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Eur J Cardiothorac Surg 2005;28:443-447
© 2005 Elsevier Science NL
Original articles |
a Department of Cardiovascular Surgery, Pitié Salpêtrière Hospital, Paris, France
b Department of Biostatistics-Health, UMR CNRS 5558, Lyon, France
Received 1 February 2005; received in revised form 6 May 2005; accepted 9 May 2005.
* Corresponding author. Address: Department of Cardiovascular Surgery, Hôpital de la Pitié-Salpêtrière, 50-52 boulevard Vincent Auriol, 75013 Paris, France. Tel.: +33 1 42 16 56 85; fax: +33 1 42 16 56 78. (Email: c.acar{at}psl.aphp.fr).
Abstract
Objective: The aim of this study was to describe the pattern of lesions responsible for commissural prolapse, the techniques of valve repair and their long-term results. Methods: Between 1992 and 2004, 128 mitral valve repairs were consecutively performed for commissural prolapse. There were 86 males and 42 females, the median age was 57.5 years (range 14–84 years). Forty-six percent of patients were in NYHA III or IV, mean ejection fraction was 61±9.4%. The diagnosis of commissural prolapse was recognized by preoperative echocardiography in 32% of the patients and was revealed by intraoperative inspection of the valve in the other cases. The site of the prolapse was the posteriomedial commissure (n=94), the anterior commissure (n=30) or both (n=4). The aetiologies were: infective endocarditis (n=56), degenerative (n=46), ischemic (n=25), congenital mitral regurgitation (n=1). The commissural prolapse was associated with another mitral valvular lesion requiring a specific treatment in 61 cases (47.7%). An associated procedure was carried out in 45 patients. Results: The operative treatment of the commissural prolapse included: commissural closure 65 (50.8%), leaflet resection 31 (24.2%), transposition or shortening of chordae 19 (14.8%), reimplantation or shortening of papillary muscles 3 (2.3%), and replacement of the commissural area by a partial mitral homograft 10 (8%). In-hospital mortality included three deaths (2.3%) and four patients (3.1%) were reoperated: three pericardial drainages for hemopericardium and one for mediastinitis. During the follow-up, one patient died (0.8%) from myocardial infarction and eight patients (6.3%) were reoperated including six (4.7%) for recurrent mitral regurgitation. After a median follow-up time of 76.9 months (range from 15 days to 160 months), 116 patients (90.1%) were in NYHA I. Echocardiographs showed no or minimal insufficiency in 112 patients (87.5%) and mild or moderate insufficiency in 10 patients (7.8%). Conclusions: The diagnosis of commissural prolapse is difficult by preoperative echocardiography. The aetiology of the mitral disease is variable (endocarditis, degenerative or ischemic mitral regurgitation). Using a variety of techniques, commissural prolapse can be repaired with excellent clinical and echographic long-term results.
Key Words: Mitral valve repair • Mitral valve regurgitation • Homograft • Endocarditis
1. Introduction
Mitral valve repair offers a reduced operative mortality and a better event-free survival when compared to mitral valve replacement [1]. The surgical techniques and results for posterior leaflet or anterior leaflet prolapse [2–4] have been extensively described. The long-term results of the surgical treatment of commissural prolapse, however, remain unclear. Sporadic experiences have been reported in limited series [5–7]. Recently, a series has shown that commissural prolapse which frequently involved both leaflets was a risk factor for reoperation [8]. The aim of this study was to describe the pattern of lesions responsible for commissural prolapse, the techniques of valve repair and their long-term results.
