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Ann Thorac Surg 2002;73:614-621
© 2002 The Society of Thoracic Surgeons

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Original article: cardiovascular

Repair of congenital malformations of the mitral valve: early and midterm results

^a G. Pasquinucci Hospital, CREAS-IFC-CNR, Massa, Italy
^b IRCCS Neuromed, Isernia (Pozzilli), Italy

* Address reprint requests to Dr Prifti, G. Pasquinucci Hospital, CREAS-IFC-CNR, Via Aurelia Sud, Massa, 54100, Italy
e-mail: edvinprifti{at}hotmail.com

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. The aims of this study were to determine early and midterm survival and freedom from reoperation, and to identify the predictors for poor postoperative outcome in children undergoing mitral valve (MV) repair owing to congenital malformations of the mitral valve.

Methods. Between January 1990 and February 2001, 94 consecutive children with congenital MV disease underwent valve repair. The mean age was 5.2 ± 3.3 years (range 20 days to 15 years). Twenty-five (26.6%) children were less than 1 year old. Isolated MV disease was found in 21 (22.4%) patients. MV stenosis was the predominant lesion in 21 (22.4%) patients with a mean left atrial to left ventricle diastolic peak gradient of 24.5 ± 9.2 mm Hg. MV regurgitation was the predominant pathophysiology in 73 (77.6%) patients with a mean regurgitation grade of 3.3 ± 0.7.

Results. The hospital mortality was 8.5% (8 of 94). Three patients required permanent pacemaker implantation owing to complete atrioventricular block. Two patients underwent mediastinal exploration for significant bleeding. Postoperatively the echocardiography color Doppler study demonstrated a significantly lower mean end diastolic left atrium to left ventricle gradient 8.7 ± 2.2 mm Hg (p < 0.001) in patients with MV stenosis and a mean regurgitation grade of 0.9 ± 0.6 (p < 0.001) in patients with MV regurgitation. Actuarial survival and actuarial reoperation-free survival were 89.2% and 76.3%, respectively. Multivariate analysis demonstrated that age less than 1 year (p = 0.035), hammock MV (p = 0.0093), cardiothoracic ratio greater than 0.6 (p < 0.0001), and associated cardiac anomalies (p = 0.003) were strong predictors for poor overall freedom from reoperation and midterm survival.

Conclusions. Mitral valve repair for congenital mitral valve disease yields acceptable early and midterm mortality and reoperation rates. Strong predictors for poor overall freedom from reoperation and midterm survival were age less than 1 year, hammock MV, cardiothoracic ratio greater than 0.6, and associated cardiac anomalies.

	Introduction

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Congenital malformations of the mitral valve (MV) are relatively rare and present with a wide spectrum of morphologic abnormalities [1] and a high incidence of concomitant cardiac anomalies [2–4]. The surgical management of congenital MV malformations in the pediatric age group has been a major therapeutic challenge for many years [4–7]. Despite the development of new techniques, MV repair still carries considerable morbidity and mortality [8, 9]. Several groups have demonstrated excellent results with repair of complex MV abnormalities [4, 9–16]. Promising outcomes have been reported in pediatric patients with MV stenosis [13], which remains a uniquely challenging group of patients. Good results have also been reported in patients with residual or recurrent left atrioventricular valve (LAVV) insufficiency after atrioventricular septal defect (AVSD) repair [14]. Acceptable outcomes have also been demonstrated in patients undergoing MV surgery during the first year of life [15]. Most reports of MV replacement in children have documented considerable perioperative and late morbidity and mortality and a high incidence of subsequent reoperations when performed in younger patients [15], although a recent report has suggested improved mortality and long-term freedom from reoperation among pediatric patients undergoing MV replacement [17].

Given the relative rarity of MV abnormalities in the pediatric population, there is a comparatively small and limited experience with MV repair at each institution. We reviewed our 10-year experience with repair of MV malformations in the pediatric age group with two main objectives: (1) to evaluate the early and midterm outcome in terms of survival and freedom from reoperation; and (2) to identify the predictors for poor postoperative outcome in this group of patients.

