturing the remaining portion of the pericardial patch to the atrium with a continuous polypropylene suture. The coronary sinus was routinely left in the right atrium unless this would produce an abnormal deviation of the atrial patch suture line, in which case it was allowed to drain into the left atrium. In the region of the mouth of the coronary sinus, sutures were placed quite superficially again to avoid injury to the conduction system.
For much of this series, multiple monitoring catheters including right atrial, left atrial, and pulmonary arterial were placed. In the past several years, the use of left atrial and pulmonary artery lines has decreased remarkably to the point that they are now rarely used. Temporary atrial and ventricular pacing wires were uniformly placed.
Routine intraoperative echocardiography (transesophageal since 1990) has been used in the most recent 118 patients to assess ventricular function, to detect residual shunts, and most importantly, to assess mitral valve function and competence. In the unusual event that a significant residual shunt or significant mitral valve incompetence is detected, bypass is resumed and the residual defect repaired.
Extracorporeal membrane oxygenation has not been used in any patient postoperatively. The patient was returned to a specialized pediatric cardiothoracic intensive care unit where care was provided by the surgeon and in recent years by dedicated pediatric cardiology intensivists. Postoperative management was aimed at avoiding pulmonary hypertensive crises by avoiding pain, hypoxia, respiratory acidosis, and hypercarbia. Cardiac function was optimized with inotropic agents (epinephrine, dobutamine) and vasodilators (nitroprusside) as necessary. Until recently, patients were sedated and paralyzed, sometimes for several days postoperatively without attempts to wean from the ventilator. Recently, however, if the patient is stable hemodynamically, sedation and paralysis were discontinued about 12 hours postoperatively, and the patient was weaned from the ventilator and extubated as quickly as possible. A repeat transthoracic echocardiogram was obtained before discharge from the hospital, and postoperative follow-up was provided by pediatric cardiologists throughout the state in the South Carolina Children’s Heart Network.
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Results |
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Twelve of 157 operative survivors (7.6%) have developed severe mitral regurgitation from 1.6 months to 8.5 years after repair of complete atrioventricular septal defect. Ten (6.4%) have undergone reoperation (9 mitral valve repair, 1 mitral valve replacement) for mitral regurgitation. Overall freedom from late reoperation for severe mitral regurgitation was 89.9% ± 3.1% at 10 and 15 years postoperatively (Fig 2). There was no difference between patients with and without Down syndrome (p = 0.2801). At the time of reoperation, mitral regurgitation was found to be secondary to dehiscence of the cleft closure (6 patients), incomplete closure of the cleft at original operation (2), single papillary muscle (1), and a dilated annulus with central leak (1 patient). Mitral valve repair was possible in 9 patients and consisted of reclosure of the cleft in all and with placement of annuloplasty sutures in most. This resulted in a satisfactory result except in 1 patient who also required tricuspid valve replacement and who died intraoperatively. One patient required mitral valve replacement at initial reoperation and did well. However, of the 8 patients who survived and initially did well after mitral valve repair, 4 subsequently required mitral valve replacement at 1, 3, 4, and 10 months postoperatively and are long-term survivors. Two of these mitral valve replacements were required because of recurrent severe mitral regurgitation, one because of severe hemolysis from a small leak, and one because of endocarditis. Two additional patients currently have severe recurrent mitral regurgitation at 3.6 and 9.0 years after the initial operation. No patient has developed mitral stenosis postoperatively.
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Intraoperative echocardiography reports were available for review in 116 patients. Intraoperative (after repair) moderate to severe regurgitation was noted in 4 patients, and no to mild MR was noted in 112 patients. Of the 4 with significant residual intraoperative MR, one required reoperation. Nine of those with no to mild MR required reoperation. Freedom from early or late reoperation for those with significant residual intraoperative MR was 75.0% ± 21.7% at 5 and 10 years. Those with no or mild MR experienced freedom from early or late reoperation of 92.8% ± 2.9% and 85.1% ± 5.1% at 5 and 10 years, respectively (p = 0.2805).
The incidence of late reoperation for recurrent mitral regurgitation increased slightly from the first to second decade (Fig 3). Freedom from reoperation at 5 and 10 years postoperatively was 100% and 94.5% ± 3.1% for patients operated on during the first decade. Second decade patients experienced freedom from reoperation of 92.4% ± 3.4% and 84.2% ± 6.6% at 5 and 10 years, respectively (p = 0.0679). Because the follow-up is shorter for second decade patients, it is possible that additional patients may require reoperation, thus making the incidence in the second decade even higher. It should be noted that no patient has required reoperation for MR more than 9 years postoperatively.
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Comment |
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One hundred sixty-two (94.2%) of the patients in this series underwent initial complete correction making the incidence of initial palliation by pulmonary artery banding lower (5.8%) than other contemporary series [9, 10, 12, 15, 31]. Operative mortality did not differ between patients undergoing primary repair and those undergoing initial palliation followed by correction (10.0% versus 8.6%, p = 1.000). Despite the movement toward initial primary correction, age at the time of correction has steadily decreased. We prefer elective correction between age 3 and 6 months, believing this to minimize the risk of postoperative problems associated with increased pulmonary vascular resistance.
