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J Thorac Cardiovasc Surg 2006;132:1390-1397
© 2006 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease

Recurrent mitral regurgitation after repair: Should the mitral valve be re-repaired?

Rakesh M. Suri, MD, DPhil*, Hartzell V. Schaff, MD, Joseph A. Dearani, MD, Thoralf M. Sundt, III, MD, Richard C. Daly, MD, Charles J. Mullany, MB, MS, Maurice Enriquez-Sarano, MD, Thomas A. Orszulak, MD

Division of Cardiovascular Surgery, Mayo Clinic College of Medicine, Rochester, Minn.

Read at the Eighty-sixth Annual Meeting of The American Association for Thoracic Surgery, Philadelphia, Pa, April 29-May 3, 2006.

Received for publication April 30, 2006; revisions received June 30, 2006; accepted for publication July 12, 2006.

* Address for reprints: Rakesh M. Suri, MD, DPhil, Division of Cardiovascular Surgery, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905 (Email: suri.rakesh{at}mayo.edu).


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
OBJECTIVE: We sought to evaluate the clinical and echocardiographic outcomes of reoperation for failed mitral valve repair.

METHODS: One hundred forty-five patients with recurrent mitral regurgitation after primary mitral valve repair of degenerative leaflet prolapse underwent mitral valve reoperations between January 1, 1970, and January 1, 2005. The mean age was 66 years, and 102 (70%) were men.

RESULTS: The mean duration from initial repair to reoperation was 4.1 years (standard deviation = ± 5.1 years). Indications for reoperation were regurgitation alone (n = 109 [75%]), hemolysis (n = 27 [19%]), obstruction from systolic anterior motion (n = 3 [2%]), endocarditis (n = 3 [2%]) and stenosis-other (n = 3 [2%]). New pathology was found in 80 (55%) patients, and failure of the initial repair was found in 61 (42%) patients. The mitral valve was re-repaired in 64 (44%) patients and replaced in 81 (56%) patients. Early operative mortality was similar after re-repair and replacement (1.6% vs 4.9%, P = .38). Independent predictors of improved survival on multivariate analysis were mitral re-repair (hazard ratio = 0.44, P = .03), younger age (hazard ratio = 1.06, P = .001), and an operative indication of mitral regurgitation alone (hazard ratio = 0.31, P = .005). Seven patients had a third mitral operation (all replacements), 6 after re-repair and 1 after replacement. At last follow-up echocardiogram (n = 96), ejection fraction was greater (P < .001) and left ventricular end-systolic dimension was smaller (P = .009) in patients undergoing re-repair compared with values in those undergoing valve replacement.

CONCLUSION: Recurrent mitral regurgitation after prior repair is frequently caused by new valve pathology. Mitral re-repair is performed in almost half of patients and is associated with superior survival, improved ejection fraction, and greater regression in ventricular dimension compared with valve replacement.



Abbreviations and Acronyms AL = anterior leaflet; LV = left ventricular; MR = mitral regurgitation; MV = mitral valve; PL = posterior leaflet



    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Mitral valve (MV) repair is the standard of care for the correction of significant mitral regurgitation (MR) caused by degenerative valve disease.1-5Go Valve repair is associated with superior survival and equivalent, if not better, durability compared with valve replacement. MV reoperation after primary repair has been reported to occur with a linearized hazard rate of 0.5% to 1.5% per year.6Go There has been hesitance to perform a second mitral repair because of concern that patients with a failed initial repair might have poor tissue quality, limiting the durability of re-repair. Also, there has been speculation that secondary MV repair might have greater risk than valve replacement.

Little is known regarding the effects of re-repair versus replacement on survival, durability, and normalization of left ventricular (LV) size and function. The objective of this study was to examine patients presenting with recurrent regurgitation after primary MV repair of leaflet prolapse, to analyze causes of technical failure after the first repair, and to determine factors predicting survival and durability after reoperation.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
This was a retrospective review of patients undergoing surgical correction (repair or replacement) of recurrent MV regurgitation after primary MV repair for regurgitation caused by degenerative leaflet prolapse. The study was reviewed and approved by the Mayo Clinic College of Medicine Institutional Review Board. The need for individual patient consent was waived because relevant identifiers were not included in the database. Included were those having concomitant coronary bypass (coronary artery bypass grafting) or closure of a secundum atrial septal defect/patent foramen ovale. We excluded patients who declined involvement in clinical research, those who underwent conversion to replacement at the time of the initial operation, and those who had an initial diagnosis of MR caused by congenital or ischemic heart disease or other forms of cardiomyopathy. Also excluded were patients with significant MV stenosis or those with endocarditis causing leaflet defects/subvalvular abscess at the time of primary MV repair.