	Material and methods

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Between January 1990 and February 2001, 106 consecutive children with congenital MV malformations underwent surgical repair or replacement. MV repair was successful in 94 patients and they constitute the study group for this report. Twelve children underwent MV replacement and were excluded from this study. In all 12 patients MV repair was attempted but they underwent valve replacement during the same surgical procedure owing to failure of the repair efforts. Patients with AVSD undergoing initial definitive repair, significant left ventricular (LV) hypoplasia, and ventriculoarterial discordance, or with a single functional ventricle were excluded from this study. Patients with persistent or residual LAVV insufficiency after AVSD repair were included in this report. Of the 94 patients in this report, 36 (38%) had undergone previous repair of some form of AVSD. During the same period, 213 patients with various forms of AVSD were operated on: 140 (66%) patients had complete AVSD, and 73 (34%) patients had partial or transitional AVSD. Nine of these 36 patients had undergone primary repair at another institution.

Patient characteristics
The mean age in the study group was 5.2 ± 3.3 years (range 20 days to 15 years). There were 52 boys and 42 girls. Twenty-five children (27%) were less than 1 year old. Twenty-one patients (22.4%) had isolated MV malformations. Two patients with severe congestive heart failure required mechanical ventilation and inotropic support prior to operation. The preoperative demographic data are shown in Table 1.

Cardiac catheterization
Preoperative cardiac catheterization was performed in 59 patients (63%). Pulmonary hypertension was severe (defined as pulmonary pressure greater than 50% of systemic systolic pressure) in 4 patients (Table 1).

Mitral valve congenital malformations anatomical presentation
Congenital malformations of the MV were classified according to Carpentier (Table 2) [2]. The most common MV malformation resulting in regurgitation were anterior leaflet cleft (type I) in 42 (45%) patients, annular dilatation (type I) in 28 (30%) patients, and elongated chordae (type II) in 14 (15%) patients. Multiple left heart obstructions (Shone’s anomaly) involving the MV were found in 2 patients. Associated valve malformations in patients with residual LAVV insufficiency after AVSD repair are given in Table 3. Associated cardiac anomalies were seen in 73 patients (78%) and are listed in Table 4. Ventricular septal defect (VSD) (17%) and subaortic stenosis (12%) were the most commonly associated lesions. Of the 16 patients with a VSD, 9 had undergone prior AVSD repair. In the other patients with a VSD, leaflet perforation was found in 3 patients, anterior leaflet cleft in 1, elongated chordae in 2, and parachute MV (type III) in 1 patient. Two of the 3 patients with tetralogy of Fallot and LAVV insufficiency had concomitant previous AVSD repair. The other patient with tetralogy of Fallot had chordal elongation and accessory MV tissue. All patients with VSD and tetralogy of Fallot, regardless of the presence of AVSD, presented with dilatation of the LAVV.

Surgical technique
Intraoperative transesophageal echocardiography was employed in all patients. The MV was exposed either through a left atriotomy posterior to the interatrial groove in 54 patients or through the interatrial septum in 40 patients, depending on the need for treating an associated heart defect. The MV apparatus was carefully inspected, with the aid of four everting pledget stitches placed at the annulus site (Fig 1) [12]. Cold saline solution was routinely injected into the LV cavity to test the valve competence and to assess the leaflet motion and coaptation. Annular dilatation producing central valve incompetence was treated by means of different reduction annuloplasty techniques (Table 5). Single mattress sutures reinforced with pledgets were employed to treat regurgitation at the commissural sites. A Carpentier prosthetic ring was used in 4 patients more than 10 years of age who had a simple annular dilatation. Attempts were made to reduce the diameter of the MV annulus to the normal values according to the patient’s age and weight [18]. In cases with elongation of chordae, the "split and tuck" technique was used. Splitting and fenestration of interchordal spaces were performed in cases with single papillary muscle. Details of the surgical MV reconstruction techniques are summarized in Table 5. The MV annulus was sized with appropriate obturators after repair. Thirty-seven patients (39%) underwent simultaneous repair of associated intracardiac heart defects. The associated surgical procedures are summarized in Table 6.