A variety of surgical techniques has been used successfully in complete atrioventricular septal defect correction. Initially the single patch technique dominated [3–5], and we and other researchers continue to prefer this technique [6–8, 11, 14]. The two-patch technique, introduced by Trusler [32], was initially believed by some investigators to be superior because of theoretic advantages related to postoperative atrioventricular valve function [10, 12, 13, 15]. Careful review of published series of repairs using the one- or two-patch technique fails to definitively document that one technique is preferable to the other. Recently Wilcox [33] and Nicholson [34] and their colleagues have described good outcomes in small series in which the common atrioventricular valve was attached directly to the crest of the ventricular septum as was described originally by Lillehei and associates [1]. It is clear from contemporary series that excellent results may be obtained using any of these techniques. Perhaps more important than the technique itself is the surgeon’s experience with a particular technique and the ability to adapt it to varying anatomy and circumstances [35].
In recent years we have used left atrial and pulmonary artery monitoring catheters much less frequently. We have noted that pulmonary artery pressure frequently increased as sedation was withdrawn and as the infant was weaned from the ventilator and that this frequently resulted in the patient being resedated and placed back on increased ventilatory settings. Once pulmonary artery monitoring lines were no longer used (and thus pulmonary artery pressures were unknown), progress toward extubation appeared to move more rapidly. As noted, this recent change in philosophy has been associated with a significantly decreased time on the ventilator, time in the intensive care unit, and overall hospital stay. There has been a progressive decline in operative mortality in most contemporary series from 15% to 20% to a current rate of 3% to 6% [8–15], coincident with (1) a change to primary repair at an early age to avoid complications of pulmonary hypertension, (2) a decreased incidence of postoperative low output syndrome, (3) fewer hemodynamically significant residual defects, and (4) a lower incidence of complete heart block. This decreased operative mortality over time has been noted in this series as well, declining from 16.4% in the first decade to 3.0% in the most recent decade. As noted, year of operation was the most significant variable related to operative mortality by multivariate analysis. The complete absence of operative mortality since 1995 in the last 51 patients in this series has obviously been extremely gratifying but will be extremely difficult to maintain over an extended period of time. Long-term survival in this series is comparable or slightly better than noted in other series [9, 10, 12, 15, 29].
Unfortunately what has not improved and what continues to be the limiting factor of this procedure, especially insofar as long-term results are concerned, is left atrioventricular valve competence. Reoperation for severe mitral regurgitation continues to be necessary in 5% to 15% of survivors regardless of operative technique (one or two patch) [8–11, 14, 15, 29, 30, 35, 36]. The incidence (8.7%) in this series is lower than many other series. Of concern is that the incidence has not decreased from the first decade to the second decade of this series, despite a commitment to achieving an optimal repair by carefully studying the anatomy at the time of cleft closure, the liberal use of annuloplasty sutures, and the use of intraoperative transesophageal echocardiography. Unquestionably working with these abnormal valves is more difficult in the 3-month-old compared to the 1-year-old, and it may be that improved understanding of the anatomy and operative techniques have been in turn counterbalanced by the increased number of very young, small infants currently being operated on. Because this incidence is so constant in most contemporary series, another possibility is that in 5% to 10% of patients, the atrioventricular valve may be so abnormal that long-term competence may be impossible to achieve in this group.
At reoperation, leakage through the commissural cleft, whether sutured or left open at the time of original repair, is the most common etiology of mitral regurgitation both in this series and in others [7–10, 13, 34, 37]. Most surgeons now agree that the cleft should always be closed except perhaps in double-orifice mitral valves or when closure would produce obstruction. However, uniform closure of the cleft as in this series does not always prevent recurrent MR as dehiscence of the closed cleft may occur, and alternative methods of closure of the cleft should be considered. We have not used pledgetted sutures for cleft closure but are currently reconsidering this policy based on the data from this series. Perhaps reinforcement of the cleft closure with small pledgets or by a thin pericardial strip on each side (or some alternate technique) might prevent what now appears to be the remaining problem with repair of complete atrioventricular septal defects. Fortunately, successful repair can be accomplished in many of those patients requiring reoperation for mitral regurgitation. Although some will subsequently require valve replacement, it is our belief that an initial attempt at valve repair should be tried to avoid problems associated with valve replacement in young children. Obviously, unfavorable anatomy or unsuccessful repair documented by visual inspection and transesophageal echo may dictate valve replacement at the first reoperation.
This relatively large series is unique in that it documents results from a single surgeon using essentially the same operative technique over a 20-year period. Despite significant improvement in operative mortality, postoperative mitral regurgitation continues to be a problem. Once residual mitral regurgitation can be eliminated as successfully as have other problems that once plagued this repair (low cardiac output, residual ventricular septal defect, heart block), the pediatric cardiologist and surgeon can confidently offer to the parents of a child with complete atrioventricular septal defect the possibility of an operation with a very low operative mortality and excellent long-term outcome without the need for future reoperation.
