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Ann Thorac Surg 2009;87:1735-1740. doi:10.1016/j.athoracsur.2009.03.009
© 2009 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

Extending the Scope of Mitral Valve Repair in Rheumatic Disease

Bachar El Oumeiri, MD*, Munir Boodhwani, MD, MMSc, David Glineur, MD, Laurent De Kerchove, MD, Alain Poncelet, MD, Parla Astarci, MD, Agnes Pasquet, MD, Jean-Louis Vanoverschelde, MD, PhD, Robert Verhelst, MD, Jean Rubay, MD, PhD, Philipe Noirhomme, MD, Gébrine El Khoury, MD

Department of Cardiovascular and Thoracic Surgery, Cliniques Universitaires Saint-Luc, Brussels, Belgium

Accepted for publication March 6, 2009.

* Address correspondence to Dr El Oumeiri, Service de Chirurgie Cardiovasculaire et Thoracique, Cliniques Universitaires, Saint-Luc UCL 90, Avenue Hippocrate 10, Brussels, B-1200, Belgium (Email: beloumei{at}ulb.ac.be).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: Repair of rheumatic mitral valves has met with limited success because hemodynamic obstruction may persist after repair because of residual diseased leaflet tissue and lack of suppleness. Over the past decade, we have developed and implemented an aggressive approach to rheumatic mitral valve repair with radical excision of the diseased leaflets area, and subvalvular apparatus and subsequent reconstruction, with the objective of removing all diseased valvular tissue.

Methods: From July 1996 to June 2007, 78 patients underwent mitral valve repair for rheumatic valve disease. Over the same time interval, 54 patients underwent mitral valve replacement. Mean age was 56.4 ± 16 years. Clinical follow-up (mean 60 ± 36 months) was complete in 100% of patients, and echocardiographic follow-up (mean 52 ± 37 months) was 96% complete.

Results: There was no hospital mortality or early reoperations. Overall survival was 94% ± 6% at 8 years, and 95% of patients were in New York Heart Association functional class II or less. Three patients (4%) required reoperation for mitral restenosis and 2 underwent re-repair. At 8 years of follow-up, freedom from cardiac death and mitral valve reoperation were 98% ± 2% and 94% ± 5%, respectively. Freedom from valve-related events at 5 and 10 years was 90% ± 8% and 86% ± 11%, and freedom from significant mitral regurgitation was 98% ± 2% at 5 years and 83% ± 9% at 8 years.

Conclusions: A more aggressive approach to resection of diseased valvular tissue with subsequent reconstruction is feasible, with good midterm results, and may extend the scope of valve repair in rheumatic disease patients.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Mitral valve repair has been demonstrated to be superior to valve replacement for degenerative mitral valve disease. Valve repair is associated with improved ventricular function [1, 2] through preservation of the normal valvular tissue and subvalvular apparatus, reduced valve-related complications, as well as lower in-hospital and late mortality [3-5]. Repair of rheumatic mitral valves remains controversial, with significant variability in the technical feasibility of repair as well as long-term outcomes [6]; however, many of the advantages of valve repair with regard to ventricular function, valve-related events, and survival are likely applicable to patients with rheumatic valve disease as well.

Rheumatic mitral valve disease affects the valve leaflets as well as the subvalvular apparatus, making it difficult to apply techniques of degenerative mitral valve repair to this situation. Rheumatic mitral valves often have fibrosis or calcification of the leaflet free margin with fused chordae, as well as occasional fibrosis and calcification of the papillary muscle or the commissural regions. Classical techniques used to repair these valves include commissurotomy, shaving of diseased tissue, and splitting of papillary muscle to improve valve mobility, often accompanied by an annuloplasty to enhance leaflet coaptation. Inevitably, diseased tissue is left behind, and despite good anatomic valve opening intraoperatively, some hemodynamic obstruction persists and can progress to clinically important mitral stenosis over time. This phenomenon has been described by Carpentier's group [7] who found that reoperation (2% per year) was due to progressive fibrosis and was related to the degree of preoperative valve fibrosis.

