Ann Thorac Surg 2009;88:733-739. doi:10.1016/j.athoracsur.2009.05.033
© 2009 The Society of Thoracic Surgeons
Original Articles: Adult Cardiac
Long-Term Outcome of Mitral Valve Repair for Infective Endocarditis
Tomoki Shimokawa, MDa,*,
Hitoshi Kasegawa, MDa,
Shigefumi Matsuyama, MDa,
Hiroshi Seki, MDa,
Susumu Manabe, MDa,
Toshihiro Fukui, MDa,
Satoshi Morita, MD, PhDb,
Shuichiro Takanashi, MDa
a Department of Cardiovascular Surgery, Sakakibara Heart Institute, Tokyo, Japan
b Department of Biostatistics and Epidemiology, Yokohama City University Medical Center, Yokohama, Japan
Accepted for publication May 13, 2009.
* Address correspondence to Dr Shimokawa, Department of Cardiovascular Surgery, Sakakibara Heart Institute, 3-16-1 Asahicho, Fuchu City, Tokyo, 183-0003, Japan (Email: tshimokawa-circ{at}umin.ac.jp).
Presented at the Forty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Francisco, CA, Jan 26–28, 2009.
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Abstract
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Background: In patients with mitral endocarditis, reconstruction of the damaged mitral valve (MV) is still challenging, and its durability remains unknown. We evaluated the long-term outcomes of MV repair for mitral regurgitation (MR) in patients with infective endocarditis.
Methods: From 1991 to 2006, 633 patients had MV repair for MR caused by leaflet prolapse: 78 had endocarditis (active in 14, healed in 64) and 555 had degenerative disease. Durability was assessed by reoperation and recurrent MR.
Results: The overall hospital mortality rate was 1.0% (endocarditis 0% vs degenerative 1.1%; p = 0.99). The 10-year survival and freedom from reoperation were 91.1 ± 1.6% and 92.2 ± 1.7%, respectively, with no differences between endocarditis and degenerative disease. Older age, New York Heart Association class III or IV, impaired ventricular function, and no use of annuloplasty were independent predictors of all-cause death. Freedom from moderate or severe MR was 99.8 ± 0.2% at 2 weeks, 91.9 ± 1.5% at 5 years, and 83.3 ± 2.3% at 10 years, for all patients and did not differ between groups at 10 years (p = 0.388). Anterior leaflet prolapse, preoperative atrial fibrillation, and no annuloplasty were independent predictors of recurrent MR. In endocarditis patients, recurrent MR was mainly caused by leaflet thickening and calcification, but not by recurrence of endocarditis.
Conclusions: MV repair for endocarditis is associated with low operative mortality and morbidity, and its long-term durability is comparable with that of repair for degenerative disease. This study suggests that a degenerative process causes late failure after MV repair for endocarditis.
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Introduction
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Mitral valve repair is now considered the preferred treatment of mitral regurgitation (MR) caused by leaflet prolapse (type II) [1–3]. In the setting of infective endocarditis, however, some concerns have been raised about the efficacy and durability of complex valve repair, particularly when performed on infected tissue during the acute phase. Surgical intervention for endocarditis can be technically challenging because of the extensive tissue destruction and abscess formation that can arise, and reconstruction after radical débridement might be required.
Several studies have suggested a better survival after mitral valve repair than after valve replacement [4–6]. We initiated this study to evaluate the long-term clinical and echocardiographic outcomes of mitral valve repair for MR in patients with infective endocarditis compared with degenerative disease and to clarify the mechanism of recurrent MR after repair of mitral endocarditis, which remains unclear.
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Material and Methods
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The protocol for this retrospective study was approved by the Institutional Review Board, and the need for informed consent in each patient was waived.
Patient Characteristics
From July 1991 to December 2006, 633 patients had mitral valve repair for type II MR at Sakakibara Heart Institute. Among them, 78 consecutive patients who were diagnosed with infective endocarditis were enrolled in this study: 14 patients were operated on during the course of antibiotic treatment (active endocarditis) and 64 after the completion of antibiotic treatment (healed endocarditis). Clinical and echocardiographic outcomes of these patients were retrospectively compared with the remaining 555 patients with degenerative disease.