Between January 1, 1970, and January 1, 2005, a total of 145 patients underwent mitral reoperations for recurrent MR at Mayo Clinic Rochester. One hundred seven patients had their first MV repair at Mayo Clinic Rochester (5% of 2122 patients undergoing primary MV repair for degenerative leaflet prolapse during the study interval), and 38 had their first operation elsewhere. A total of 64 (44%) patients underwent MV re-repair, and 81 (56%) underwent replacement of the previously repaired valve. The mean interval between the initial operation and reoperation was 4.1 ± 5.1 years. The date of reoperation occurred within the first 3 months after the primary repair in 26 (18%) patients. A total of 6 patients undergoing re-repair and 1 undergoing replacement had a third mitral operation (second mitral reoperation). All 7 of these had valve replacement. The indications for reoperation were recorded from preoperative clinical assessments and echocardiograms. Findings at the time of the operation were determined from a review of the operative notes. The mean duration of follow-up in survivors was 3.3 (± 4.1) years.

Surgical Procedure
Both the indications for primary MV repair and the surgical techniques used evolved over the 35-year period. During the third decade of the study (1990s), we adopted a strategy of earlier primary MV repair for regurgitation caused by leaflet prolapse on the basis of quantitative echocardiographic criteria.2Go The most frequent lesion for which patients underwent initial surgical correction of MR at Mayo Clinic was isolated posterior leaflet (PL) prolapse of the middle scallop caused by either chordal elongation or chordal rupture. The most common method of correction during the initial operation was triangular resection and suture repair of the involved portion of the PL supplemented by a standard-length (63-mm) flexible posterior annuloplasty band.7,8Go During the first 2 decades of the study, anterior leaflet (AL) prolapse was corrected by means of chordal shortening, chordal transfer, or commissural annuloplasty. More recently (after 1990), we used artificial polytetrafluoroethylene* neochordae8Go for repair of AL prolapse and, in selected patients, leaflet plication. Indications for reoperation were recurrent MR with or without associated complications. Techniques used for MV re-repair were generally similar to those used in primary MV repair.

Statistical Analysis
Group statistics were expressed as means ± 1 standard deviation. Categoric variables were compared between groups by using the {chi}2Go test for independence or the Fisher exact test. Two-sample t tests were used to compare continuous variables between groups. Survival and reoperation end points were estimated by using the Kaplan-Meier method (actuarial). Multivariate models to identify potential risk factors for these end points were investigated by using Cox proportional hazards and were constructed with stepwise selection techniques. P values of .05 or less were considered significant.


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Baseline Characteristics
Baseline characteristics of patients are presented in Table 1. Patients undergoing MV replacement were slightly more symptomatic and had greater left atrial dimensions before reoperation than patients undergoing valve re-repair. All other aspects of the preoperative risk profiles were similar comparing those who underwent MV re-repair versus those who underwent prosthetic replacement.


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TABLE 1. Baseline characteristics
 
Indications for Reoperation
The indications for a second MV procedure are shown in Table 2. A total of 109 (75%) patients underwent reoperations for significant regurgitation alone. The remaining factors responsible for a decision to reoperate were hemolysis in 27 (19%), dynamic outflow tract obstruction caused by systolic anterior motion of the anterior mitral leaflet in 3 (2%), endocarditis in 3 (2%), MV stenosis in 1 (1%), and "other" in 2 (1%). Patients were more likely to have valve replacement at reoperation if the preoperative indication was MR alone and were more likely to have re-repair if hemolysis was the cause. Of the 27 patients with hemolysis, the mean MR grade at reoperation was 3.4, and the mean interval from first operation to reoperation was 1.1 years.


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TABLE 2. Indications for reoperation
 
Reoperation
The findings at reoperation are shown in Table 3. Overall, the surgically determined factor or factors contributing to recurrent MR included the AL in 65 (45%), the PL in 61 (42%), ring annuloplasty dehiscence in 42 (29%), and chordal rupture in 20 (14%). New valve pathology was determined to be the responsible cause of recurrent MR in 80 (55%) patients, and technical failure of the primary repair was most responsible in 61 (42%) patients. The cause of MR at reoperation was unclear in 4 (3%) patients. Patients having MV re-repair were more likely to have a specific anatomic cause for recurrent MR identified by the surgeon at reoperation, such as annuloplasty dehiscence or technical failure of the prior repair. Discovering new pathology was associated with a tendency to replace the MV.