In response to these challenges, we have developed an approach over the past decade that involves aggressive excision of the diseased leaflet tissue and of the supporting fused subvalvular apparatus to remove all valvular tissue that is affected by rheumatic disease. This excision is followed by reconstruction with pericardial path, artificial chordae, as well as the use of tricuspid valve autograft or mitral homograft in selected situations. Here, we present our 11-year single-institution experience with this approach to the repair of rheumatic mitral valves, with a focus on the description of the surgical techniques as well as on clinical and echocardiographic outcomes.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Patient Population
This study was approved by the Institutional Review Board of the hospital and written informed consent was waived for this retrospective review. From July 1996 to June 2007, 78 patients with rheumatic mitral valves disease underwent mitral reconstructive surgery at our institution. During the same time interval, 54 patients underwent mitral valve replacement for rheumatic disease. All patients were preoperatively assessed with transthoracic echocardiography and intraoperative transesophageal echocardiography. Echocardiographic assessment included mitral annulus, leaflet thickness and mobility, commissural and chordal fusion, calcification, regurgitation jet, thickness of chordae tendinae, and left atrial thrombus and other valvular lesions.

Preoperative patient characteristics are given in Table 1. Eight patients (10.2%) had had previous mitral valve surgery. Pure mitral regurgitation (MR) was present in 38 patients (49%), stenosis was present in 3 patients (4%), and combined mitral stenosis and MR was present in 37 patients (47%). The presenting symptom was dyspnea on exertion. Forty patients (52%) were in New York Heart Association (NYHA) functional class III or IV. Congestive heart failure and atrial fibrillation was present in 8% and 44% of patients, respectively.


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  		Table 1 Preoperative and Operative patients Characteristics (n = 78)
 
Surgical Technique
Surgical approach was through a median sternotomy, and ascending aortic and bicaval canulation was used along with antegrade normothermic blood cardioplegia. Left atriotomy was performed through the interatrial groove. A thorough and systematic assessment of the valve was performed focusing on the quality of the valve tissue (thickness, pliability, calcification, commissural inspection) and of the subvalvular apparatus. Evaluation of the mitral valve revealed a dilated mitral annulus in 10 patients (12.8%), commissural fusion in 25 (32%), calcification in 12 (15.3%), and leaflet fibrosis or calcification in 61 (78%).

Valve assessment was followed by cautious but complete resection of the diseased valve tissue and decalcification when necessary. We have found that in the classical "fish mouth" rheumatic mitral valve, the disease largely affects the free margin of both anterior and posterior leaflets and the associated subvalvular apparatus. The leaflet tissue a few millimeters beyond the free margin can often be quite mobile and acceptable. The goal was to resect all affected tissue but preserve as much normal leaflet and subvalvular tissue as possible (Fig 1). After the resection was complete, the quantity and quality of remaining tissue was analyzed, and a decision was made to either preserve or replace the valve. In cases where large amounts of native valve tissue were resected, valve preservation was facilitated by nonclassical techniques for reconstruction, including anterior leaflet augmentation with pericardial patch (n = 2), polytetrafluoroethylene neochordae implantation (n = 24; Fig 1C), use of a tricuspid autograft for reconstruction of a commissure (n = 19), or the use of a partial mitral homograft (n = 2). Types of techniques used for mitral valve repair are listed in Table 2. An annuloplasty ring was implanted in 63 patients (81%) to treat annular dilatation, in the setting of significant preoperative MR, to support a complex mitral valve repair and improve coaptation area.


Figure 1
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  		Fig 1. (A) Rheumatic mitral valve with classic "fish mouth" appearance. (B) The dotted line indicates the area to be resected. (C) Appearance after resection of leaflet edge and supporting chordae and reconstruction with polytetrafluoroethylene neochordae.

 

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  		Table 2 Surgical Techniques for Mitral Valve Repair
 
The techniques for neochordae implantation [8], the harvest and implantation of the tricuspid autograft [9, 10], pericardial patch extension [11], and partial mitral homograft [12] have been previously described. When the tricuspid autograft is needed, the posterior leaflet of the tricuspid valve was carefully examined, removed with its chordae and papillary muscle attachment, and transferred to the commissural area of the mitral valve (Fig 2). The stress on the papillary muscle suture was relieved by reinforcement of the free edge of the transferred leaflet by natural or artificial chordae. The tricuspid valve was repaired using either a sliding plasty or an annuloplasty.


