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Ann Thorac Surg 2007;84:444-450
© 2007 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Reoperation After Mitral Valve Repair for Degenerative Disease

^a Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic, Cleveland, Ohio
^b Department of Quantitative Health Sciences, The Cleveland Clinic, Cleveland, Ohio

Accepted for publication March 26, 2007.

^_* Address correspondence to Dr Gillinov, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic, 9500 Euclid Ave/Desk F24, Cleveland, OH 44195 (Email: gillinom{at}ccf.org).

Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29–31, 2007.

Dr Gillinov discloses that he has a financial relationship with Edwards Lifesciences, LLC; Viacor, Inc; Medtronic, Inc; St. Jude Medical, Inc; and Guidant, Corp.

 

	Abstract

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

 
Background: With recent increases in frequency of mitral valve repair for degenerative disease, surgeons will encounter more patients with recurrent mitral regurgitation after repair. Objectives of this study were to determine (1) mechanisms for and timing of failed repair of degenerative disease and approach to reoperation, (2) durability of re-repair, and (3) long-term survival after reoperation.

Methods: From January 1980 to January 2005, 188 patients underwent reoperation for recurrent mitral regurgitation. Follow-up averaged 6.5 ± 5.0 years.

Results: Mechanisms of failure were procedure related in 71 patients, valve related in 84, both in 25, or uncertain in 8. Intervention was early (median, 19 days) for procedure-related failure and later (median, 5.4 years) for valve-related failure (p < 0.0001). Procedure-related failure was caused by suture dehiscence in 40 (42%) of 96 patients, rupture of previously shortened chordae in 20 (21%), systolic anterior motion in 20 (21%), hemolysis in 21 (22%), and incomplete initial correction in 11 (11%). Valve-related failure was caused by progressive disease in 100 (92%) of 109 patients and endocarditis in 11 (10%); these were not mutually exclusive. Mitral valve replacement was performed in 64% and re-repair in 36% (65% of recent reoperations). Freedom from a second mitral reoperation after re-repair was 93% at 10 years. Survival at 1, 5, and 10 years was 88%, 81%, and 62%, respectively.

Conclusions: When reoperation occurs late after repair of degenerative mitral valve disease, new valve pathology is usually the culprit, and re-repair is less common. In contrast, reoperation for procedure-related failure occurs early and is often amenable to re-repair. When performed, valve re-repair is durable.

Mitral valve repair is the procedure of choice for mitral regurgitation (MR) caused by degenerative disease [1–8]. Reported advantages of mitral valve repair compared with replacement include better preservation of left ventricular function, greater freedoms from thromboembolism, anticoagulant-related hemorrhage, and endocarditis, and improved long-term survival [1–12]. However, mitral valve repair has not been demonstrated to confer superior long-term freedom from reoperation when compared with bioprosthetic mitral valve replacement [11]. Mitral valve reoperation after primary repair has been reported to occur at a linearized rate of 0.5% to 1.5% per year [13]. Thus, reoperation to treat recurrent MR is an important clinical consideration after mitral valve repair [14].

Few data exist concerning the mechanisms of recurrent valve dysfunction after mitral valve repair or success of subsequent treatment modalities [15–17]. There has been reluctance to perform a second mitral repair at reoperation because of concern that patients with a failed initial repair might have poor tissue quality or other factors that might limit the durability of re-repair. Thus, objectives of this study were to determine (1) mechanisms for and timing of failed repair of degenerative disease and approach to reoperation, (2) durability of a re-repair, and (3) long-term survival after reoperation.

	Patients and Methods

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

 
Study Population
Between January 1980 and January 2005, 188 patients underwent mitral valve reoperation at The Cleveland Clinic for recurrent MR after initial mitral valve repair for degenerative disease. These consisted of replacement in 120 (63%) and re-repair in 68 (36%). This included all patients receiving reoperation for failed repair, even if the initial repair was performed at an outside hospital. However, patients having unsuccessful mitral valve repair, followed by replacement during the same operative procedure, were not included. Patients having concomitant tricuspid valve surgery or coronary revascularization at the initial surgery or reoperation were included; those having aortic valve procedures, ascending aortic procedures, myectomy, or a Dor procedure at the initial or reoperative procedure were excluded. Patients with etiology of MR other than degeneration (ischemic, rheumatic, endocarditis, functional, congenital) were also excluded.

During the time frame of this study, 4024 patients with degenerative disease had primary mitral valve repair at The Cleveland Clinic. Mean age at the time of reoperation was 61 ± 12 years (15th and 85th percentiles, 46 and 72 years; Table 1). Data were retrieved from the prospective Cardiovascular Information Registry (CVIR), which has been approved by the Institutional Review Board (IRB) for use in research, with patient consent waived. Additional details of reoperative findings were abstracted and synthesized from review of imaging studies and operative notes.