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TABLE 3. Findings at reoperation
 
At reoperation, 64 patients underwent MV re-repair, and 81 underwent valve replacement. During re-repair, a modification of the annuloplasty was carried out in 52 of 64, an AL procedure was performed in 33 of 64, and the PL was addressed in 32 of 64. Concomitant procedures were performed in 38 patients and included coronary artery bypass grafting in 14 (10%), tricuspid valve repair in 12 (8%), aortic valve replacement in 8 (6%), the Cox maze procedure in 4 (2.8%), atrial septal defect closure in 1 (0.7%), and patent foramen ovale closure in 1 (0.7%). The operative mortality after valve replacement was 4.9% (4 patients), and that after mitral re-repair was 1.6% (1 patient). Where data were available on predismissal echocardiography, 97% (59/61) of patients undergoing re-repair and 98% (64/65) of those undergoing valve replacement had no greater than mild MR.

Univariate and Multivariate Predictors of Late Mortality
Univariate analysis and multivariate models were constructed to determine the influence of preoperative and intraoperative variables on late mortality (>30 days) after reoperation. The univariate survival advantage associated with re-repair is shown in Figure 1. On multivariate analysis, 3 independent factors were associated with improved survival: MV re-repair, younger age, and the preoperative indication of pure MR (Table 4).


Figure 1
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Figure 1. Kaplan-Meier probability of late survival (>30 days or after discharge from the hospital) after mitral valve re-repair or replacement at reoperation for recurrent mitral regurgitation. The late survival associated with mitral valve re-repair is greater than that seen after mitral replacement (mortality hazard ratio for re-repair, 0.49; P = .05 vs valve replacement).

 

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TABLE 4. Univariate and multivariate predictors of late mortality
 
Univariate Predictors of Third Mitral Operation
A total of 7 patients (6 undergoing re-repair and 1 undergoing replacement) underwent a third MV operation at a mean of 5.7 years after the second operation (operative mortality, 0%). The actuarial survival free of subsequent reoperation after the first MV reoperation was 93% at 5 years overall. The 5-year actuarial freedom from reoperation after re-repair was 83%, and the linearized risk of reoperation was 3.4% per year. The only univariate predictor of a third MV operation was performance of an AL procedure at the time of re-repair. The number of events was insufficient to perform multivariate modeling.

Follow-up Data
At the date of last contact, 43 (100%) of 43 patients undergoing re-repair were in New York Heart Association class I/II versus 31 (91%) of 34 after replacement. The final available follow-up echocardiograms (between 1-5 years, n = 96) were analyzed to assess LV size and function after MV re-repair versus replacement. These were performed a mean of 946 days after re-repair and 915 days after valve replacement (Table 5). Patients undergoing MV re-repair at the second operation had significantly better ejection fraction and smaller LV end-systolic dimension during follow-up compared with those undergoing MV replacement.


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TABLE 5. Follow-up echocardiographic data
 

    Discussion
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
This is the first study to compare the outcomes of MV re-repair versus replacement for recurrent MR after primary repair of degenerative MV prolapse. Our results indicate that reoperation was most often required for recurrent regurgitation and that the cause was similarly distributed between failure of the previous repair and new valve pathology. MV re-repair was performed in just under half of all patients in our series. Importantly, we found that re-repair is clearly beneficial, conveying improved survival, along with better recovery of LV function and greater LV regression, compared with valve replacement. If MV re-repair is technically possible, it should be the favored choice at reoperation.

The indications for reoperation and intraoperative findings both influenced the choice of surgical procedure. Significant MR alone was the most frequent indication for reoperation after initial MV repair, as has been shown in prior reports,9Go and was associated with a tendency to perform valve replacement over re-repair (85% vs 63%, P = .002). Technical reasons for failure of the primary MV repair were discovered to be important in 42% of patients, which more frequently led to be re-repair (56%) over replacement (31%, P = .002). Discovering a specific anatomic cause for disruption of the prior repair and, specifically, annuloplasty dehiscence was more prevalent in those undergoing re-repair (47% vs 15%, P < .001). This observation underlines the fact that the ability to discern an anatomic reason for failure of the first repair is important if a second repair is to be considered. It also reaffirms the importance of reliable intraoperative and predischarge echocardiography to identify those with early repair failure so that surgical reintervention can be undertaken before leaving the hospital, as others have suggested.9Go Finding new valve pathology at reoperation might have influenced the decision to replace the MV (42% vs 65%, P = .005). This tendency might have been associated with a concern that disease progression in remaining leaflet tissue would increase the likelihood of a third MV operation.

The observation that roughly half of all patients (55%) have new MV pathology causing recurrent MR after primary repair differs from the reports of others, who have suggested that technical failure was the most common finding at reoperation.9,10Go It is possible that the prevalence of rheumatic and ischemic MV disease in these studies might have influenced both the cause of repair failure and the stated preference for valve replacement at reoperation.