Figure 2
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  		Fig 2. (A) Harvested posterior leaflet of tricuspid valve with its chordae and papillary muscle. (B) Reconstruction of anterior commissure with tricuspid autograft tissue.

 
At the completion of repair, mitral valve competence was tested by injecting cold saline into the left ventricular cavity. Transesophageal echocardiography was used to assess the result intraoperatively. Associated procedures were performed in 41 patients (52.5%), as listed in Table 1. Postoperatively, patients were treated with warfarin for 2 months after valve repair, and if at that time they were in sinus rhythm with no other indications for anticoagulation, they were treated with aspirin alone.

Follow-Up
All patients underwent transthoracic echocardiography before discharge. Mean clinical follow-up was 60 ± 36 months (range, 1 to 137) and was 100% complete. Survival and functional status were obtained by telephone contact with the patients, their relatives, or the referring physician, and from review of visit or hospital records. Cause of death was categorized as cardiac or noncardiac. Cardiac death was defined as related to congestive heart failure, myocardial infarction, cardiac arrest, or sudden death. Valve-related complications were defined according to published guidelines [13].

Statistical Analysis
Continuous variables are reported as mean ± SD, and categorical variables are reported as number (%). Survival and event-free survival were calculated using Kaplan-Meier curves. Univariate analyses were performed to identify predictors of reoperation or significant recurrent mitral insufficiency using the log-rank test. Statistical analyses were performed using SAS version 9.1 (SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
Early Clinical Outcomes
There was no hospital mortality. Sixteen patients (20.5%) had postoperative complications consisting of reexploration for bleeding (n = 3), low-output syndrome (n = 1), prolonged mechanical ventilation longer than 48 hours (n = 5), myocardial infarction (n = 1), cerebrovascular accident (n = 1), acute renal failure requiring dialysis (n = 2), mediastinitis (n = 1), and reoperation for wound infection (n = 2). No patients needed a MV reoperation during the index hospital admission.

At discharge, transthoracic echocardiography indicated no MR in 32 patients (41%), MR of grade 1 in 42 patients (54%), and MR of grade 2 in 4 patients (5%). The mean gradient across the mitral valve was 5.5 ± 2.4 mm Hg (data available for 85% of patients). There was 1 early death due to leukemia 1 month after surgery.

Late Clinical Outcome
There were 6 late deaths (7.6%) after a mean period of 63 ± 17 months (range, 39 to 87), due to heart failure (n = 1), cerebrovascular accident (n = 1), trauma (n = 1), septicemia (n = 1), and cancer (n = 2). Freedom from late death was 94% ± 3% at 5 years and 81% ± 7% at 10 years, whereas freedom from cardiac death was 98% ± 2% at 10 years (Fig 3A).


Figure 3
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  		Fig 3. Clinical and echocardiographic outcome in patients undergoing rheumatic mitral valve repair. (A) Overall survival (dashed line) and freedom from cardiac death (solid line) were 81% ± 7% and 98% ± 2%, respectively, at 10 years. (B) Freedom from mitral valve reoperation (due to severe recurrent mitral stenosis) was 94% ± 5% at 10 years. (C) Freedom from recurrent mitral regurgitation (>2+) was 83% ± 9% at 8 years.

 
Three patients (3.84%) underwent reoperation for severe valve restenosis, resulting in a freedom from mitral valve reoperation rate at 10 years of 94% ± 5% (Fig 3B). The first reoperation occurred 8 months after initial repair using classical techniques including commissurotomy, triangular resection of the posterior leaflet, and an annuloplasty ring. This patient underwent mitral valve replacement at another center owing to recurrence of mitral stenosis likely due to inadequate resection of diseased tissue at initial operation. The second patient had undergone commissurotomy, posterior leaflet resection, and neochordae at the time of first repair and underwent mitral valve replacement with a mitral homograft 53 months later owing to progression of rheumatic disease. Lastly, the third patient had undergone commissurotomy and a large commissural resection with the insertion of a tricuspid autograft for anterior commissural reconstruction at the index operation and presented at 52 months with progression of rheumatic disease, which also involved the tricuspid autograft. This patient underwent re-repair using a partial mitral homograft along with commissurotomy and an annuloplasty ring.