Follow-Up
An IRB-approved questionnaire was sent to patients every 2 years, supplemented by a telephone interview with families or outside physicians, with patient consent. Mean follow-up was 6.5 ± 5.0 years, with 15% of patients monitored for more than 13.5 years. A total of 1215 patient-years of follow-up data were available for analysis.

Data Analysis
Timing
The cumulative distribution of interval from the initial mitral valve repair to reoperation, stratified by mechanism of repair failure, was estimated nonparametrically by the Kaplan-Meier method, Probability density function was assessed parametrically by using hazard function technology [18]. (For additional details, see http://www.clevelandclinic.org/heartcenter/hazard.)

Approach
Factors associated with approach to failure at reoperation (valve re-repair versus replacement) were identified by bagging [19], using the variables listed in the Appendix, automated stepwise analysis of 500 bootstrap resamplings, and a p = 0.05 for retention. Thereafter, the analyses were aggregated and variables or closely correlated clusters of variables appearing in 50% or more of analyses were retained in the final model. In particular, trends with time were closely analyzed by using transformations of scale that best linearized the relationship.

Freedom from reoperation
Freedom from a second reoperation after re-repair was estimated nonparametrically using the Kaplan-Meier method. For comparison, estimates of freedom from a second reoperation after valve replacement are also given.

Survival
Overall and stratified nonparametric estimates of survival after reoperation were obtained with the Kaplan-Meier method. A parametric method was used to resolve the number of phases of instantaneous risk (hazard function) and to estimate shaping parameters [18]. Thereafter, multivariable analysis was performed in the hazard function domain by using bagging for variable selection, as described previously under "Approach."

Presentation
Categoric data are summarized as frequencies and percentages and continuous variables as means ± standard deviations or, when their distribution was skewed, as medians and 15th and 85th percentiles (equivalent to ± 1 standard deviation).

	Results

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

 
Repair Failure
Mechanisms for mitral valve failure leading to reoperation were procedure related in 71 patients, valve related in 84, both in 25, or uncertain in 8 (Table 2). Procedure-related failure was caused by suture dehiscence in 40 (42%) of 96 patients, rupture of previously shortened chordae in 20 (21%), SAM in 20 (21%), hemolysis in 21 (22%), and incomplete initial correction in 11 (11%). Suture dehiscence occurred at the site of leaflet repair in 30 patients, the anuloplasty in 7, or at both sites in 3. Valve-related failure was caused by progressive degenerative disease in 100 (92%) of 109 patients and endocarditis in 11 (10%). These were not mutually exclusive. Progressive degeneration most commonly manifested as leaflet prolapse.

View larger version (8K): [in this window] [in a new window]   Fig 1. Timing of reoperation for repair failure after mitral valve repair for degenerative disease according to mechanism of failure. Patients having both procedure-related (top line) and valve-related failure (bottom line) appear twice in these graphs. Cumulative distribution of times to failure is shown with each step representing a failure. The median time to failure is the point at which each curve crosses the 50% line.

View larger version (13K): [in this window] [in a new window]   Fig 2. Re-repairs versus valve replacement for repair failure after mitral valve repair for degenerative disease by date of reoperation. Solid circles represent means by yearly groupings and the solid line is a trend line. (A) Overall results. (B) Results stratified by mechanism for repair failure. Patients experiencing both procedure-related (top line, filled circles) and valve-related mechanisms (bottom line, open circles) of failure appear in both strata.

View larger version (10K): [in this window] [in a new window]   Fig 3. Freedom from reoperation after mitral valve re-repair (line). Each solid circle is a reoperation, vertical bars are asymmetric confidence limits equivalent to ± 1 standard error, and numbers in parentheses patients are remaining at risk.

View larger version (19K): [in this window] [in a new window]   Fig 4. (A) Risk-unadjusted overall survival after mitral valve (MV) reoperation for repair failure. Each open circle represents a death, vertical bars are asymmetric confidence limits (CLs) equivalent to ± 1 standard error, and numbers in parentheses are patients at risk. Solid lines are parametric estimates enclosed in CLs equivalent to ±1 standard error (dashed line). (B) Unadjusted survival stratified by approach to reoperation (repair [top set of lines] versus replacement (bottom set of lines]). Filled circles (repair) and open triangles (replacement) represent a death, vertical bars are asymmetric confidence limits (CLs) equivalent to ±1 standard error, and numbers in parentheses are patients at risk. Solid lines are parametric estimates enclosed in CLs equivalent to ±1 standard error (dashed lines).