The preoperative characteristics of both groups are summarized in Table 1. Patients in the degenerative group were significantly older and had more hypertension, hyperlipidemia, and a larger left atrium than patients in the endocarditis group. Other characteristics were not significantly different between the two groups. Active endocarditis was defined as positive blood cultures obtained preoperatively or intraoperatively, an infected valve detected macroscopically, or patients undergoing operations during the first 6 weeks of antibiotic therapy. Causative microorganisms were identified in 12 patients with active endocarditis: Staphylococcus aures in 5, Streptococcus viridans in 1, S mitis in 2, S constellatus in 1, Cardiobacterium hominis in 1, Gemella in 1, and Lactococcus lactis in 1. In patients with healed endocarditis, 61 patients had a history of endocarditis diagnosed by a cardiologist, and the remaining 3 patients were diagnosed intraoperatively by compatible valvular lesions.
Surgical Technique
In patients with active endocarditis, operation was indicated mainly in cases with complications, including the presence of congestive heart failure due to severe regurgitation, persistent sepsis despite adequate antibiotics, or large vegetations on echocardiography with risk of emboli. In patients with healed endocarditis, the indications for operation were severe MR, and these criteria were similar to those for degenerative disease. Before 1993, mitral valve replacement was initially indicated for acute endocarditis. Valve repair was performed in both active and healed endocarditis patients.
Standard cardiopulmonary bypass techniques were used, including bicaval cannulation. Myocardial protection was achieved with antegrade and retrograde intermittent cold blood cardioplegia and retrograde terminal warm blood cardioplegia. A combined transseptal superior approach was used in most patients.
The techniques used for valve repair included chordal replacement with expanded polytetrafluoroethylene (ePTFE) sutures for anterior mitral leaflet (AML) prolapse and quadrangular resection or sliding technique for posterior mitral leaflet (PML) prolapse in most cases. Resection of a part of the AML was indicated in patients with leaflet infection or fibrotic thickening. In patients with extended prolapse of the PML, chordal replacement with ePTFE sutures was added to the PML resection.
For mitral annuloplasty in active endocarditis patients, we commonly used posterior annuloplasty with autologous pericardium. In healed endocarditis patients, selection of the ring was similar to that of degenerative disease. Carpentier-Edwards Classic annuloplasty ring (Edwards Lifesciences Inc, Irvine, CA), posterior annuloplasty using part of a flexible Duran Annuloplasty ring (Medtronic Inc, Minneapolis, MN), or autologous pericardium, and Carpentier-Edwards Physio annuloplasty ring (Edwards Lifesciences Inc) were used sequentially in most patients.
During the operation, we decided whether a second pump run and intraoperative redo were necessary, depending on the maximum regurgitant jet area (MRA) and length as measured on transesophageal echocardiography. Intraoperative redo was conducted when the MRA was 2.0 cm2 or more, or even when the MRA less than 2.0 cm2, especially in those patients with AML prolapse [7].
Echocardiographic Evaluation and Clinical Follow-Up
Follow-up transthoracic echocardiography was performed before discharge, at 6 months, and annually thereafter (average, 5.5 ± 3.8 years; range, 0.1 to 16.4 years). The degree of residual MR was classified according to the MRA [8]. Data on 6 patients with degenerative disease were lost during the follow-up period; follow-up was 99.1% complete. Follow-up was continued until an end point of death or completion of the study (July 1, 2008). The clinical follow-up represented 3957.2 patient-years, with a mean follow-up of 6.3 ± 4.0 years (range 0.1 to 16.9 years).
Statistical Analysis
Statistical analyses were performed with SPSS software (SPSS Inc, Chicago, IL). Continuous data were expressed as means ± standard deviation and categoric data as the number of patients. Univariate analysis was performed with a Mann-Whitney test for continuous variables or Fisher two-tailed exact test for categoric variables. Late survival and freedom from events were estimated using the Kaplan-Meier method. The log-rank test was used for statistical comparison of Kaplan-Meier curves. Stepwise Cox multivariate regression analysis was used to identify the independent predictors of late outcomes. Preoperative and operative variables with a univariate p < 0.1 or those judged to be clinically important were entered into the multivariate Cox model (Appendix 1). All values of p < 0.05 were taken as significant.
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Results
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Early Outcome
The valve lesions and surgical procedures are listed in Tables 2 and 3.
