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Eur J Cardiothorac Surg 2000;18:54-61
© 2000 Elsevier Science NL
a Division of Cardiovascular Surgery, Hospital for Sick Children, University of Toronto, 555 University Avenue, Suite 1525, Toronto, ON M5G 1X8, Canada
b Toronto Congenital Cardiac Centre for Adults, Toronto, ON, Canada
c Division for Paediatric Cardiology, Hospital for Sick Children, Toronto, ON M5G 1X8, Canada
Received 8 September 1999; received in revised form 11 January 2000; accepted 22 February 2000.
Corresponding author. Tel.: +1-416-813-6419; fax: +1-416-813-7984
e-mail: bill.williams{at}sickkids.on.ca
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Abstract |
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 Top Abstract 1. Introduction 2. Patients and methods...3. Results4. Discussion Appendix A. Conference...References |
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Key Words: Atrioventricular septal defect • Left atrioventricular valve • Mitral valve repair • Reoperation
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1. Introduction |
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TopAbstract1. Introduction 2. Patients and methods...3. Results4. Discussion Appendix A. Conference...References |
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Sparse data are available on the outcome following reintervention for LAVVR [9–12]. The frequency of repair versus valve replacement at reoperation is unknown. Prosthetic replacement of the LAVV should be avoided in young children and especially in infants, because of poor survival, high incidence of valve-related complications and the need for multiple subsequent valve replacements as the child grows [13,14].
We believe that when there is adequate valve leaflet tissue, reoperation can be successfully accomplished by closing the cleft and narrowing the annulus. However, if the leaflets are dysplastic, valve repair at reoperation is prone to failure. There may be too much tension to allow cleft closure and an annuloplasty may have to be so extensive that it causes stenosis [9,10,12,15].
We propose a novel repair for patients with AVSD and dysplastic leaflets. Its use may avoid failure of conventional repair and/or need for valve replacement.
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2. Patients and methods |
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TopAbstract1. Introduction 2. Patients and methods...3. Results4. Discussion Appendix A. Conference...References |
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2.1. Estimation of prevalence of reoperation for LAVVR
To estimate the prevalence of reoperation for LAVVR after AVSD repair, we reviewed the clinical data of 761 patients (partial AVSD (n=240, 31.5%) and complete AVSD (n=521, 68.5%)) who underwent AVSD repair at the Hospital for Sick Children, Toronto or the Toronto Congenital Cardiac Centre for Adults between July 1982 and December 1998. Patients whose initial repair was performed prior to 1982 or at other centers are excluded for this part of the analysis. There were 64 early deaths (8.4%). Seven (2.9%) deaths occurred after repair of a partial AVSD (six of seven were less than 1 year old) and 57 (10.9%) after repair of a complete AVSD. The mean follow-up of hospital survivors is 5.3 years (range 0–18 years, median 4.2 years). Follow-up is available on 44% of the patients beyond 5 years after repair and 77% have been seen since January 1, 1997. The prevalence of the reoperation for LAVV was analyzed by the Kaplan–Meier method.
2.2. Patient demographics and operative techniques
Three different operative techniques were utilized at reoperation for LAVVR: (1) conventional repair, consisting essentially of closing a residual cleft with or without a De Vega type annuloplasty, (2) valve replacement, or (3) patch augmentation of the superior and inferior bridging leaflets. The demographic features of the three groups of patients are outlined in Table 1.
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2.3. Group 1: conventional repair
Conventional repair of the LAVVR was performed in 54 patients. Although they appear younger (median age of 3 years (1 month to 38.4 years; mean 5.3±6.8 years)) than the other two groups of patients, the difference is not statistically significant. Eleven infants aged less than 1 year (20%) are counted in this group. Thirty-five patients have complete AVSD, and the remaining 19 partial AVSD, including three transitional type (AVSD with a restrictive VSD and fusion of the anterior and posterior bridging leaflets above the ventricular septum, thus dividing the common AVV into distinct left and right components). A parachute LAVV was noted in five patients and double orifice in three patients. The initial AVSD repair had been performed a median of 16 months (range 1–27 years, mean 3±5 years) beforehand. Postoperative echocardiographic data following the initial repair of the AVSD was available for 38 of the 54 patients among whom 17 (45%) had moderate to severe LAVVR and the remainder minimal incompetence.
