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Division of Cardiothoracic Surgery; Washington University School of Medicine and Barnes Jewish Hospital, St Louis, Missouri
Accepted for publication January 23, 2008.
* Address correspondence to Dr Crabtree, Barnes-Jewish Hospital, Washington University School of Medicine, One Barnes Jewish Hospital Plaza, 3108 Queeny Tower, St. Louis, MO 63110 (Email: crabtreet{at}wustl.edu).
Presented at the Fifty-fourth Annual Meeting of the Southern Thoracic Surgical Association, Bonita Springs, FL, Nov 7–10, 2007.
| Dr Damiano discloses that he has a financial relationship with Atricure Inc, Medtronic Inc, and Medical CV Inc; Dr Moon with Edwards Inc.
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Abstract |
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Methods: A retrospective study was performed on 257 consecutive patients undergoing mitral valve repair exclusively for IMR from 1996 to 2005. Potential preoperative and perioperative risk factors for death and postoperative echocardiographic data were recorded.
Results: Preoperative echocardiography demonstrated 3+ to 4+ MR in 98.4% (252 of 257). Concomitant coronary artery bypass grafting was performed in 80.9% (208 of 257). Operative mortality was 10.1% (26 of 257). Overall survival by Kaplan-Meier analysis was 68.3% at 3 years and 52.0% at 5 years. Factors associated with late mortality by multivariate analysis include advanced age (relative risk [RR], 1.037; 95% confidence interval [CI], 1.016 to 1.059; p 
0.001), preoperative dialysis (RR, 3.504; 95% CI, 1.590 to 7.720; p = 0.008), and diabetes (RR, 2.047; 95% CI, 1.319 to 3.177; p = 0.001). Echocardiographic data at 20 ± 25 months were available in 57% (147 of 257). Their survival by Kaplan-Meier analysis was 76.4% at 3 years and 65.1% at 5 years with 0 to 2+ MR postoperatively (n = 106) vs 61.3% and 35.8% with 3+ to 4+ MR (n = 41; p = 0.003). Cause of death was available in 72.3% (60 of 83) of late deaths, with 42.2% (35 of 83) attributed to cardiac causes and 30.1% (25 of 83) noncardiac.
Conclusions: Mortality for IMR remains high despite surgical management and may be related to risk factors for progression of coronary artery disease. Despite repair, MR progresses in many patients and is associated with poor survival, although more detailed prospective data are needed to characterize this relationship.
The incidence of functional ischemic mitral regurgitation (IMR) in the setting of ischemic heart disease has been reported to be as high as 50%, although the cause of MR in patients with coronary artery disease may be heterogeneous, thus complicating its prognostic significance [1–3]. The presence of IMR portends a much worse prognosis after a Q-wave myocardial infarction (MI), with 5-year mortality of 62% and 39% with and without IMR, respectively [2]. Even mild degrees of MR after an MI have been associated with a significant increase in long-term mortality [4, 5]. Furthermore, there has been a clear graded independent association between the degree of IMR and the development of congestive heart failure after an acute MI [4].
Unfortunately, the treatment of IMR remains challenging, and the late survival for these patients has been generally poor [1, 2, 4–10]. Although mitral valve repair has been an essential component of this management, some studies with mixed populations of patients who had moderate and moderate-severe IMR demonstrated similar 5-year survival for patients undergoing coronary artery bypass grafting (CABG) or CABG with mitral valve repair [11, 12]. In addition, operative mortality for CABG plus mitral valve repair has ranged from 8.8% to 21% compared with operative mortality of 2% to 9% for patients undergoing CABG alone. However, a propensity analysis study from our institution demonstrated similar operative mortality between the two groups when matched for comorbidities and degree of MR [15]. Unfortunately, most groups have demonstrated poor long-term outcomes among patients undergoing mitral valve repair, with many studies reporting 5-year mortality of 40% to 50% [11, 13–18].
The purpose of this study was to analyze the mortality and morbidity associated with mitral valve repair among patients with IMR and to identify characteristics associated specifically with operative and long-term mortality. A further goal was to examine postoperative echocardiographic data as it relates to late mortality, hypothesizing that MR progression is a poor prognostic marker for these patients.
