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Ann Thorac Surg 1999;68:537-541
© 1999 The Society of Thoracic Surgeons

Original Articles

The long-term results of commissure plication annuloplasty for congenital mitral insufficiency

Hideaki Ohno, MDa, Yasuharu Imai, MDa, Masatsugu Terada, MDa, Takeshi Hiramatsu, MDa

a Department of Pediatric Cardiovascular Surgery, The Heart Institute of Japan, Tokyo Women’s Medical University, Tokyo, Japan

Address reprint requests to Dr Ohno, Department of Pediatric Cardiovascular Surgery, The Heart Institute of Japan, Tokyo Women’s Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan;
e-mail: ohno{at}mxu.mesh.ne.jp


   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Comment
 References
 
Background. Mitral valve repair in the pediatric population remains demanding because of a diversity of apparatus anomalies and the young age of the patients.

Methods. We reviewed our clinical results for mitral valve repairs for congenital mitral insufficiency. Forty-nine consecutive patients aged 2 months to 34 years (mean, 4.4 years) had mitral valve repair between June 1984 and December 1996. Forty-one patients (83.7%) had associated cardiac anomalies. The predominant pathologies for the regurgitations were chordal anomalies in 34 patients (69%), annular dilatation in 8 (16%), and leaflet anomalies in 7 (14%). Mitral valve repair included commissure plication annuloplasty in 43 patients (88%), modified DeVega in 11, cleft closure in 5, plication of the anterior leaflet in 3, triangular resection of the anterior leaflet in 2, chordal shortening in 1, and placement of artificial chordae in 1. Several combined techniques were required in 19 patients.

Results. There were no early or late deaths. The follow-up period was from 6 to 166 months (mean, 88.4 months). Forty-seven patients (95.9%) were in New York Heart Association class I. The long-term echocardiographic studies showed that 2 of 30 patients without reoperation had moderate regurgitation. The actuarial freedom from reoperation was 85.6% (95% confidence limits, 72.8%, 98.4%) at 13 years. Five patients (10.2%) required valve replacement from 13 days to 75 months after the valve repair. Two patients had cerebral ischemic events as a result of cardiomegaly and atrial fibrillation.

Conclusions. Valve repair for congenital mitral insufficiency gave adequate results in combination with commissure plication annuloplasty and other techniques with excellent long-term functional status.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 References
 
Although congenital mitral valve insufficiency is rare, it is a clinically important entity because some patients become severely symptomatic during early infancy because of congestive heart failure and pulmonary hypertension in association with a large left-to-right shunt.

We prefer reconstructive mitral valve operations as treatment because pediatric valve replacement poses clinical and technical difficulties, including high mortality rate; small-sized mitral annulus, left atrium, and left ventricle; accelerated tissue calcification and degeneration of the bioprosthesis; difficulty in maintaining anticoagulant therapy; and reoperation for prosthetic valve replacement with growth [1–6]. Mitral valve repair in adults is a well-established and safe procedure with long-term follow-up [7–10]. However, a congenitally malformed mitral valve has a wide spectrum of morphologic abnormalities. In addition, it is difficult to manage surgically and requires multiple valve-repair techniques. Several recent reports have described long-term results that show remarkable improvement in a large series of patients treated by mitral valve repair [11–14]. We reviewed our clinical experience in valve repairs for congenital mitral insufficiency.


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 References
 
Between June 1984 and December 1996, 49 consecutive patients had mitral valve repair for congenital mitral insufficiency at an initial operation. There were 17 male and 32 female patients whose age at operation ranged from 2 months to 34 years (mean, 4.4 years), with 13 patients less than 1 year old. Excluded from this study were patients with atrioventricular canal defect, single ventricle, left ventricular hypoplasia, corrected transposition of the great arteries, coronary arterial anomalies, Marfan syndrome, and metabolic disease. Five patients who had mitral valve replacement at the initial operation were also excluded. The abnormality resulting in infeasible mitral repair was a direct leaflet-papillary muscle attachment in 2 patients, short chordae to anterior leaflet in 1, absent chordae to the middle scallop in 1, and single papillary muscle in 1.