All patients left the operating room with an MR grade of 0 or trivial on transesophageal echocardiography. During the study period, mitral valve replacement was performed for native endocarditis in 9 patients with active endocarditis and in 3 with healed endocarditis. Feasibility of the repair was 86.7% (78 of 90) in all, 60.9% (14 of 23) in active, and 95.5% (64 of 67) in healed. No hospital deaths occurred among the 78 patients who underwent valve repair for endocarditis. Postoperative complications were cerebral infarction in 3 patients, cerebral hemorrhage in 1, ventricular tachycardia in 1, and mediastinitis in 1. There were no reoperations during the same hospitalization.
The overall hospital mortality rate after valve repair for type II mitral regurgitation was 1.0% (6 of 633), with no differences between endocarditis and degenerative disease (0% vs 1.1%; p > 0.99).
Survival and Reoperation Rate
During late follow-up, 4 endocarditis patients died of noncardiac causes. One reoperation was needed for recurrent severe regurgitation. In degenerative patients, there were 34 late deaths, including 12 cardiac deaths, and 28 reoperations including 5 patients requiring repeat repairs. Survival was 95.2 ± 1.0% at 5 years, 91.1 ± 1.6% at 10 years, and 80.1 ± 4.1% at 15 years for all patients, and was identical between the patients with endocarditis and degenerative disease (89.6 ± 4.7% vs 91.4 ± 1.7% at 10 years, p = 0.610; Fig 1). Freedom from reoperation was 97.1 ± 0.8% at 5 years, 92.2 ± 1.7% at 10 years, and 85.6 ± 3.9% at 15 years for all patients, and at 10 years was 97.8 ± 2.2% in the endocarditis patients compared with 91.3 ± 1.9% in those with degenerative disease, although the difference did not reach statistical significance (p = 0.080; Fig 2). In Cox multivariate regression analysis, older age, New York Heart Association functional class III or IV, impaired ventricular function (left ventricular ejection fraction < 0.50), and nonuse of ring or band annuloplasty were independent predictors of all-cause death. Anterior leaflet prolapse was the only independent predictor of reoperation (Table 4). There were no significant differences in survival and freedom from reoperation between active and healed endocarditis at 10 years (100% vs 88.4 ± 5.1%, p = 0.398; 100% vs 97.4 ± 2.5%; p = 0.672).
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Fig 1. Survival curve in patients with endocarditis (solid line) and degenerative disease (dashed line).
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Fig 2. Freedom from reoperation in patients with endocarditis (solid line) and degenerative disease (dashed line).
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Recurrence of MR
The latest follow-up echocardiography revealed moderate or severe MR in 7 endocarditis patients (Table 5). The mean duration from operation to recurrent MR was 5.4 ± 5.4 years. One of 2 patients with severe MR underwent valve replacement 4.6 years after operation, and the cause of recurrent regurgitation was leaflet calcification due to chronic hemodialysis. Another patient with severe MR died of malignancy 7.9 years after operation. Two of 5 patients with moderate MR refused reoperation, and the remaining 3 patients were observed carefully because of the lack of symptoms. As determined by echocardiography, recurrent regurgitation was mainly caused by leaflet thickening and calcification in 4 patients and leaflet prolapse in 2. No findings recurrent endocarditis was found.
Freedom from moderate or severe MR was 99.8 ± 0.2% at 2 weeks and decreased to 91.9 ± 1.5% at 5 years, 83.3 ± 2.3% at 10 years, and 74.9 ± 4.3% at 15 years for all patients, and was identical between the patients with endocarditis and degenerative disease (91.9 ± 3.6% vs 81.7 ± 2.6% at 10 years; p = 0.388, Fig 3). Anterior leaflet prolapse, preoperative atrial fibrillation, and nonuse of ring or band annuloplasty were independent predictors of recurrent MR (Table 4). There was no significant difference in freedom from recurrent regurgitation between active and healed endocarditis (100% vs 90.3 ± 4.2% at 10 years, p = 0.310).
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Fig 3. Freedom from recurrent mitral regurgitation in patients with endocarditis (solid line) and degenerative disease (dashed line). The linearized rate of recurrent regurgitation was 2.0% per year (endocarditis, 1.5% vs degenerative, 2.1%; p = 0.569).