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Addendum |
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TopAbstractIntroductionMaterial and methodsResultsCommentAddendumAcknowledgmentsDiscussionReferences |
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Discussion |
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The improvement in survival no doubt reflects your own increased familiarity with the anatomy of this defect as well as a number of concurrent changes: improved myocardial protection, routine use of intraoperative echo, improvements in anesthesia.
Your 3% mortality during the most recent decade sets a benchmark for all surgeons, and the absence of mortality in your last 51 patients indicates that the survival results for repair of complete atrioventricular canal can be brought to match those of less complex cardiac lesions such as perimembranous ventricular septal defect.
On the other hand, you have also indicated that there is still work to be done, that is, the elimination of late mitral valve regurgitation in all patients.
I would like to ask three questions.
The first, of all of the factors that you have described that have positively impacted your results, which factor do you think has had the greatest impact and is the one factor that other surgeons must emulate to achieve the results that you have achieved?
The second question relates to your method of myocardial protection. You have shown that it has changed from single-dose antegrade crystalloid cardioplegia to multidose blood cardioplegia that is administered primarily in a retrograde fashion. Do you have a sense of what part of the change in technique has been most important? Has it been the blood? Has it been the multiple dosing? Has it been the retrograde technique. And what is the advantage of administering it retrograde?
The final question is, how do you determine the true extent of the septal commissure or cleft? And is not a potential pitfall in the repair? In my own personal experience I have noted that if I do not take a great deal of care in identifying the points of transition from the unsupported leaflet edge within the cleft to the beginning of the chordal attachment, I may not achieve a long-standing, competent valve.
I thank you for asking me to comment on this and thank the Society.
DR CRAWFORD: I do not know what the single most important factor is, because there are several things going on at the same time. Clearly, operator experience is an important factor and it is going on as this series developed. I suspect that that probably has as much effect as anything.
Two others are clearly important. One is a commitment to myocardial preservation. Because early in the series, as you saw, the cross-clamp times were short and there was the fear that I had to rush through the operation and get it done before I did some harm to the heart. Now I no longer do that because I have confidence in myocardial preservation.
You asked, is it the retrograde technique, is it multiple dose, is it blood? I do not know how to separate all those things out. I use retrograde after the initial dose of antegrade cardioplegia for one reason, but I have no data whatsoever to support it. I spend a fair amount of time injecting saline into the ventricles trying to find out where the valves coapt, and in that process I think you introduce bubbles that find their way into the aortic root and then into the coronary arteries. And it is my hypothesis that perhaps retrograde cardioplegia may wash some of those bubbles back out of the coronary and may prevent some damage from that, but I have no proof.
DR ROSS M. UNGERLEIDER (Portland, OR): Fred, I, too, appreciated the opportunity to review your manuscript, which is beautifully written, and I think that the members of your profession will enjoy reading it when it does come out in print. Your results are exceptional. I will ask two brief questions.
First, it was intriguing that your long-term mitral valve outcomes seemed to be better in the patients operated on in the first decade. And I wonder whether at a time when you are spending more time with a cross-clamp and presumably more time repairing the valves and inspecting the valves in the second decade, how could you explain those results? Do you think it has to do with operating on older patients, perhaps those previously banded? Does that perhaps make the valve outcomes better?
The second question I would ask you also relates to the fact that reoperation is a risk of bad outcome in your series, and I wonder whether you could explain for us how you evaluate the valves at the time of operation. What do you do with the valve that seems to be persistently leaking every time you fill the ventricle? How do you interpret the intraoperative echo?
Once again, I think this is a marvelous series. You’re to be congratulated on your outcomes.
DR CRAWFORD: Sometimes you find something when you review your data that you do not want to find. And I really can not explain why the mitral regurgitation is no better, and perhaps worse, in the second decade. Again, several things are going on. The babies are getting smaller. We are operating on them earlier. And in my opinion, there is no question that it is harder to deal with a valve in a 2-month-old, 2.5-kg child than it is a 6-month-old, 4- or 5-kg child.
But there is at least one report in the literature that says that the results are better in children under 4 kg. And so I do not know.
The second thing, intraoperative echo is something that you have had a lot of experience with. Three of the patients that had echoes were placed back on cardiopulmonary bypass because they had severe mitral regurgitation in the operating room. Two of those have done well without the need for future operation. One of those subsequently had to have a mitral valve repair about 2 years later.
At the same time we have other patients who left the operating room with mitral regurgitation that I could not make any better, who by 6 to 12 months postoperatively, the mitral regurgitation has decreased. So the presence of mitral regurgitation by echo in the operating room does not necessarily predict what it is going to be like 6 to 12 months down the road.
What I try to do now is to spend time and get it the best I can possibly get it the first time around. And I am somewhat reluctant to go back on the pump because by that time I am not sure there is anything else I can do.
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