Forty-one patients (83.7%) had associated cardiac defects (Table 1). Of these 41, 33 patients, including 12 infants, were associated with volume overload diseases of the left ventricle, such as ventricular septal defect or patent ductus arteriosus. Five patients had previous operations, including repair of aortic coarctation in 2 and closure of an atrial septal defect, closure of a ventricular septal defect, and repair of tetralogy of Fallot in 1 each.


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  		Table 1. Associated Cardiac Defects

 
The degree of preoperative mitral regurgitation was assessed by echocardiography, cardiac catheterization, or both methods. According to the criteria of Sellers and associates [15], the degrees of regurgitation on angiogram were 1/4 in 1 patient, 2/4 in 9, 3/4 in 19, and 4/4 in 6 patients. Echocardiographic studies showed that 31 of 40 patients had regurgitation to a moderate or greater degree. Echocardiographic grades were based on the length of regurgitation jet relative to left atrial size [16], so regurgitation on echocardiography was more severe than on angiogram in some patients.

Thirty-four patients had chordal anomalies that were the most common cause for the mitral regurgitation, including chordal elongation in 16 patients, absent chordae in 7, scant chordae in 4, short chordae in 2, and mixed lesions of chordae in 5. Seven patients had leaflet anomalies, including cleft mitral valve in 6 and hypoplastic posterior leaflet in 1. Among the patients mentioned above, 6 (5 with absent chordae and 1 with cleft anterior leaflet) had abnormal papillary muscles that were directly attached to the anterior leaflet. Three patients had anomalous papillary muscles; in 2 of the 3 patients, the anterior papillary muscle was hypoplastic and associated with isolated and malpositioned papillary muscle. Eight patients had annular dilatation, including asymmetric posterior leaflet caused by large commissural leaflet or scallop in 6 patients [17], and symmetric annular dilatation in 2 (Table 2).


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  		Table 2. Main Lesions Responsible for the Regurgitation

 
Surgical techniques
All operations were done using cardiopulmonary bypass at moderate systemic hypothermia. After aortic cross-clamping, the mitral valve was exposed and cold cardioplegic solution was injected into the left ventricle to test the valve competence.

Our policy of mitral valve repair was as follows (Table 3): chordal anomalies, annular dilatation, and dilated commissural leaflet were treated by commissure plication annuloplasty (CPA), as reported by Kay and associates [18] and Reed and colleagues [19]. We have recently become reluctant to use foreign materials except for suture materials and to treat the chordae directly. Commissure plication annuloplasty was applied to the side where regurgitation was dominant or the commissural leaflet was dilated, or to the side where the papillary muscle was hypoplastic, bifid, bifurcated, or separated in patients with central regurgitation. Bilateral CPA was done if the residual regurgitation after unilateral CPA persisted as a result of redundant anterior leaflet. When needed, DeVega-type circular annuloplasty (a modified DeVega) with absorbable polydioxanone was added to the CPA. A Hegar obturator was used to reduce the annular diameter according to the criteria established by Rowlatt and associates [20]. Cleft was treated by interrupted sutures with reinforcement of fresh autologous pericardial strips on the atrial and ventricular sides. Mild regurgitation was repaired concomitantly in cases of associated cardiac lesions indicated for operation. A combination of several techniques was required in 19 patients.


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  		Table 3. Surgical Procedures

 
The following cases were exceptions to our policy. In 2 patients with chordal elongation, chordal shortening was added to the CPA. Artificial chordae with a fresh autologous pericardium was used in a 2-year-old boy for whom the central portion of the anterior leaflet had no chordal support. The autologous pericardium in a trousers-like shape was sutured to a flail edge of the anterior leaflet.

Follow-up
We obtained all information from outpatient medical records or through telephone calls to the referring pediatricians or directly to the families of the patients. Long-term data were available in 47 of 49 patients, with a mean follow-up time of 88.4 months (95% confidence limits [CL] 75.3, 101.6 months). Two-dimensional echocardiographic and Doppler studies were done in 30 patients within several months after discharge, and the latest postoperative studies were conducted 88.2 ± 7.94 months after the surgical procedure. Patients with residual regurgitation were followed up regularly with two-dimensional echocardiography. We did not examine the remaining 12 patients without valve replacement with two-dimensional echocardiography because all of them had no or faint heart murmur except 1 who was followed up at a referring hospital. Actuarial freedom from reoperation was calculated by the Kaplan-Meier method.