2. Patients and methods
2.1 Population and mitral valve characteristics
A retrospective analysis included 128 consecutive patients who underwent mitral valve repair for commissural prolapse between 1992 and 2003. There were 86 males to 42 females, median age was 57.5 years (range 14–84 years). Thirteen percent of the patients were in New York Heart Association functional class I, 41% were in class II, 35% were in class III and 11% were in class IV. Mean ejection fraction was 61.1±9.4%. The clinical preoperative data are presented in Table 1
. The diagnosis of commissural prolapse was recognized by preoperative echocardiography in 32% of the patients and was revealed by intraoperative inspection of the valve in the other cases. The site of the prolapse was the posteriomedial commissure (n=94), the anterior commissure (n=30) or both (n=4). The specific mechanism of the commisural prolapse is described in Table 2
. The aetiologies were: infective endocarditis (n=56), degenerative (n=46), ischemic (n=25), congenital (n=1) mitral regurgitation (MR). In the case of endocarditis, there were 11 (8.6%) acute endocarditis and 45 (35.2%) healed endocarditis. In the ischemic cases, there were 12 (9.4%) sequelae of myocardial infarction but not in acute period and there were 13 (10.2%) patients with ischemic heart disease suffering from angina pectoris. The commissural prolapse was associated with another mitral valvular lesion requiring a specific treatment in 91 cases (71.1%). An associated procedure was carried out in 45 patients (35.1%): coronary bypass 24 (18.8%), aortic valve replacement 8 (6.3%), coronary bypass associated with aortic valve replacement 3 (2.3%), Bentall 3 (2.3%), tricuspid valvular plasty 3 (2.3%), others 4 (3.1%).
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2.4 Statistical analysis
Description of continuous variables was expressed as mean±SD of the mean, or as median with the extremes. Categorial variables were presented as absolute numbers of patients and percentages. The statistical significance of the comparisons between two or several groups was tested using a Log Rank test and the Cox regression analysis when needed. Survival was calculated using a Kaplan–Meier method. A P-value less than 0.05 was considered as statistically significant. The analyses were carried out using SPSS software (version 11.5.1, SPSS, Inc.).
3. Results
3.1 Early results
There were three in-hospital deaths (2.3%). The cause of death was: sepsis (n=1), cardiogenic shock (n=1) and respiratory distress syndrome (n=1). There were two transient cerebral ischemia attacks, one rectal bleeding, and one gluteal hematoma. Four patients (3.1%) required an early reoperation: three pericardial drainages for hemopericardium and one for mediastinitis. There was no early valve failure. Transthoracic echocardiographs at discharge showed no residual mitral insufficiency in 94 cases (73.4%) and grade 1 in 34 cases (26.6%).
3.2 Late results
One hundred and sixteen patients were in NYHA class I (90.1%), six in NYHA II (4.7%), and two in NYHA III (1.6%). At follow-up transthoracic echocardiography, no insufficiency or a minimal insufficiency was present in 112 patients (87.5%), mild insufficiency (grade 2) in five patients (3.9%) and moderate insufficiency (grade 3) in five patients (3.9%) were detected. At this control, the median of the pressure gradient across the mitral valve was 4.0mmHg (range 1.5–4.0mmHg) and the median of the mitral valve area by planimetric evaluation was 3.0cm2 (range 2.2–3.5cm2). The cumulated survival rates were 97.7% at 30 days, 97.7% at 1 year, 96.7% at 5 and 10 years (Fig. 2
). There was one late death (0.8%), due to myocardial infarction 4 years after repair. A reoperation was required in eight patients (6.3%). Six patients (4.7%) required a mitral valve replacement for severe mitral regurgitation (grade 4) due to failure of the repair (n=4) or recurrence of mitral endocarditis (n=2) with secondary cordal rupture. The lesions responsible for the failure of the repair were: mitral valve stenosis (n=1), dehiscence at the site of papillary muscle reimplantation (n=1), elongation of chordae (n=2). In addition, a reintervention was needed for a false aneurysm on the proximal suture line of a Ross procedure and aortic root replacement for an aortic dissection. The cumulative rates of freedom from reoperation were 95.2% at 1 year, 91.6% at 5 years and 87.6% at 10 years. The cumulative rates of freedom from reoperation involving the mitral valve were 98.4% at 1 year, 96.6% at 5 years and 92.5% at 10 years (Fig. 3
). There was no statistically predictive factor for mitral reintervention: etiology (P=0.616), site of prolapse (P=0.314), associated mitral lesion (P=0.797), age (P=0.090), surgical technique (P=0.139), concomitant surgical procedure (P=0.828). There was no cerebrovascular accident throughout the follow-up.