During the follow-up period, 2 patients (3%) had thromboembolic complications (0.77 events per 100 patient-years) in the late postoperative period, with 1 resulting in mortality. One of those patients was in atrial fibrillation. No patient had bacterial endocarditis. Freedom from valve-related events, including valve-related death, reoperation, infective endocarditis, or thromboembolism, was 90% ± 8% at 5 years and 86% ± 11% at 10 years. Of the 71 late survivors, 49 (69%) were in NYHA class I, 19 (27%) were in NYHA class II, and 3 (2.81%) were in NYHA class III/IV. A total of 47 patients (60%) were in normal sinus rhythm, 28% were in atrial fibrillation, and 5% had a permanent pacemaker.

At a mean follow-up of 52 ± 37 months, transthoracic echocardiography showed no MR or MR grade 1 in 55 patients (71%), MR grade 2 in 19 patients (24%), and MR grade 3 in 4 patients (5%). There were no patients with severe MR. Of the 4 patients with grade 3 MR, 1 was in NYHA class I and 3 were in NYHA class II. Freedom from development of significant MR was 98% ± 2% at 5 years and 83% ± 9% at 8 years.

Univariate analyses were performed using the composite endpoint of mitral valve reoperation and recurrent mitral insufficiency (>2+). Patient age, type of mitral disease (stenosis, insufficiency, or mixed), preoperative atrial fibrillation, and use of nonclassical technical reconstruction techniques all yielded nonsignificant relationship with outcome (all p > 0.7).


   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
Classical techniques for the repair of rheumatic mitral valves inevitably leave behind diseased tissue that can lead to both intraoperative and late failure of repair [7]. In this study, we demonstrate that an aggressive approach to resection of disease tissue with subsequent reconstruction of leaflet and subvalvular apparatus is feasible and can result in a successful repair in a large proportion of patients (approximately 60%) with rheumatic valve disease, and with a low recurrence of mitral stenosis (3.8%). The use of nonclassical reconstructive techniques including the use pericardial patch, polytetrafluoroethylene neochordae, mitral homograft, and tricuspid autograft produces stable results with freedom from cardiac death and MV reoperation rates of 98% and 94%, respectively, at 10 years, and freedom from recurrent MR rate of 98% at 5 years. This approach to the surgical management of rheumatic mitral valve disease can extend the scope of valve repair for these patients.

Although the incidence of rheumatic heart disease in developed countries is declining, the afflicted patients present a challenging problem for cardiac surgeons. The demonstrated benefits of mitral valve repair over replacement in degenerative disease with respect to survival and left ventricular function can likely be translated to the rheumatic population. However, repair failures are higher in rheumatic disease [14]. Furthermore, these patients tend to be younger and are more likely to undergo mechanical valve replacement [15] with the associated risks of thromboembolic and hemorrhagic events that accrue over time. Lastly, rheumatic mitral valve disease is more prevalent in many parts of the developing world where adequate facilities for monitoring of prosthetic valve function and management of anticoagulation therapy are not easily available. For all these reasons, repair of rheumatic mitral valves is a desirable alternative to replacement.

Conversely, repair of a rheumatic mitral valve presents unique challenges due to the presence of fibrosis and calcification in the leaflet tissue as well as the to subvalvular apparatus and generally poorer quality tissue compared with degenerative disease. Isolated rheumatic mitral stenosis can be treated by balloon valvuloplasty in the presence of suitable anatomy, although the presence of mitral insufficiency remains a contraindication. Classical surgical techniques for rheumatic mitral valve repair, including commissurotomy, shaving of leaflet tissue, papillary muscle splitting, and annuloplasty, inevitably leave behind diseased valve tissue, which has been shown to be a risk factor for repair failure [7]. Other risk factors for failure in rheumatic mitral valve repair have also been demonstrated, and include younger age [16] and the presence of mixed mitral stenosis and insufficiency. These methods have demonstrated a repair rate between 20% and 50% and a freedom from MV reoperation rate that varies approximately between 50% and 80% at late follow-up (10 to 12 years; Table 3).