   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 References
 
There were no hospital deaths or late deaths. Forty-seven of 49 patients (95.9%) were in New York Heart Association functional class I. Reoperation was defined as the necessity for valve replacement or rerepair of the mitral valve and was indicated when congestive heart failure occurred because of severe residual regurgitations. Actuarial rate of freedom from reoperation was 89.9% at 6 years and 85.6% (95% CL, 72.8%, 98.4%) at 13 years after operation (Fig 1). Five patients required valve replacement with a St. Jude Medical prosthetic valve from 13 days to 75 months after the initial valve repair (Table 4). All lesions responsible for residual regurgitation were chordal (three absent chordae, one chordal elongation, and one scant or short chordae), and the preoperative grade of regurgitation was 3/4 or 4/4. All of these patients were treated by CPA and other techniques at the initial operation. Patient 3 required a valve replacement 13 days after the repair because the sutures lacerated the anterior leaflet. We did not encounter any cases requiring reoperation in which annular redilatation was responsible for the residual regurgitation. All patients who had valve replacement received anticoagulants, either warfarin potassium and aspirin in 3, and only warfarin potassium in 2.



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  		Fig 1. Actuarial freedom from reoperation.

 

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  		Table 4. Profile of Patients Requiring Mitral Valve Replacement After Valve Repair

 
Long-term echocardiographic studies of 30 patients showed moderate regurgitation with no stenotic findings in 2, none or trivial degree in 10, mild in 18, and moderate in 2 (Fig 2). Three of seven patients who had regurgitation to a moderate or greater degree at discharge required valve replacement, and the regurgitation improved to become only mild or less in 3 patients.



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  		Fig 2. Comparison of preoperative and long-term regurgitation grades. *Indicates patients after valve replacement were excluded. **Six patients were assessed only by angiogram, according to the Sellers’ criteria. (LVG = left ventriculogram; Post-Op = postoperative; Pre-Op = preoperative; UCG = ultrasonic echocardiogram.)

 
Two patients had cerebral ischemic events because of atrial fibrillation after the valve repair. The first patient was an 18-year-old woman who had trivial regurgitation on echocardiography at discharge from the hospital. The second was a 34-year-old woman who had the valve repair for mitral regurgitation after repair of tetralogy of Fallot. Both patients had cardiomegaly with a cardiothoracic ratio of more than 0.6 and did not receive anticoagulants before the events. We usually give antiplatelet agents for small children with prosthetic valve or atrial fibrillation and add warfarin for older children, so these two cases deviated from our usual anticoagulant regimen.


   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
References
 
The diversity of congenital mitral valve anomalies remains a therapeutic challenge because of the young age of the patients and the high incidence of associated complex cardiac defects. Recent surgical results have improved, with the overall mortality rates reported in the literature ranging from 0% to 22.2% for a large series [11–14, 21, 22]. We also obtained satisfactory results without early or late deaths and with the achievement of excellent long-term functional status, with 95.9% of patients in New York Heart Association functional class I. These data encouraged us to favor valve repair operations not requiring foreign materials.

The mean age of our patients was lower than that reported from western countries [11, 13, 21]. As many as 83.7% of our patients had other cardiac anomalies that might have contributed to an earlier appearance of congestive heart failure and early surgical intervention. All patients who had valve repair during infancy were in New York Heart Association functional class I and needed no reoperation. We therefore believe that the associated cardiac defects and the young age per se might not be risk factors for operative death or repair failure.

Chordal abnormalities are the most frequently encountered lesions. In our experience, the patients with chordal anomalies, except for elongation, more often require valve replacement. An unsupported area of the leaflets is wider in cases of absent chordae associated with the direct leaflet-papillary muscle attachment. Posterior papillary muscle has a broader attachment of the chordal branches to the posterior commissural leaflet. Therefore, subvalvular anomalies in the posterior papillary muscle could cause the leaflets to coaptate poorly, with resultant mitral regurgitation.