The incidence of hemolysis after MV repair is unknown, and the optimal clinical management is still a topic of debate. In this series hemolysis as a cause for reoperation after initial MV repair of degenerative leaflet prolapse was unusual (19%) but was also a factor favoring re-repair. A recent report suggested that 90% of patients presenting with hemolysis after prior MV repair required MV reoperations for surgical correction.11Go The operative techniques used to eliminate the regurgitant jet and to prevent the recurrence of hemolysis while preserving the native MV have been described elsewhere.11-14Go Several groups have published their experience with reoperation for this condition,11-13,15,16Go and there has been a suggestion that MV replacement might be the treatment of choice.11Go Our current data indicate that re-repair for hemolysis is effective and is not a risk factor for a third mitral operation.

Operative mortality in our study was 1.6% after re-repair and 4.9% after replacement. El Asmar and colleagues10Go found an overall reoperative mortality of 1.4% in a series in which 85% of repair failures were followed by replacement. Gillinov and associates9Go studied a mixed population of patients (degenerative, 59%; rheumatic, 20%; ischemic, 16%; endocarditis, 4%; and congenital, 1%), reporting an early mortality after re-repair of 8.6%. A similar operative risk, 8.9%, was reported by Niederhauser and coworkers.17Go Our study examines a cohort of patients who are relatively homogeneous. In limiting our review to degenerative MV disease, we have attempted to focus on the actual reoperative risk associated with re-repair versus replacement in this population.

MV re-repair was an independent predictor of improved late survival in our study, despite similar preoperative risk profiles to those undergoing MV replacement. Moreover, re-repair led to superior recovery of ejection fraction and more complete regression of LV dimensions toward normal, as has been shown after primary valve repair.6Go It has also been demonstrated elsewhere that greater LV function and smaller LV dimensions after primary MV surgery are associated with a survival advantage during long-term follow-up.18-20Go This might explain the observed benefit in late survival that we have seen in our current series after re-repair. The findings in this report challenge the assumption that MV replacement is the conservative choice for correction of recurrent MR. The previously established benefits of primary MV repair on survival, LV size, and function persist after re-repair.

Although the durability of MV replacement was slightly greater than that of re-repair at reoperation, the difference between the 2 groups could not be statistically differentiated. Surgical correction of the AL during MV re-repair was performed in 33 (52%) of 64 patients undergoing re-repair and was the only univariate risk factor to be associated with the need for a third mitral operation. Because the majority of the procedures in this report were carried out between 1980 and 2000, many patients had correction of AL prolapse with methods that are now known to be less durable than chordal replacement.5,21Go Our recent results concur with those of others who have found no significant difference in MV reoperation rates after primary repair of isolated PL prolapse versus that involving the AL in the current era.6,22,23Go The improved durability of primary AL repair will also likely influence the results of re-repair in the future.

Limitations
This is a retrospective review and is associated with the traditional limitations. It is possible that we selected a group of patients who were more likely to be followed for some distinguishing feature. Although we captured all patients presenting for reoperation at our institution, regardless of the location of the first repair, it is conceivable that this group differs from those who had reoperations elsewhere. Finally, because of the length of the period over which this study was completed, there are variations in the frequency and extent of echocardiographic follow-up.

Clinical Implications
Delaying surgical reintervention for recurrent severe MR after primary MV repair can be deleterious. Identification of MV-related hemolysis, an anatomic abnormality of the prior repair, or technical failure at reoperation all increase the likelihood of performing a second MV repair. Just under half of all patients in this study underwent re-repair at reoperation. The proportion of those who have anatomy amenable to re-repair is likely higher than this. Re-repair frequency might be limited either by surgeon bias or patient concern regarding a third operation. Whereas patients have previously been counseled to accept MV replacement as the more conservative choice after failure of primary MV repair, the survival advantage, durability, and improvements in LV size and function associated with re-repair should motivate clinicians to offer this opportunity to patients.


    Conclusions
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Mitral re-repair is currently performed in almost half of all patients with recurrent MR after failed primary repair of degenerative MV disease. The reoperation rate after re-repair is 3.4% per year, and will likely improve as the results of more recent valvuloplasty techniques for AL repair become available. MV re-repair should be offered as the preferred approach to preserve longevity along with LV size and function at reoperation.


    Footnotes
 
Maurice Enriquez-Sarano reports consultant fees, lecture fees, and grant support from Edwards Lifesciences.

* Gore-Tex neochordae, registered trademark of W. L. Gore & Associates, Inc., Newark, Del. Back


    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 

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