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Comment
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The present study demonstrated the several important findings: First, in endocarditis patients, 10-year survival was 89.6 ± 4.7%, freedom from reoperation was 97.8 ± 2.2%, and freedom from recurrent was 91.9 ± 3.6%. These results were similar to those of degenerative patients. Second, Cox multivariate regression analysis showed endocarditis was not an independent predictor of late survival, reoperation, or recurrent mitral regurgitation after repair in mitral valve prolapse. Third, recurrent regurgitation in endocarditis patients was mainly caused by leaflet thickening and calcification in 5 patients and leaflet prolapse in 2, but importantly, not by recurrences of endocarditis.
Despite improvements in diagnosis and therapy, the in-hospital mortality rate for endocarditis remains between 20% and 25%, without significant improvement in the past 2 decades [9, 10]. Appropriately timed and performed surgical treatment of the infected heart valve is important to reduce early and late death [11]. Our surgical indications for infective endocarditis were previously described. We believe that operation should not be delayed once surgical indications are present, although delaying intervention is advised if neurologic complications are present [12].
Valve replacement has been the standard surgical therapy for patients with mitral valve endocarditis. More recently, several single-institution series have suggested the feasibility, effectiveness, and durability of valve repair for endocarditis [4–6]. In a multicenter study conducted in North America, Gammie and colleagues [13] recently reported a 20% and 48% feasibility rate of valve repair in active and healed endocarditis, respectively, with a progressive increase of both rates during the last decade. In published studies, the feasibility of repairing infected valves varies from 33% to 78% for active and from 36% to 86% for healed infections [14], and this is similar to the results of our study.
There were important differences in the rate of repair between active and treated endocarditis patients, with repair significantly more likely in patients with treated endocarditis. The difference in repair rates likely reflects that patients with greater leaflet destruction were more likely to require intervention in the acute phase, whereas those with less tissue damage were more likely to undergo operations in the chronic phase [13]. In our experience, valve replacement was indicated in 3 patients before 1993, 3 with preoperatively severe conditions, and 2 with concomitant procedures. The remaining 4 patients required conversion to valve replacement based on the results of operative finding in 2 and transesophageal echocardiography in 2.
Patients undergoing successful valve repair do better compared with those undergoing valve replacement in the setting of preoperative endocarditis [14]. In addition, early valve repair may prevent worsening of heart failure and progression of valve destruction by the infectious process. Zehr [15] mentioned this is likely true for two reasons: First, prosthetic valve replacement is an abnormal anatomic construct. The recreation of the anatomy by valve repair allows for nonturbulent inflow into the left ventricle and unimpeded laminar flow through the left ventricular outflow tract. The left ventricular dimensions are maintained with the chordal preservation associated with repair. This translates to normalizing flow and contractility. In patients with replacement, turbulent flow patterns likely place the patient at an incremental risk for recurrent endocarditis. Even partial or complete chordal-sparing valve replacement does not recreate normal hemodynamics due to flow disturbances. The second reason is the often-underemphasized long-term morbidity and mortality associated with valve replacement, the requirement for anticoagulation, paravalvular leak, valve thrombosis, embolism, structural deterioration, pannus formation, endocarditis, and biocompatibility issues.
A recent meta-analysis found that patients undergoing valve replacement had significantly poorer outcomes for early death (14.4% vs 2.3%), late death (40.5% vs 7.8%), early cerebrovascular events (11.5% vs 4.7%), late cerebrovascular events (24.4% vs 1.6%), and late recurrent endocarditis (7.3% vs 1.8%) [14]. This meta-analysis also demonstrated low rates of early and late repeat mitral valve operation (2.2% and 4.7%, respectively) after valve repair, suggesting favorable long-term durability.
De Kerchove and colleagues [16] reported that freedom from reoperation and endocarditis recurrence at 10 years in 63 patients with acute endocarditis was 72 ± 24% and 98 ± 0.1%, respectively. During the follow-up period, only 11% had grade II mitral regurgitation on echocardiography. The use of a patch to restore leaflet defect was not predictive for reoperation in their experience, and only the presence of paravalvular abscesses and calcified or rheumatic disease were considered significant risk factors for mitral valve reoperation. In this study, we used autologous pericardium patch, depending on the size and location of the lesions. Moreover, after radical débridement of infected and necrotic tissue, the use of chordal replacement with ePTFE and prosthetic ring or pericardial band annuloplasty was not associated with reinfection, even in active endocarditis.
