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Ann Thorac Surg 2005;79:607-612
© 2005 The Society of Thoracic Surgeons
a Department of Pediatric Cardiology
b Department of Cardiothoracic Surgery
c Department of Epidemiology and Biostatistics, Erasmus MC-Sophia, Rotterdam, the Netherlands
Accepted for publication July 6, 2004.
* Address reprint requests to Dr Ten Harkel, Erasmus MC-Sophia, Department of Pediatric Cardiology, Dr Molewaterplein 60, 3015 GJ Rotterdam, the Netherlands (E-mail: a.tenharkel{at}erasmusmc.nl).
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Abstract |
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METHODS: Retrospective review of clinical, operative, and echocardiographic data was performed. From 1990 until 2001 164 patients underwent correction of their atrioventricular septal defect.
RESULTS: Five patients died in the immediate postoperative period, and 2 patients were lost to follow-up. During follow-up (median, 66 months; range, 9 months to 12 years), 30 patients (19%) had severe left-sided atrioventricular valve regurgitation. Sixteen patients had severe left-sided atrioventricular valve regurgitation in the immediate postoperative period; 4 of them showed spontaneous regression to near-normal valve function during follow-up. Fourteen patients exhibited left-sided atrioventricular valve regurgitation during follow-up; 8 of them remained stable with medication only. Fifteen of the 30 patients with severe left-sided atrioventricular valve regurgitation underwent reoperation. A significant risk factor for the development of severe left-sided atrioventricular valve regurgitation and reoperation was the presence of preoperative severe left-sided atrioventricular valve regurgitation.
CONCLUSIONS: Severe left-sided atrioventricular valve regurgitation develops in a significant number of patients after correction of atrioventricular septal defect, and preoperative severe left-sided atrioventricular valve regurgitation is an important risk factor. Although reoperation usually results in good valve function, spontaneous regression after the immediate postoperative period is possible and should be given a fair chance.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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In this paper, we present our analysis of LAVVR and consequent reoperation after AVSD correction. We examined several preoperative, operative, and postoperative risk factors for the development of severe LAVVR and for the risk of reoperation.
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Patients and Methods |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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Measurements
To determine predisposing factors of LAVVR and left atrioventricular (AV) valve reoperation, we evaluated the following variables: sex, presence of syndrome, degree of preoperative LAVVR, presence of additional heart defects, age at operation, valvuloplasty of the left AV valve during first operation, and obstruction of the left ventricular outflow tract. End points were severe LAVVR, reoperation for LAVVR, or death.
The degree of LAVVR was measured by color Doppler echocardiography. We used a modification of the grading system as previously described by Moran and associates [2]. The degree of mitral regurgitation as assessed by the width of the vena contracta in two orthogonal planes was subjectively categorized on a scale of 1 to 3, where 1 is none or mild, 2 is moderate, and 3 is severe. All assessments that gave unequivocal results were independently reviewed by one of the investigators (A.D.J.T.H.).
Surgical Techniques
The surgical technique has been described extensively in a previous study [3]. Surgery was performed using continuous extracorporeal circulation with moderate hypothermia (rectal temperature, 28°C) and cardioplegic arrest (a single antegrade dose of St. Thomas's Hospital cardioplegic solution, 10 mL/kg body weight). The surgical reconstruction in complete AVSD consists of a two-patch technique [3]. All operations were done through a right atriotomy parallel to the right AV groove, extending from the right atrial auricle to the level of the entrance of the inferior caval vein. Cold saline solution was used to fill the ventricular chambers and float the AV valve tissue into a closed position to establish the line of coaptation between the superior and inferior components of the valve and to identify the proper line of division into right and left parts of these components in Rastelli types B and C. In Rastelli type A, no surgical division is necessary. The chordal anatomy is left intact. The distance from the AV valve level to the crest of the interventricular septum was accurately assessed to reconstruct the AV valves at the appropriate height to prevent subaortic stenosis.