View larger version (42K): [in this window] [in a new window]   Fig 1. Transseptal approach. Enhanced mitral valve apparatus exposure with the aortic insufficiencies of four everting pledget stitches placed at the annulus site. (AO = ascending aorta; IVC = inferior vena cava; RA = right atrium; SVC = superior vena cava; TV = tricuspid valve.)

Statistical analysis
Group statistics are expressed as mean ± SD. The generalized Wilcoxon test was performed for the statistical analysis between groups. Fisher’s exact test was used for the noncontinuous variables. The relationship between preoperative and postoperative variables within the same group was assessed by the McNemar test. The univariate analysis was performed to identify risk factors for early and overall mortality. The multivariate Cox regression analysis, including stepwise analysis (Biomedical Data Processing Program [BMDP2L-Survival analysis with covariates]; BMDP Statistical Software, Inc, Los Angeles, CA), was performed to determine independent variables associated with death. Long-term survival rates were calculated using the Kaplan-Meier method and statistical significance was calculated by the log rank test. Significance between data was considered achieved when p was less than 0.05.

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Eight (8.5%) hospital deaths occurred in this series. Causes of death included progressive heart failure in 4 patients, multiple organ failure in 2, sepsis in 1, and respiratory failure in 1 patient. Three patients (1 of whom underwent subaortic stenosis resection and another of whom required closure of a perimembranous VSD) required permanent pacemaker implantation because of a complete atrioventricular block. Transient neurological deficits were identified in 3 patients (2 of whom underwent circulatory arrest), all of which reversed completely within 2 weeks after the surgical procedure. Two patients required mediastinal exploration owing to significant bleeding. Two boys, 10 and 13 years old, required subsequent MV replacement owing to infective endocartitis and severe MV insufficiency within the first year after the surgical procedure.

Univariate analysis of the preoperative variables demonstrated that age less than 1 year (p = 0.004), MV stenosis as the predominant lesion (p = 0.013), hammock MV (p = 0.006), pulmonary hypertension (p = 0.001), congestive heart failure (p = 0.004), cardiothoracic ratio greater than 0.6 in patients with MV insufficiency (p = 0.006), and left atrium to aorta ratio greater than 1.5 (p = 0.012) are strong predictors for poor early postoperative outcome (Table 7). All 5 deaths in patients with MV stenosis occurred in patients with a hammock MV. Reoperation or prior AVSD repair is not a risk factor for postoperative mortality. Prolonged cardiopulmonary bypass and aortic cross clamping times and use of circulatory arrest were associated with failed attempts at MV repair (Table 7), demonstrating the presence of a more complex valvular abnormalities or associated heart defects.

The actuarial survival was 89.2% at 5 years and actuarial reoperation-free survival at 5 years was 76.3% (Fig 2). Six patients required subsequent MV replacement. The incidence of reoperation during follow-up was significantly higher among patients who had stenotic lesions compared with patients who had regurgitation. Among the 16 survivors with preoperative MV stenosis, 5 (31%) required reoperation versus 6 reoperations among 70 survivors (8.6%) with preoperative MV insufficiency (p = 0.028). Nine patients died during follow-up. Two of these patients had a hammock MV and 4 were less than 12 months of age at the time of operation. All the preoperative, intraoperative, and postoperative variables were analyzed. Variables reaching or approaching statistical significance (p < 0.1) were included in the multivariate model (Table 8). The multivariate analysis demonstrated that the age less than 1 year (p = 0.035), hammock MV (p = 0.0093), cardiothoracic ratio greater than 0.6 (p < 0.0001), and associated heart defect (p = 0.003) were strong predictors for poor event-free survival (Table 8).