The advantages of mitral valve repair compared with replacement are well established for degenerative disease and include better preservation of left ventricular function, low perioperative death, avoidance of long-term anticoagulation, low long-term rate of thromboembolic complications, low risk of endocarditis, excellent freedom from reoperation, and improved long-term survival [1–3]. Long-term studies indicate freedom from reoperation at 10 years exceeds 90% [17, 18]. However, David and colleagues [18] indicated that rates of reoperation underestimate the rates of failure of mitral valve repair by about 15% to 20%. To assess the durability of valve repair, late echocardiographic evaluation is an absolute requirement.
In this study, freedom from recurrent MR in endocarditis patients was 91.9 ± 3.6% at 10 years, and these results were better than those of our degenerative patients with 81.7 ± 2.6% at 10 years or the David series with 73 ± 3% at 12 years. Recurrent regurgitation in our endocarditis patients was mainly caused by leaflet thickening and calcification in 5 (7.4 ± 5.1 years) and leaflet prolapse in 2 (0.3 ± 0.1 years). Although it is difficult to clarify the mechanism of recurrent regurgitation based only on late echocardiography, we suspect that the mechanism and timing of failure in endocarditis is similar to that in degenerative disease. With degenerative disease, failure related to the procedure is the primary mechanism of early valve dysfunction, and failure related to the valve is the predominant mechanism of late failure [19, 20].
A few limitations of this study must be recognized. First, this was a retrospective study of a clinical experience at a single institution. Second, this study focused only on the durability of mitral valve repair for endocarditis and compared it with that for degenerative disease, regardless of the study populations and surgical indications. Therefore, we did not perform extensive analyses of outcomes for valve repair compared with replacement. We included also patients with concomitant procedures. Our data demonstrate important preoperative differences between patients. Patients with endocarditis were younger, had fewer risk factors and changes in cardiac morphology, and had a higher incidence of prolapse of the anterior leaflet or both leaflets. These differences were similar to those of the multicenter study in North America. Third, our study was limited by relatively small number of endocarditis patients. Although the number of patients with endocarditis was small, it was larger than the number of cases previously published to date with long-term follow-up. Fourth, echocardiograms obtained during this study included semiquantitative assessments of MR according to the MRA in most patients. Recently, quantitative echocardiography has been performed routinely in selected patients. Moreover, echocardiographic follow-up was not obtained on a fixed schedule in patients monitored beyond 10 years. It is possible, therefore, that patients with recurrent MR were more symptomatic, prompting them to seek medical attention and obtain echocardiograms and leading to an underestimation of durability.
In conclusion, mitral valve repair for endocarditis is associated with low operative mortality and morbidity. Long-term durability of mitral valve repair for endocarditis is comparable with that of repair for degenerative disease. This study suggests that late failures after mitral valve repair for endocarditis result from degenerative processes.
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Appendix
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Discussion
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DR MICHAEL A. ACKER (Philadelphia, PA): During the period of this study, how many times did you actually find yourself forced to replace the valves and not repair them, and what are your criteria that you could suggest to the audience, what is the limit of endocarditis involvement that would not be amenable to repair?
DR SHIMOKAWA: During the study period, the mitral valve was replaced in 9 active and 3 healed native endocarditis patients.
DR ACKER: So how many times did you find that you had to replace? I know sometimes, though, I try to repair these. Sometimes the destruction of the valve is so severe I find that I can't repair it. Did you ever find a valve that you could not repair?
DR SHIMOKAWA: In this study, the indications of valve replacement were the patients with complex destructed lesion and preoperative poor condition such as shock, acute renal failure needed dialysis, or acute lung injury. And before 1993, for acute endocarditis, mitral valve replacement was initially indicated.
DR ACKER: So you never had a valve that was completely studded with vegetations, anterior and posterior leaflet, you never encountered that, or how would you repair that valve?
DR SHIMOKAWA: We should try to repair in all endocarditis patients, we believe. However, in some patients in poor condition, shorter operative time would be beneficial. In our experience, conversion to valve replacement was needed in 4 patients based on the results of operative finding in 2 and transesophageal echocardiography in 2. In these patients, the destructed lesion of the valve was too severe to repair. We speculate that the critical factor that determines the operative procedure is the original lesion of the mitral valve before the onset of infective endocarditis. The degree of the long-standing lesion may be more decisive.
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Acknowledgments
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We gratefully thank Ko Bando, MD, for reviewing the article.
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References
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Abstract
Introduction