	Comment

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

We, and others, previously studied relatively small series of patients with recurrent mitral valve dysfunction after mitral valve repair and devised classification systems for categorizing repair failure. In a review of 72 patients undergoing late reoperation after mitral valve repair, El Asmar and colleagues [15] proposed that failure could be classified as surgeon related or valve related. In that experience, most repair failures were surgeon related in degenerative disease. Our group published a similar report [16] in which most patients had degenerative mitral valve disease and found procedure-related factors to be the most common cause of recurrent valve dysfunction necessitating reoperation. In that experience, rupture of previously shortened chordae was the single most common mechanism of repair failure.

The current study reports 188 reoperations for failed mitral repair. In these patients, the mechanisms of failed repair were nearly equally distributed between procedure-related and valve-related causes. Some patients had more than one mechanism of repair failure, which emphasizes the importance of careful echocardiographic and surgical examination of the valve at the time of reoperation. Potentially preventable technical problems remain an important cause of repair failure. Procedure-related or technical reasons for failure of the primary repair were important in 96 of 188 patients. Suture dehiscence was the most common procedure-related issue, occurring at sites of leaflet resection and at the anuloplasty ring. This underscores the importance of careful surgical technique and creation of a tension-free repair. In the case of a large posterior leaflet resection, we now favor a sliding repair to reduce tension on suture lines.

Repair failures occurred during the entire follow-up period, indicating the need for continued echocardiographic surveillance after mitral valve repair: there is no "safe" period after which a patient can be deemed free of risk of repair failure. Others have demonstrated that mitral valve repair is followed by a high initial instantaneous risk of valve failure and a subsequent low constant risk of late valve failure [4, 7, 13]. Amplifying this finding, we have clarified the relationship between mechanism and timing of failure, identifying procedure-related failure as the primary mechanism of early valve dysfunction and valve-related failure as the predominant mechanism of late failure.

Approach to Reoperation
In the past, surgical treatment of recurrent MR after mitral valvuloplasty was controversial. El Asmar and colleagues [15] performed a second valve repair in only 15% of patients with failed valvuloplasty, and others suggested that failed mitral valve repair should always be treated by replacement [17]. During the period of this study, our approach to reoperation in these patients evolved. With increased understanding of the mechanisms and timing of repair failure, we adopted a more aggressive approach to re-repair; today, re-repair is used in 65% of patients. Re-repair is most frequently chosen for patients with procedure-related repair failure, who tend to present early and to have discrete anatomic problems amenable to re-repair; an increased repair rate in these patients is responsible for the overall increased proportion of re-repairs in recent years. Re-repair is less likely in those who present late with valve-related mechanisms of repair failure or multiple mechanisms of valve dysfunction.

Freedom From Reoperation and Long-Term Survival
Freedom from reoperation and long-term survival were excellent after valve re-repair. Supporting this finding, echocardiographic follow-up from Suri and colleagues at [20] the Mayo Clinic confirms good long-term valve function after re-repair. In our study, there was a trend toward better survival after re-repair than after replacement, but it did not reach statistical significance. However, Suri and colleagues [20] identified re-repair as an independent predictor of improved survival in these patients. This suggests that the benefits of repair on left ventricular size and function may persist after re-repair, or alternatively, that the replacement group represents patients with more advanced cardiac disease and more comorbidities, resulting in decreased survival.

Limitations
This is a retrospective clinical study associated with traditional limitations. Postoperative echocardiographic follow-up was limited, and insufficient data were available to describe the course of MR after re-repair. In 8 patients, the mechanism of repair failure could not be determined, and these were classified as unknown.

Conclusions and Clinical Implications
Reoperation for procedure-related failure occurs early; in such cases, the mechanism of failure is usually discrete, and we favor re-repair. When performed, mitral valve re-repair is durable. If reoperation occurs late after repair of degenerative mitral valve disease, new valve pathology is usually the culprit, and re-repair is less common. In the setting of progressive valve disease, particularly if diffuse or complex, consideration should be given to mitral valve replacement.

	Appendix

 
Variables Used in Multivariable Analyses
Demography
Age (year), sex, height (cm), weight (kg), body surface area (m²), body mass index (kg/m²).

Preoperative status
New York Heart Association functional class, Canadian angina class, emergency operation.

Mitral valve pathology
Fibrosis or thickening, calcification, elongated chordae (to anterior or posterior leaflet), chordal rupture (to anterior or posterior leaflet), leaflet prolapse (anterior, posterior, bileaflet), elongated papillary muscle, dilatation of mitral anulus, dilated left ventricle, regurgitation grade: 0 to 4+ scale.

Left ventricular function
Left ventricular dysfunction grade (1 = none, 2 = mild, 3 = moderate, 4 = severe), previous myocardial infarction, left ventricular ejection fraction.