At reoperation, in addition to closing the cleft and annuloplasty, leaflet perforation or leaflet dehiscence was sutured in 12 patients (22%), chordae were shortened in four (7.4%), papillary muscles were split in three (6%) and a commissurotomy performed in one patient. Concomitant procedures (n=13, 25%) included the closure of a residual atrial septal defect in four (7.4%) and a ventricular septal defect in four (7.4%) patients, right atrioventricular valve repair in three (6%) and a pulmonary valvotomy in two patients (4%) with associated tetralogy of Fallot.
2.4. Group 2: valve replacement
Valve replacement was performed in 14 patients (19%). They were the eldest of the three groups of patients with a median age of 11.3 years (0.9–51.4 years; mean 16.2±15.5 years), although their age is not statistically different from the other groups. Partial AVSD was present in ten patients (71.4%) and the remaining four (29%) had complete AVSD, all Rastelli type A. Two patients had a parachute LAVV, and one a double orifice. The interval between the initial repair and reoperation for LAVVR was a median of 5.5 years (4.3–35 years; mean 8.6±9.9 years) which appeared longer than the other two groups of patients, but did not reach statistical significance.
A mechanical prosthesis was implanted in 13 patients (eight Bjork–Shiley (Shiley, Inc., Irvine, CA), four St. Jude (St. Jude Medical, Inc., St. Paul, MN) and one CarboMedics (Sulzer Medica, Austin, TX) valves). Valve size ranged from 16 to 33 mm. An inverted 16-mm aortic homograft was implanted in one child. The subvalvular apparatus was partially preserved in four patients (29%). Concomitant procedures included a residual ASD closure in two patients, and a subaortic resection in one.
2.5. Group 3: patch repair
Eight patients (11%) underwent a novel patch repair illustrated in Fig. 2). The leaflet augmentation technique consists of detaching the bridging leaflets radially 2 mm from the annulus from within 2 mm of one commissure to the other (Fig. 1)
. Abnormal chordal attachments to the ventricular side of the leaflet are resected to mobilize the valve tissue. A crescent-shaped patch of glutaraldehyde-treated autologous pericardium is sutured in place to augment the leaflet surface. The pericardial patch is prepared by suspending it using silk sutures at its four corners, wrapping it in a sponge, placing it in a solution of 0.625% glutaraldehyde for 5 min, then rinsing it in 100% dehydrated alcohol for 30 s and storing it in 0.9% sodium chloride solution until it is used. The augmented leaflet area allows for better leaflet coaptation and a tension-free closure of the cleft, further improving competency. An annuloplasty was performed in three of the eight patients.
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2.6. Follow-up interval
Follow-up information is available for all but five operative survivors for a follow-up rate of 93%. The mean follow-up is 4±5 years (1 month to 24 years, median 3 years); 3.9 years (1–23.9 years, median 2.4) for conventional repair, 5.2 years (0.1–15.5 years, median 3.8) for mitral valve replacement, and 2.3 years (0.2–8.5 years, median 1.0) for patch repair.
2.7. Mechanisms for LAVVR
We attempted to determine which patients failed conventional repair or underwent valve replacement and might have benefited from a patch repair. Clinical and echocardiographic data of the 68 patients who underwent a conventional repair or a valve replacement were analyzed. The patients were divided into two populations. Group 1: valve replacement or ‘failed conventional repair’ (n=23, 34%) included the postoperative cardiac deaths, and patients with residual LAVV disease necessitating early replacement (<1 year) following a conventional repair; and group 2: ‘successful repairs’ (n=45, 64%). A univariate analysis was performed using the variables listed in Table 4.
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2 for categorical variables. Cumulative reintervention rate over time and survival were calculated by the Kaplan–Meier method and compared using log rank test. A P value less than 0.05 was considered as statistically significant. |
3. Results |
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TopAbstract1. Introduction 2. Patients and methods...3. Results4. Discussion Appendix A. Conference...References |
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The LAVV repair was the only procedure in 47 patients (72%) and was associated with a concomitant surgical repair in the remaining 18 patients (28%).
The overall 10-year freedom from reoperation for LAVVR following AVSD repair is 86%. The 10-year freedom from reoperation for LAVVR was marginally better (P=0.053) in patients with partial AVSD with a rate of 89 vs. 83% in patients with a complete AVSD (Fig. 2) .