The ventricular septal defect was closed by sewing in a semioval Gore-Tex patch (W.L. Gore & Assoc, Flagstaff, AZ) onto the right side of the defect with running 5.0 Surgilene (American Home Products, Madison, NJ) suture. At the AV level, the superior bridging leaflet and the right superior leaflet in Rastelli type A and the respective parts of both superior and inferior bridging leaflets in Rastelli types B and C were included in the running suture line and sewn to the ventricular septal defect patch, taking care of adequate coaptation at the meeting point of the superior and inferior leaflets on both the right and the left sides. In both partial AVSD and complete AVSD closure of the atrial septal defect was begun with a running Prolene (Johnson & Johnson, New Brunswick, NJ) suture to fix a glutaraldehyde-pretreated autologous pericardial patch, starting in the commissure between the right mural leaflet and the inferior bridging leaflet, following the hinge-point level of the leaflet and, for complete AVSD, continuing onto the previous suture line at the AV level of the ventricular septal defect patch. At this stage, the suturing at the left AV valve circumference at the septal level is complete, and valve testing can be done. Using horizontal interrupted Prolene 6-0 sutures, the left-sided cleft was then completely closed in patients with a trileaflet left AV valve after reconstruction, or partially closed in patients with bileaflet left AV valve in the absence of a left lateral leaflet. Valve competence was repeatedly tested with saline injection through the valve orifice. If considered indicated, commissuroplasty was applied. The closure of the atrial septal defect was then completed by further sewing in the pericardial patch. From the commissure between the right mural leaflet and the inferior bridging leaflet, the patch follows the right atrial wall to the bottom of the coronary sinus to avoid the AV nodal area with preservation of coronary sinus drainage to the right atrium. From this point on the border of the atrial septal defect was followed superiorly to reach the AV ring again. In case of a second atrial septal defect, both were closed with the pericardial patch. The right AV valve was floated into a closed position, and, if indicated, the right-sided coaptation area of the superior and inferior bridging leaflets was closed with interrupted Prolene 6-0 sutures. In all patients the correction was evaluated by intraoperative transesophageal or epicardial echocardiography. After completion of surgery all patients went to the intensive care unit for at least an overnight stay.
Statistics
Statistical analysis was performed with SPSS 10.1 (SPSS, Inc, Chicago, IL). Data are presented as median and ranges unless stated otherwise. Continuous and categorical data are compared between groups using the Mann-Whitney and 
2 tests, respectively. Cumulative incidence of severe LAVVR with time and reoperation rates were calculated by the Kaplan-Meier method. Univariate analyses with the log rank test were performed to assess whether there was a difference between categories of possible predictors regarding these event rates. Multivariate Cox regression analyses were performed to assess the impact of selected variables simultaneously. A p value less than 0.05 was considered statistically significant.
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Results |
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Before operation 110 patients (70%) had absent or mild LAVVR, 34 patients (22%) had moderate LAVVR, and 13 patients (8%) had severe LAVVR. No differences were found in this regard between partial and complete AVSD (Table 1). One week after surgical correction of the AVSD 103 patients (68%) had none or mild LAVVR, 34 patients (22%) had moderate LAVVR, and 16 patients (10%) had severe LAVVR. In 4 patients no echocardiogram was performed at that moment; as they were in good clinical condition and had no cardiac murmur at physical examination, they presumably had no or only mild LAVVR.
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Sixteen of the 30 patients had severe LAVVR immediately after corrective surgery, as confirmed by echocardiography at 1 week. The other 14 patients exhibited LAVVR after a median of 29 months (range, 1 month to 8 years). Of the 16 patients who had severe LAVVR immediately after surgery, 4 patients showed a decrease in LAVVR without any surgical intervention. Nine of the 16 patients underwent reoperation. The other 3 patients were initially managed by medication. One of these 3 patients is now stable for 11 years, 1 patient has stopped medication after 9 months and is now stable for another 7 months, and 1 patient was scheduled for valve replacement at the end of the study. Of the 14 patients who experienced LAVVR after the immediate postoperative period, 6 patients underwent reoperation and 8 patients were managed by medication during a follow-up period of 29 months (range, 1 to 37 months). These 8 patients remained stable.