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  		Table 3 Summary of Case Series Reporting Repair Rate and Outcome in Rheumatic Mitral Valve Repair
 
Our approach to the repair of rheumatic mitral valves is based on the idea that the quality of residual valve tissue at the end of the repair is an important determinant of long-term outcome. Thus, after careful inspection of all components of the valve, we begin with parsimonious resection of the affected tissue. The goal is to resect all diseased valve tissue, but also to leave behind as much unaffected valve tissue as possible. At the end of this resection, a decision is made as to whether adequate quantity and quality of tissue remain to perform valvular reconstruction. To this end, techniques that are not classically described for rheumatic mitral valve repair are utilized. These nonclassical techniques include resuspension of the leaflets using polytetrafluoroethylene neochordae after resection of the primary chordae, use of tricuspid autograft or mitral homograft, or both, to reconstruct a large portion of resected valve, typically a commissural region, and pericardial patch augmentation of a leaflet. Although each of these techniques has each been individually described previously [8, 10], their use in the setting of rheumatic valve disease is novel and adds to the surgeon's armamentarium of techniques to reconstruct the valve after aggressive tissue resection. This approach to the rheumatic mitral valve increases the repair rate (approximately 60% in our series) compared with that of the published literature and also provides excellent midterm to long-term durability, with 94% freedom from reoperation at 10 years (Table 3).

Thromboembolic complications and anticoagulation-related hemorrhage are important considerations in the surgical management of mitral valve disease. The rates of thromboembolic after bileaflet mechanical mitral valve replacement despite oral anticoagulation therapy can be between 2.2% and 4.1% per year. Furthermore, in these patients, a relatively high target international normalized ratio of 3.0 is recommended, and that can result in a risk of important bleeding events of 2.5% per year [17]. Added to that are the inconveniences of oral anticoagulation therapy, including the variability in dosing, need for blood sampling, activity restrictions, and minor hemorrhagic complications. Thus, the benefits of mitral valve repair are clearly greatest for patients who would normally undergo mechanical mitral valve replacement. That applies to a large proportion of patients with rheumatic mitral valve disease (mean age 56 years in our study). Consistent with previous reports [18], the rate of thromboembolic complications after repair was extremely low in our series (0.7% per patient year) without the burden of oral anticoagulation therapy.

Study Limitations
Limitations of this study are that it is a single-center study and retrospective. As such, it is susceptible to referral bias and reflects institution-specific practices. Furthermore, quantitative data on mitral valve area and gradients at late follow-up were not available for all patients.

In conclusion, repair of rheumatic mitral valves remains a challenging problem. An aggressive approach to resection of diseased tissue with subsequent reconstruction can increase the repair rate and provides excellent midterm to long-term outcome. This approach can extend the scope of mitral valve repair for patients with rheumatic disease.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

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  3. Carpentier A, Chauvaud S, Fabiani JN, et al. Reconstructive surgery of mitral valve incompetence: ten-year appraisal J Thorac Cardiovasc Surg 1980;79:338-348.[Abstract]
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  8. Chiappini B, Sanchez A, Noirhomme P, et al. Replacement of chordae tendineae with polytetrafluoroethylene (PTFE) sutures in mitral valve repair: early and long-term results J Heart Valve Dis 2006;15:657-663.[Medline]
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  12. Acar C, Tolan M, Berrebi A, et al. Homograft replacement of the mitral valve. Graft selection, technique of implantation, and results in forty-three patients. J Thorac Cardiovasc Surg 1996;111:367-380.[Abstract/Free Full Text]
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  15. Grossi EA, Galloway AC, Miller JS, et al. Valve repair versus replacement for mitral insufficiency: when is a mechanical valve still indicated? J Thorac Cardiovasc Surg 1998;115:389-396.[Abstract/Free Full Text]
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  18. Yau TM, El-Ghoneimi YA, Armstrong S, Ivanov J, David TE. Mitral valve repair and replacement for rheumatic disease J Thorac Cardiovasc Surg 2000;119:53-60.[Abstract/Free Full Text]
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