3.2. Operative mortality at reintervention for LAVVR
Among the 76 patients (65 from our center and 11 referred from elsewhere) who have undergone reoperation for LAVVR, there are six operative deaths: five following a conventional repair (9%), one after a valve replacement (7%) and none after a leaflet augmentation procedure. The operative results are outlined in Table 2. The cause of death was heart failure in all six, in combination with sepsis in two (mediastinitis, endocarditis). Four of the six deaths were in infants aged less than 1 year, who had an initial AVSD repair 1 week to 4 months prior to reoperation for severe LAVVR and progressive heart failure. The only death after LAVV replacement occurred in a child aged 10 months with a double orifice and parachute LAVV in whom an inverted aortic allograft was implanted. She developed significant prosthetic stenosis and died of mediastinitis and congestive heart failure 10 days postoperatively.
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3.3. Operative morbidity
One third of the patients had postoperative complications. The prevalence of complications was not different among the three groups (Table 3). Five patients required pacemaker implantation for complete atrioventricular block after reintervention; four (31%) after LAVV replacement, one (2%) after conventional repair and none after patch augmentation.
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3.5. Subsequent reintervention
Nine patients underwent further reintervention after conventional repair at a median interval of 12 months (1 month to 12.8 years, mean 3±2.5 years). A valve replacement was performed in seven patients and two had a rerepair, after which one patient required a prosthetic valve implantation 1 year later for persistent LAVVR.
In the valve replacement group, two patients were reoperated for paravalvular leak/recall at 9 years in one patient and for outgrowth of the prosthesis at 14 years.
Amongst the eight patients who underwent a patch repair, two required further surgery and were successfully rerepaired. One of these patients was rerepaired at 5 years for subaortic stenosis and moderate LAVVR. The other patient was rerepaired at 41 months for severe LAVVR. At reoperation, the pericardial patches had not retracted, were compliant, and had not calcified. Annular dilation was responsible for the regurgitation and was corrected with an annuloplasty. Replacement of the valve was not required.
The 5-year freedom from reintervention is comparable for the three techniques (P=0.92), estimated at 81, 82 and 50% for conventional repair, valve replacement and patch repair, respectively (Fig. 3) .
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3.7. Echocardiographic assessment
Late echocardiographic follow-up is available for 55 (85%) survivors. Among the conventional repair patients, mild LAVVR was present in 85% and moderate LAVVR in 15%.
All eight of the patch-repair patients had echocardiographic evaluations with six patients showing mild LAVVR and two with moderate LAVVR. Mild LAVV stenosis (mean Doppler gradient=4 mmHg) was present in only one patient. None of the patients have systolic anterior motion (SAM) or left ventricular outflow tract obstruction. All of the patients with a patch augmentation repair have preserved left ventricular function.
Eighteen survivors of a valve replacement with long-term echocardiographic follow-up showed normally functioning prostheses although one patient has a 3-mm paravalvular leak. The cardiac function is mildly depressed in all valve replacement patients.
3.8. Mechanisms of LAVVR
All of the patients with a successful repair had mild to moderate dysplasia as described intraoperatively. The mechanism of LAVVR was primarily due to cleft incompetence and/or annular dilation. The presence of a parachute or double-orifice mitral valve, type of AVSD (partial or complete) and age at reoperation did not influence significantly the outcome of the repair.
At reoperation, 34% of the patients had a subsequent valve failure or required a valve replacement (Table 4). All of the patients who failed conventional surgery had severely dysplastic valves. We believe that the novel patch repair technique would have avoided a failure or valve replacement in some of these patients.
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4. Discussion |
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TopAbstract1. Introduction 2. Patients and methods...3. Results4. Discussion Appendix A. Conference...References |
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Improvements in echocardiographic evaluation and an increasing clinical experience with this pathology have helped to identify mechanisms of regurgitation. The pathophysiology of LAVVR appears to be multifactorial. Abnormalities of one or more of the atrioventricular valve components, the annulus, leaflets, chordae or the papillary muscles, can contribute to incompetence. Cleft incompetence is the most frequent finding. Other valvular abnormalities have been observed in our patient population and also reported by other authors including isolated annular dilation, chordal abnormalities, parachute valve and double-orifice valve [9,10,12,15]. LAVV dysplasia has been identified as a potential deterrent to a successful repair [9,10,15]. Acar et al. [16] demonstrated that a relative decrease in leaflet surface area, as calculated by three-dimensional echocardiography, could be responsible for regurgitation at the level of the cleft and also at the commissures.
Cleft incompetence, annular dilation and lesser degree of dysplasia appear to lend themselves to a successful conventional repair consisting of a cleft closure with or without an annuloplasty [9,10].