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Patients and Methods |
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Perioperative risk factors and demographics were determined from the database and supplemented by chart review. Postoperative data were collected from patients' hospital charts. Echocardiographic data were collected from patients' charts and hospital records. The data were supplemented by interviews with primary care physicians and cardiologists. Strategies for surgical revascularization and for choice of mitral prosthesis were at the discretion of the surgeon. Mortality data were obtained from chart review and supplemented from the United States Social Security Death Index database, physician interview, and review of death certificates.
Preoperative and postoperative echocardiographic data were recorded. In most instances, the assessment of the degree of MR was made by a third-party cardiologist uninvolved in the clinical care of the patient. Based on echocardiography, MR severity was graded as absent (0+), trace (1+), mild (2+), moderate (3+), or severe (4+).
Statistical Analysis
Statistical analyses were performed with SPSS 11.0 software (SPSS Inc, Chicago, IL). Univariate analyses was performed for all relevant categoric variables by using contingency tables (
2 or Fisher exact tests for variables with small expected cell numbers) and t tests or the Mann-Whitney U test for continuous variables. Continuous data were reported as the median with the interquartile range (25th to 75th quartile). Multivariate analyses were performed using a stepwise logistic regression, in which all variables with a value of p < 0.10 in the univariate analyses or that were thought to be related were included in the initial full models. A value of p < 0.05 was considered significant.
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Results |
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There were 26 operative deaths for an operative mortality of 10.1%. The operative mortalities were attributed to cardiac causes in 65.4%, neurologic causes in 15.4%, pulmonary causes in 11.5%, and other causes in 7.7%. By multivariate analysis, only previous CABG was associated with operative mortality (n = 42), with an odds ratio of 3.072 (95% confidence interval, 1.254 to 7.525; p = 0.019). However, operative mortality for patients with postoperative stroke was 29.4% (5 of 17) and total mortality was 70.6% (12 of 17) during the length of the study. The operative mortality rate for elective cases of 9.0% (18 of 199) was not significantly different vs 13.8% (8 of 58) for urgent/emergency cases (p = 0.3).
Total overall mortality was 42.4% with mean follow-up of 3.2 ± 2.4 years. Kaplan-Meier analysis revealed 68.3% and 52.0% overall survival at 3 and 5 years, respectively (Fig 2). Late death was analyzed separately (n = 231), excluding operative deaths. Table 3 outlines factors associated with late death by multivariate analysis. Previous CABG, operative era, mitral valve ring size, and use of a full ring vs a band were not found to be significant prognostic factors. Cause of death was available in 72.3% (60 of 83) of late deaths, with 42.2% (35 of 83) attributed to cardiac causes such as MI or progressive heart failure, and 30.1% (25 of 83) were noncardiac. Preoperative left ventricular (LV) end diastolic pressure was available in 53.7% (138 of 257) of patients and was not found to be a significant predictor of decreased survival (p = 0.2).
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Comment |
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Similarly, Mihaljevic and colleagues [19] identified severe lateral wall motion abnormality and renal insufficiency as risk factors for death after CABG and mitral valve repair in patients with 3+ to 4+ IMR and also suggested a relationship between progressive coronary artery disease and the dismal prognosis associated with IMR. These data emphasize the importance of early and complete revascularization in this group of patients to prevent the loss of viable myocardium that ultimately contributes to ventricular remodeling and MR.
The operative mortality of 10.1% in this study is congruent with other reported rates ranging from 8.8% to 21% [12–14, 20]. The only risk factor for operative mortality in this group was redo operation. Although the stroke rate was only 6.6%, the mortality rate of 70.6% in these patients highlights the importance of stroke prevention in the operative and perioperative period.
A significant concern raised by this and other studies is the progression of MR after repair and the associated poor prognosis. In this study, 25% had 3+ to 4+ MR on the most recent echocardiogram, with actuarial 5-year survival in this group of 36%. Previously reported rates of recurrent moderate to severe MR after repair range from 17% to 37%, although varying patient characteristics and often limited postoperative echocardiography follow-up contribute to the variability between studies [7, 19, 21, 22]. Mechanisms involved in the deterioration of mitral valve function include continued LV remodeling and progressive worsening of posterior leaflet tethering [23, 24].