Reoperations
None of the patients required reoperation for left AV valve stenosis. Fifteen patients underwent reoperation for progressive LAVVR after a median follow-up of 14 months (range, 1 to 79 months). In 3 of these 15 patients small residual shunts at the ventricular level or atrial level were closed as well. Of the total number of 15 patients, 13 underwent repair of the left AV valve at the second operation, and 2 patients underwent valve replacement at that time; in 2 patients a third repair of the left AV valve was necessary, in 1 of these repair of the left AV valve later was followed by valve replacement. The findings during reoperation were as follows: cleft dehiscence was complete in 9 and incomplete in 3, the cleft was left open in 2, and there was a perforation in the left lateral leaflet in 1.
The reoperation consisted of a placement of a St. Jude mechanical prosthesis in 2 patients (sizes 25 and 27). All open or dehiscent clefts were closed again, in 9 patients by simple interrupted sutures, in 4 patients with pledgetted interrupted sutures. In 5 patients the re-repair was completed with two commissuroplasties and in 1 patient with one commissuroplasty.
One other patient underwent reoperation for left ventricular outflow tract obstruction. Two patients needed pacemaker implantation because of complete heart block. The main reason for reoperation because of LAVVR was a combination of left ventricular dilatation and significant complaints of cardiac failure that did not respond to diuretics and angiotensin-converting enzyme inhibitors. Of the 15 patients with severe LAVVR who did not undergo reoperation, 11 use angiotensin-converting enzyme inhibitors, but they all have left ventricular dimensions within normal limits and no significant complaints.
Of the 15 patients who underwent reoperation for LAVVR, 12 are still alive at a median value of 61 months (range, 4 months to 11 years) after the last operation. Eight patients use no medication at present and have mild LAVVR. Two patients have moderate LAVVR and are managed by medication. Two patients still have severe LAVVR. One of these patients is in a stable condition with medication; the other patient shows dilated cardiomyopathy despite extensive medication. She is known to have Down's syndrome and had repair of her complete AVSD at the age of 3 months. One month later she had an additional valvuloplasty of the left AV valve because of persistent severe LAVVR. The LAVVR did not improve, and a mechanical prosthesis (St. Jude, 25 mm) was placed at the age of 3.2 years, which was after conclusion of the study. At the age of 4.5 years her left ventricular dimension is still 48 mm (>>P95) with a fractional shortening of 15%. Her medical treatment consists of diuretics, captopril, carvedilol, and oral anticoagulation.
Mortality
The overall survival, including the five early postoperative deaths, was 94% ± 2% at 5 years and 92% ± 3% at 10 years of follow-up. There was no significant difference between patients with partial and complete AVSD. None of the 5 patients who died in the early postoperative period after their primary correction had severe LAVVR before operation (1 patient died during the operation, 1 patient died of persistent pulmonary hypertension, 1 patient died of ventricular tachycardia and pulmonary hypertension, 1 patient died of a His bundle tachycardia, and 1 patient died of persistent low output failure). Five patients died during further follow-up (1 patient suddenly died at home, 37 days postoperatively; 1 patient died during the second surgical reconstruction of the left-sided AV valve, 40 days after the primary correction; 1 patient died of progressive cardiac failure 4 months after reconstruction of the left-sided AV valve, 1.5 years after the primary correction; 1 patient died of progressive cardiac failure 1 year after valve replacement, 6 years after the primary correction; and 1 patient died of irreversible pulmonary hypertension, 8.5 years after the primary correction).
Risk Factors For Severe Left-Sided Atrioventricular Valve Regurgitation and Reoperation
In univariate analysis a preoperative LAVVR was a significant risk factor for development of severe postoperative LAVVR (Fig 1). The 5-year and 10-year freedom from severe LAVVR was 90% ± 3% and 88% ± 3%, respectively, for patients with mild preoperative LAVVR, 60% ± 8% and 50% ± 12%, respectively, for patients with moderate LAVVR, and 62% ± 13% and 62% ± 13%, respectively, for patients with severe preoperative LAVVR (p = 0.01). The absence of Down's syndrome was also a risk factor for developing severe LAVVR. The 5-year and 10-year freedom from severe LAVVR for Down's syndrome patients was 88% ± 4% and 85% ± 4%, respectively, whereas it was 72% ± 6% and 68% ± 7%, respectively, for non–Down's syndrome patients (p = 0.006). In multivariate analysis, however, both factors lost their separate significance, and the relative influence could not be determined. This could be explained by the strong correlation between preoperative LAVVR and Down's syndrome. The presence of mild, moderate, and severe preoperative LAVVR in the Down's syndrome patients was 75 of 94 patients (80%), 16 of 94 patients (17%), and 3 of 94 patients (3%), respectively, whereas this was 34 of 62 patients (55%), 18 of 62 patients (29%), and 10 of 62 patients (16%), respectively, for the non–Down's syndrome patients.