Because of the wide spectrum of lesions, multiple techniques of valve repair may be needed including modifications of those used in adults. The use of a pericardial patch augmentation has been previously described by the Carpentier group, primarily for mural leaflet enlargement in degenerative mitral disease and in the treatment of endocarditis [17]. They studied the performance of the autologous pericardial patches fixed in glutaraldehyde in a series of 64 patients followed over a 3-year period. Repeat echocardiographic studies revealed preserved pericardial tissue with normal compliance and without evidence of calcification. These satisfactory results have also been noted in children in spite of the known propensity for younger patients to prosthetic calcification. In two of our patients, at reoperation the pericardial patches were free of signs of deterioration and permitted a successful rerepair. In contrast, valve replacement was required in six of seven patients who required reoperation after a conventional repair. Durability of the patch augmentation is demonstrated by the first child in the series who continues to do well 8.5 years after repair.
Our results confirm findings of the few published series of reoperations for LAVVR after AVSD repair. Alexi-Meskishvili et al. reported the experience of the German Heart Institute in 28 patients [9]. Cleft closure combined with an annuloplasty in addition to other valve repair procedures resulted in the successful decreased LAVVR in 64% (n=18) of their patients. In five, severe LAVVR led to valve replacement. Anomalies other than cleft incompetence were predictive of recurrent severe postoperative LAVVR.
Lamberti et al. [11] reported reoperations in 14 patients who had prior AVSD repair, among whom four required valve replacement (30%). At the mean follow-up of 3 years, all ten of the repaired patients had no or mild LAVVR on echocardiographic evaluation.
Repair offers the advantage of avoiding the need for lifelong anticoagulation in children and the absence of thromboembolic complications. Following valve replacement, mortality rate in infants is especially high [14,18]. The survival was estimated at 52% at 1 year and 43% at 5 years by Koboda et al. from the Children's Hospital in Boston [14]. The survival was over 80% at 10 years in our population of patients who appeared to be slightly older.
In conclusion, there are multiple mechanisms of LAVVR after repair of an AVSD. In our experience, reoperation has been required in 14% of patients within 10 years of an AVSD repair. When these patients have adequate leaflet tissue, conventional repair may produce a satisfactory long-term outcome. However, when the LAVV leaflets are dysplastic, as they were in 34% of our patients, leaflet augmentation with autologous pericardium may lessen the risk of a failed valve repair and/or the need for valve replacement. A pericardial patch repair can be safely be performed and is durable.
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Acknowledgments |
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Footnotes |
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Appendix A. Conference discussion |
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TopAbstract1. Introduction 2. Patients and methods...3. Results4. Discussion Appendix A. Conference...References |
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Dr Poirier: Adult patients who undergo reoperation for left atrioventricular valve regurgitation do appear to have more valvular dysplasia, leaflet tissue retraction and thickening than in infants and children. We believe that with time the valves do become more dysplastic, particularly patients that had thickened leaflets and abnormal subvalvular apparatus at initial AVSD repair. The left atrioventricular valve has a complex anatomy and multiple mechanisms of regurgitation. Valve repair is not always successful and early or late valve replacement is a definite possibility. If we can guarantee repairability then we can be more aggressive and repair earlier, possibly avoiding an increase in dysplasia that renders a later repair difficult and preserving left ventricular systolic function. Otherwise a more conservative approach is appropriate.
Dr D. DiCarlo (Rome, Italy): Your technique makes a lot of sense and was very nicely presented. You state in your presentation and in your abstract that it allows for a tension-free closure of the cleft, which is obviously a major problem, and very often we find that regurgitation is due to the fact that sutures have cut across the cleft margins. I don't know if this was the case, but in your slide the way that the mitral valve was shaped showed a very small posterior leaflet, which is usually considered in the literature, whether under one-third of the circumference or not, a contraindication for closure of the cleft. So I was wondering whether it was just a case that the drawing was done this way, or whether you implied that in that particular case the cleft has to be closed at any price? That's my first question. Please also comment on your techniques of closing the cleft because we seem to continue to have a lot of dehiscence nowadays.
Dr Poirier: The illustration in not quite to scale. Left atrioventricular valves post-AVSD repair with small posterior leaflets are essentially monoleaflet valves that can benefit from the enlargement of the bridging leaflets or of the posterior leaflet, using our technique. The cleft is completely closed whenever possible unless this induces stenosis, at which time the cleft is only partially closed. Interrupted stitches using monofilament or braided suture material is used.
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References |
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TopAbstract1. Introduction 2. Patients and methods...3. Results4. Discussion Appendix A. Conference...References |
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