Annular dilatation is a second cause of regurgitation. In the present study, 71% of the annular dilatation was related to dilatation of one commissural leaflet, as pointed out by Carpentier and colleagues [23].

Various papillary muscle patterns were observed, including muscles that could be described as bifid, trifid, bifurcated, or separated. Anterior papillary muscle is often involved with hypoplasia [14]. Hypoplastic papillary muscle is rarely associated with chordal anomalies.

The commissure plication annuloplasty used here, which is similar to that described by Kay and associates [18] and Reed and colleagues [19], does not require the foreign materials. This technique was simple and clinically satisfactory in 85.9% of the patients in our series. Based on the concept of annular remodeling, Carpentier and associates [14, 23] have proposed the use of a prosthetic ring at the initial repair to prevent the redilatation of the annulus. Contrary to their reports, it was useful to apply the CPA to the posterior commissural leaflet, in which dilatation is observed frequently, or the commissural leaflet at which the side papillary muscles or chordae are abnormal, because we did not experience any annular redilatation at reoperation. We believe that one papillary muscle is sufficient to support both leaflets and that CPA is feasible for most chordal anomalies if the unilateral papillary muscle and chordal support are almost normal.

DeVega-type annuloplasty is also an effective method. In patients with abnormalities of the subvalvular apparatus, DeVega-type annuloplasty should not be a first choice surgical procedure and is better used in conjunction with CPA. We expected polydioxanone to be absorbed within several months after the DeVega-type annuloplasty, and that the mitral stenosis after the valve repair [24] could be prevented by weakening the purse-string effect of the sutures [25].

The use of CPA is limited to situations with absent chordae or restricted motion of the leaflet due to short chordae. Chauvaud and associates [14] reported that two cases with hypoplastic posterior leaflet and posterior papillary muscle were successfully treated by enlargement of the leaflet with an autologous pericardial patch and increased motion of the posterior leaflet. With few exceptions, we did not treat the chordae and leaflets directly because the mitral apparatus in small children is fragile, and the subvalvular apparatus could be congenitally abnormal.

Surgical treatment to the flail central portion of the anterior leaflet is particularly demanding. Aharon and associates [22] and Carpentier and colleagues [23] argued that the surgical results of triangular resection of the anterior leaflet are unsatisfactory. We, as well as Okita and associates [12], treated a small prolapsing anterior leaflet, caused by chordal anomalies, with plication or triangular resection. In pediatric cases, as with adult cases, with a large flail anterior leaflet, the use of artificial chordae might be the best treatment. In our series, a chordal substitute with an autologous pericardium was used in 1 patient, and he maintained a good clinical status and had less than mild regurgitation 50 months after the repair. But we do not adopt this procedure as a standard technique because there is inevitable risk of shrinkage and excessive fibrosis in the autologous pericardium, and its durability and safety during child’s rapid growth has not yet been determined [26, 27].

The need for reoperation generally occurs within 2 years of the initial valve repair [28]. The reoperation rate in the literature remains high, between 1.4% and 38% [12, 14, 28]. The actuarial freedom from reoperation in our study was 89.9% at 6 years and 85.6% at 13 years. Of the patients with prosthetic valves, 6 of 10 patients (60%) had absent chordae, and 5 of 8 patients (62.5%) with the direct leaflet-papillary muscle attachment finally had valve replacement. Because the direct leaflet-papillary muscle attachment involved a broader area of chordal defects and restricted leaflet motion, unilateral papillary muscle after CPA might not be able to support both leaflets fully, and restoration of leaflet mobility might be difficult by conventional methods. Therefore, CPA is a useful technique for pathologic mitral valves, except in cases of a decreased number of chordae associated with bilateral commissures or more than half of the leaflets.

We conclude that a combination of commissure plication annuloplasty with various repair techniques is effective and safe for congenital mitral insufficiency with good functional status over the long-term. More experiences and technical refinement will be necessary because of the limits of this type of mitral valve repair for absent or scant chordae affecting a broader area of the leaflets.


   Footnotes
 
This article has been selected for the open discussion forum on the STS Web site: http://www.sts.org/section/atsdiscussion/


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

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Accepted for publication February 18, 1999.




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