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Although not uncommon, commissural prolapse is far less frequent that prolapse of the anterior and prolapse of the posterior leaflet. The exact identification of the localization of the prolapse can be difficult and commissural prolapse is frequently overlooked as in one-third of the cases. The echocardiographic appearance of commissural prolapse can mimic leaflet perforation. The assessment of the volume of the regurgitation is occasionally difficult due to the lateral direction of the jet along the atrial wall. Thus, echo analysis has to be conducted by an experienced echocardiographer and careful intraoperative inspection of the valve by the surgeon is required to assess prolapse of a commissure [7,12]. Whereas the most frequent aetiology of mitral disease in case of anterior or posterior leaflet prolapse is degenerative insufficiency, commissural prolapse is primarily related to infective endocarditis whether as an acute lesion or as a late sequel. Barlow's disease and coronary heart disease were the other two main sources of commissural prolapse. The lesion responsible for the prolapse was extremely variable and could involve the leaflet tissue, the cordae or the papillary muscle. The most typical injury was rupture of the commissural cord. The commissural cord has a characteristic fan-like shape and is invariably inserted on the apex of the papillary muscle. The importance of the prolapse depends upon the extent of the area supported by the commissural chord. In case of a subdivided papillary muscle resulting in a separate commissural head, the commissural cord is usually short and supports a limited part of the valve; in contrast, commissural cord emerging from a single papillary muscle deep into the ventricle can be functionally very important.
The site of prolapse was most frequently the posterior commissure. This was particularly true in ischemic mitral insufficiency, the posterior papillary muscle being more prone to necrosis due to the distribution of its blood supply relying on distal branches of the circumflex and/or of the right coronary artery. The most frequently used technique for repairing the commissural area was the commissural closure in this series. On the whole, closure of the commissure did not produce any significant restriction of flow as shown by the low transvalvular gradients on the postrepair echocardiography. In one case, however, a severe infective endocarditis required an extensive leaflet resection and a small prosthetic ring had to be inserted which together with the commissural closure resulted in a secondary mitral stenosis leading to reoperation. In such circumstances, the use of a partial mitral homograft allows repair of the valve without producing stenosis as shown in a few cases in this series. The long-term results of the partial homograft for infective endocarditis have been documented and demonstrated that this alternative offers durable results in mitral valve endocarditis [14,17,18].
Because of its safety and ease, the commissural closure technique was preferred to the resection with sliding plasty of the commissure. This latter technique was found to be indicated mainly in severe forms of Barlow's disease with excess tissue. Besides the commissural prolapse, intraoperative analysis of the valve revealed an associated prolapse of another region of the valve (A3 or P3) in half of the cases; these were addressed using the classical Carpentier techniques. A prosthetic ring annuloplasty was achieved in all cases, if commissural closure had been performed, care was taken not to downsize the annuloplasty ring. A ring whose size was equal to that of the anterior leaflet was then selected.
In-hospital mortality was comparable to series of valve repair involving the other areas of the mitral valve [19,20]. The results were stable and 87.6% of the patients were free from reoperation at 10 years. The causes of reoperation were mainly technical errors (dehiscence of a reimplanted papillary muscle, stenosis) or recurrence of infective endocarditis. The statistical analysis failed to show any predictive factor for reoperation.
In conclusion, the diagnosis of commissural prolapse is difficult by preoperative echocardiography. The aetiology of the mitral disease is variable (endocarditis, degenerative or ischemic mitral regurgitation). Using a variety of techniques, commissural prolapse can be repaired with excellent clinical and echographic long-term results.
References
This article has been cited by other articles:
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  M. Enriquez-Sarano, V. T. Nkomo, and H. Michelena Principles and Practice of Echocardiography in Cardiac Surgery Card. Surg. Adult, January 1, 2008; 3(2008): 315 - 348. [Full Text]
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F. Y. Chen and L. H. Cohn Mitral Valve Repair Card. Surg. Adult, January 1, 2008; 3(2008): 1013 - 1030. [Full Text]
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 G. D. Dreyfus, O. S. Neto, and S. Aubert Papillary muscle repositioning for repair of anterior leaflet prolapse caused by chordal elongation. J. Thorac. Cardiovasc. Surg., September 1, 2006; 132(3): 578 - 584. [Abstract] [Full Text] [PDF]
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