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Comment |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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Left Atrioventricular Valve Regurgitation and Timing of Reoperation
Although the operative mortality for repair of AVSD has decreased during the past decade, the incidence of late reoperation for LAVVR has not reduced. In the present study 15 of 154 patients underwent reoperation for severe LAVVR. Major risk factors for postoperative LAVVR that have been described are preoperative LAVVR [4, 5], a cleft that was left open [3, 6, 7], or severe left AV valve anomalies [6, 7]. We also found preoperative LAVVR to increase the risk of postoperative regurgitation and reoperation. Severe LAVVR eventually leads to left ventricular dilatation, diminished contractility, and eventually cardiac decompensation. One patient in the present study had left ventricular dilatation and diminished contractility that did not improve after valve replacement. Left AV valve surgery significantly improves clinical status, with a sustained improvement in ventricular chamber size. However, the ideal timing for reoperation remains unclear. Surgery in young patients is often delayed until the appearance of severe symptoms because of the patient's size and anticoagulation requirements if an artificial valve is necessary. In the present study, 4 patients who had postoperative severe LAVVR showed spontaneous regression, indicating that postoperative LAVVR is not always definitive. If reoperation seems unavoidable, the choice has to be made between left AV valvuloplasty or valve replacement. Mitral valve replacement, especially in young children, is accompanied by a high mortality risk, and about 37% may show the development of complete heart block [2]. Furthermore, especially children after AVSD repair show a worse outcome after valve replacement [7]. The need for lifelong anticoagulation remains a disadvantage, although the incidence of anticoagulation-related complications is low [8].
In the present series we found a negative effect of not having Down's syndrome for the development of severe LAVVR. This confirms the finding of previous studies [9, 10]. In the study of Al-Hay and colleagues [10], both the absence of Down's syndrome and the presence of dysplastic valves were associated with the development of severe LAVVR. In our study multivariate analysis reduced the statistical significance of preoperative LAVVR and Down's syndrome for the development of severe LAVVR to p values between 0.05 and 0.1, with a strong correlation between Down's syndrome and the lower incidence of preoperative LAVVR. This finding confirms the results of Al-Hay and colleagues [10], who found more dysplastic AV valves in patients without chromosomal abnormalities.
Mortality Risks
The 10-year survival of 92% ± 3% in the present study is comparable to other studies [4, 8, 11]. Comparing with other studies it has to be taken into account that we limited our series to patients operated on from 1990 onward. Most studies show that mortality is mainly predicted by the era of surgical repair, decreasing from 19% before 1980 to 3% after 1990 [12].
There has been controversy about the influence of age at operation on the risk of operative mortality. Najm and associates [13] reported a higher risk for death in infants operated on for partial AVSD. However, these infants had a higher incidence of severe symptoms, which might have increased the mortality risk. Also Günther and coworkers [8] showed increased risk at an age younger than 6 months. Reddy and associates [14] did not find any influence of age on outcome for complete AVSD repair. Gatzoulis and colleagues [15] report the low operative risk of repair of partial AVSD in adults. In the present study an effect of age on mortality rate could not be found. However, 3 of 15 patients (20%) who underwent reoperation eventually died. These patients died of progressive left ventricular dilatation and progressive complaints of cardiac failure.
Conclusions
A significant number of patients after AVSD correction have to undergo reoperation for severe LAVVR. Preoperative severe LAVVR, and severe LAVVR 1 week after operation were the main risk factors. However, spontaneous regression after the immediate postoperative period is possible and should be given a fair chance. When severe LAVVR persists, redo surgery should be considered. This surgery usually has to be performed relatively early after initial surgery and contains an increased risk for morbidity and mortality. Attempts at re-repair are usually successful. Valve replacement is a last resort.
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