Other cardiac comorbidity
Atrial fibrillation, coronary artery stenosis (left main trunk, left anterior descending coronary artery, circumflex coronary artery, right coronary artery; >50%, any), number of coronary systems with >50% stenosis, family history of coronary artery disease, ventricular arrhythmia, complete heart block, history of endocarditis, history of heart failure, regurgitation grade and stenosis of aortic, tricuspid and pulmonary valves, number of previous cardiac operations.

Noncardiac comorbidity
History of hypertension, treated diabetes (insulin treated/noninsulin treated), stroke, smoking, peripheral arterial disease, chronic obstructive pulmonary disease, renal failure; concentration of blood urea nitrogen, creatinine, bilirubin, cholesterol (total, high-density lipoprotein, low-density lipoprotein), triglycerides; hematocrit.

Details of procedure
Mitral valve repair or replacement, mitral valve repair details (leaflet resection, sliding leaflet repair, chordal resection, cleft repair, leaflet suture, leaflet débridement, type of anuloplasty ring, anterior leaflet repair, posterior leaflet repair), replacement with biological or mechanical valve, concomitant tricuspid valve repair or replacement, coronary artery bypass grafting, number of internal thoracic artery grafts.

Reasons for reoperation
Valve related (progressive degeneration, endocarditis), procedure related (suture dehiscence, hemolysis, systolic anterior motion, chordal shortening, incomplete initial repair).

Experience
Date of reoperation, years from previous mitral valve operation.

	Discussion

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

 
DR MICHAEL MACK (Dallas, TX): Can you give us an idea of when you decide to reoperate? You indicated in that your entrance criteria was 2+ or greater MR. Surely that alone is not the indication for reoperation, since we heard on Sunday in the Evalve trial 2+ MR is actually considered a success of that procedure. So could you give us some idea of when you decide to reoperate?

DR DUMONT: I think you have to look at whether the patients are symptomatic or not. That would be the first criterion. Obviously, if they have hemolysis with 2+ regurgitation needing transfusion, that would be another indication. Of course if they have endocarditis with large vegetation on the mitral valve, that would be another indication.

DR MACK: And it looked like in the procedure-related ones, your average time to reoperation was about 18 days. If you have 2 to 3+ MR after repair postoperatively, is there any reason to wait, hoping that that will get better or should you just say this is not acceptable and go back and reoperate at that point?

DR DUMONT: At The Cleveland Clinic, we usually do not accept those kinds of results and we go back to the operating room within the same hospitalization, unless there are other complications involved, of course.

DR EDWARD M. BENDER (Cape Girardeau, MO): I enjoyed your talk. I thought it was very useful, and it was also interesting to note that the single most common mode of failure was ring dehiscence on your slides. Should we be changing our technique to perhaps use pledgeted sutures instead of the usual nonpledgeted sutures when placing rings? And number two, did the mode of failure change based on the type of ring used?

DR DUMONT: I will answer your second question first. No, the mode of failure did not change according to the type of ring. This study spans 25 years, so at the beginning of the study, we were using the Carpentier-Edwards classic ring during the 400 or so first mitral valvuloplasties, then we used the Periguard annuloplasty band, and in the last 15 years have been using the Cosgrove-Edwards annuloplasty ring. In a previous report, we found the Periguard ring to be a risk factor for failure of mitral valve repair. So we haven’t been using that one. But as for the Carpentier-Edwards classic versus the Cosgrove-Edwards, we saw no difference in terms of failure.

As for the dehiscence, not only the rings dehisced but also at the sites of reapproximation, of P1 and P3. That is another area where we saw dehiscence of sutures, and those were re-repaired early, as you saw from our results. And depending on the mechanisms, we either patched it up, as you saw in the case we reported, or had to take out the ring and put in another one.

DR MACK: Does the complexity of the initial repair influence whether you re-repair it or not? In other words, if you have to reoperate and the initial repair was for bileaflet disease, would you then tend to replace or would it totally depend upon what you find at the time of reoperation?

DR DUMONT: It would almost totally depend what we find at the time of reoperation. For instance, if we find a cleft that can be easily closed at the time of reoperation, that will be done. Obviously if the mechanism of failure is complex with multiple jets, I think it would be safer to just replace those valves.

	Acknowledgments

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

 
We thank Angela York for database construction and Wanda Weaver for patient follow-up. This work was supported in part by a gift from the Broyhill Family.

	References

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Eric Dumont Eugene H. Blackstone Joseph F. Sabik, III Lars G. Svensson Tomislav Mihaljevic Bruce W. Lytle Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dumont, E. Articles by Lytle, B. W. Search for Related Content PubMed PubMed Citation Articles by Dumont, E. Articles by Lytle, B. W. Related Collections Valve disease