View larger version (10K): [in this window] [in a new window]   Fig 2. Actuarial survival and freedom from reoperation among children with congenital mitral valve malformation undergoing mitral valve repair. (AS = actuarial survival; AS-R = reoperation-free actuarial survival).

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

A careful preoperative evaluation of the MV abnormality with special attention to the anatomic and functional features should be performed in each patient. We do believe that the key to a good postoperative outcome is a thorough preoperative understanding of the anatomy of the MV apparatus and the precise mechanisms causing stenosis or insufficiency.

The short-term and long-term results of MV repair compare favorably with those of replacement among patients with congenital MV malformation. Most authors have reported a significantly higher mortality rate—higher than 30%—among children undergoing MV replacement [7, 17]. However, other authors have reported acceptable early and long-term survival among children undergoing MV replacement [16]. MV replacement using a homograft is another surgical alternative but a very recent study revealed a high reoperation rate due to late development of severe MV regurgitation at 5 years after implantation [19]. MV homografts for valve replacement may be considered in highly selected cases in which conservative reconstruction techniques are not possible. Avoiding long-term anticoagulation therapy and preserving LV geometry are the main advantages of homografts over other MV prostheses [20].

We believe that any attempt to preserve the native MV should be encouraged, especially in infants and young children. MV repair offers the advantages of avoiding thromboembolism, preserving chordal and subvalvular apparatus function, and potentially reducing the need for reoperation. Because of a wide spectrum of MV lesions, which usually involve different sites of the valvular apparatus, multiple techniques of valve repair are required [2, 11, 15, 21].

In our series of patients annular dilatation and prolapsed leaflet were frequently present. Annuloplasty was performed in all patients presenting with annular dilatation. Rigid rings were employed only in patients older than 10 years presenting with pure annular dilatation so as to avoid thromboembolism episodes or complications due to anticoagulation and to not interfere with growth. In most of the patients we employed the commisure plication annuloplasty technique to correct the annular dilatation. Other techniques such as unilateral or bilateral pericardial patch annuloplasty were employed successfully in our series of patients. The need for ring annuloplasty procedure in the pediatric age group remains controversial. Chauvaud and associates [9, 22] used ring annuloplasty in children over 2 years of age, whereas other groups have demonstrated that other types of annuloplasty techniques can be employed successfully in children and the prosthetic rings are not indispensable for achieving favorable results [8, 10, 15]. MV leaflet prolapse was treated successfully in most of the cases by partial leaflet resection, papillary muscle shortening with the split and tuck-in technique, or the use of artificial chordae.

Surgical repair of congenital MV stenosis has been typically associated with greater postoperative mortality and morbidity [14, 22] and a higher reoperation rate compared with MV repairs for insufficiency [12]. The hammock MV is the most difficult malformation to correct owing to the considerable amount of muscle found beneath the MV leaflet causing severe LV inflow obstruction [2, 12, 22]. The hammock MV was defined as a very dysplastic MV, without tendinous chordae, with the apex of the papillary muscles having direct continuity with the leaflet tissue [23]. In parachute and hammock MV the single papillary muscle was split delicately at the midline in two halves [2], thus increasing the excursion of the MV during diastolic phase. When necessary a commissurotomy procedure was also performed. Eight of the 9 patients with hammock MV in this series had early or late death or required reoperation.

The mortality rate of 8.5% in this series of patients is somewhat elevated compared with some recently reported series of patients with congenital malformations of the MV [12, 14, 16]. We believe this result was related to the disproportionate number of patients less than 1 year old with MV stenosis. Statistical analysis of the early postoperative survival identified as strong predictors for postoperative mortality, age less than 1 year, MV stenosis, hammock MV, congestive heart failure, pulmonary hypertension, and associated heart defects. The multivariate analysis revealed only age less than 1 year old, hammock MV, cardiothoracic ratio greater than 0.6, and associated cardiac anomalies as risk factors for death or reoperation. Very few reports on MV repair in children identified predictors for poor outcome in this group of patients, probably because of the small numbers of patients in each report. Sousa and colleagues [15] reported excellent results in children less than 1 year of age undergoing MV surgery, with a 7-year actuarial survival of 94%. We found some very different results: 6 of 25 early deaths and 6 of 11 late deaths were patients less than 1 year old. From our data it seems that age less than 1 year is a risk factor for poor early and midterm survival. The correction of the associated heart defects also increased the operative risk, probably because of significantly longer cardiopulmonary and aortic cross clamping times, more complex anatomy, and LV hypertrophy and impaired LV function, particularly in cases with LV outflow tract obstruction and VSD. In our series, we did not find a higher mortality rate among patients undergoing LAVV repair owing to residual insufficiency after AVSD repair. The mortality rate in this subgroup of patients was 5.5% (2 patients). Other authors have reported an acceptable postoperative mortality and morbidity in this specific group as well [14, 24, 25]. We found a high incidence of concomitant anatomical abnormalities of the LAVV in patients requiring valve repair after AVSD correction, and we believe that persistent or recurrent insufficiency in such cases is closely related to the presence of these associated abnormalities. Meskishvili and associates [24] also found that the presence of these morphologic abnormalities in this subgroup of patients increased the incidence of regurgitation after AVSD repair. In such situations, the surgeons should not hesitate to perform associated LAVV reconstruction procedures during AVSD correction. This may reduce significantly the risk of reoperation due to insufficiency [25].

Improvements noted in the degrees of both regurgitation and stenosis were still present 6 months after surgery. An acceptable postoperative outcome was obtained in 84 of 86 survivors. Moderate stenosis was noted in only 1 of the 6 surviving patients who originally presented with MV stenosis. Among the 70 surviving patients who initially presented with insufficiency as the predominant lesion, only 1 patient was graded as having moderate regurgitation at 6 months after valve repair.

The actuarial survival and the actuarial reoperation-free survival were 89.2% and 76.3%, respectively, at 5 years follow-up. These results are comparable with other published data. Moran and colleagues [14] demonstrated a survival of 89.9% and 86.6% at 1 and 10 years of follow-up among patients requiring valve repair due to LAVV insufficiency after AVSD correction. Stellin and colleagues [12] demonstrated an excellent long-term outcome in a series of 34 patients with MV dysplasia, with 96.8% and 86.5% actuarial survival and reoperation-free survival, respectively, at 12 years of follow-up. Yoshimura and coauthors [16] demonstrated an actuarial survival of 87.2% and 90.3% at 10 years in children undergoing MV repair and replacement, respectively. Serraf and associates [13] in their series of 72 children with MV stenosis undergoing surgery demonstrated a 69.6% actuarial survival and 70.8% freedom from reoperation at 15 years of follow-up, and they concluded that the associated anomalies significantly increased the early postoperative mortality and morbidity among these patients. Patients requiring repair of associated lesions in addition to undergoing valve repair for MV stenosis appear to be at an increased risk for postoperative morbidity and mortality.

Study limits
This study has several limitations. It is a retrospective study, and a relatively small number of patients are included in the study. All congenital MV malformations were included in the study group. It would be interesting to study congenital MV stenosis and insufficiency separately, but that would necessitate a longer study period and data collection from multiple institutions. The operations were performed by three different surgeons, which may have an impact in terms of postoperative outcome and homogeneity of surgical procedures performed. Patients with residual LAVV insufficiency after AVSD correction were included in the study. Although most of these patients presented with associated MV lesions, we believe that separate analysis in this group should be made.

We conclude that repair of congenital MV malformations yields acceptable early and midterm outcome in terms of mortality and freedom from reoperation. Strong predictors for poor overall survival appear to be age less than 1 year, hammock MV, congestive heart failure, and associated cardiac anomalies.

	Acknowledgments

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We are grateful to Professor Sylvain Chauvaud for his technical assistance and collaboration. We also would like to express our appreciation to Dr Ralph Delius of the Childrens Hospital of Michigan for his support regarding manuscript revision, suggestions, and technical comments.

	References

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