Kuwahara and colleagues [24] have demonstrated that increased posterior leaflet tethering was the primary determinant for late MR after annuloplasty and recommended further downsizing of the annuloplasty device to accommodate for such tethering. Braun and colleagues [20] demonstrated 2-year actuarial survival of 85.6% with strict downsizing by two ring sizes, with no progression to 3+ to 4+ MR at 18 months of follow-up. Like other studies, however, ours failed to demonstrate a clear association between band or ring size and recurrent MR [25]. Furthermore, mitral valve ring size was not found to be associated with prognosis in this study, and some reports have questioned whether undersized annuloplasty provides any long-term survival benefit compared with revascularization alone [19, 26].
Division or elongation of secondary cords may prove to be a beneficial adjunct to annuloplasty as a method to prevent late recurrent MR, although data are limited on this point [27]. Other techniques or devices that directly impact reshaping of the left ventricle may provide survival benefit, although current data are limited [7]. Pre-revascularization variables that may factor into the progression of MR include the presence of extensive myocardial scar and the volume and location of viable myocardium [28].
This study was plagued by many of the same limitations reported in other retrospective, nonrandomized, single-institutional studies. This study addressed only those patients that underwent mitral valve repair for IMR and does not address those that were either treated medically or those that underwent CABG alone. We previously published a propensity analysis that demonstrated no difference in operative mortality or long-term survival between patients undergoing CABG with mitral valve repair vs a matched group undergoing CABG alone for IMR [13]. In addition, follow-up echocardiographic data were only available in 57% of patients at 20 ± 25 months. Given our wide referral base and the length of the study, there is likely wide variability in the interpretation of echocardiographic data performed at many different institutions by different cardiologists. Other studies have discussed the impact of recurrent postoperative MR with less than 50% follow-up echocardiographic data, although other contemporary series have provided more complete follow-up echocardiographic data [20, 25, 29, 30].
Furthermore, the Survival and Ventricular Enlargement (SAVE) trial demonstrated that ejection fraction was similar between post-MI patients with and without mild MR, but that patients with mild MR had larger end-systolic and end-diastolic volumes and more spherical ventricles, with a significant increase in cardiac-related death [5]. More complete echocardiographic follow-up that also includes more detail regarding LV geometry and remodeling may allow for identification of surrogate markers that predict more rapid progression of disease.
An additional limitation of this study that is an essential component of management of these patients is evaluation of adequacy of medical therapy, including the routine use of β-blockers, angiotensin-converting enzyme inhibitors, and statins. These agents play an important role in the treatment of patients with ischemia and LV dysfunction and should be an important part of any trial that studies these patients [26].
Studies with detailed preoperative echocardiographic data have identified LV end-diastolic dimension as the single most important factor in predicting reverse remodeling and progression of MR postoperatively [20, 30]. The variability in long-term outcomes between studies in the literature may be related to selection of patients with widely variant LV end-diastolic dimensions although, as in our study, these data are not always available or incomplete.
Despite the limitations, this study reaffirms the grave prognosis associated with significant IMR and identifies predictors of early and late death. These data emphasize the role of progressive coronary disease to the pathology in these patients and again demonstrate that despite repair, MR progresses in some patients and is associated with poor survival. Our current practice involves measuring the intertrigonal distance to size the annulus and downsizing the device by at least two sizes at the time of annuloplasty. Our data, consistent with other reports, failed to demonstrate a clear association between ring size, or downsizing, and the progression of MR or late death. These results, in association with others demonstrating poor long-term survival, as well as recent publications questioning the benefit of the addition of mitral valve repair to revascularization, emphasize the importance of developing alternative therapies and multicenter trials to deal with this complex problem [19].
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Discussion |
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First, if we address the adverse prognosis, it seems that extreme preoperative risk profiles are a fundamental feature of ischemic MR and perhaps are the major factor accounting for the poor prognosis. Your average age was 66 years compared with 60 for standard coronary bypass. Your mean ejection fraction was 35%, and 46% for your patients who had pulmonary hypertension. These values are virtually identical to Don Glower's paper presented at the AATS [American Association for Thoracic Surgery] a few years ago (J Thorac Cardiovasc Surg 2005;129:860–8), and when Don adjusted for differences in baseline characteristics, it turned out that the 8-year risk-adjusted survival after repair was statistically similar for ischemic and prolapse patients. This finding has been confirmed since by The Cleveland Clinic and also in a recent excellent paper from Virginia. Additionally, Dr Carmelo Milano has another study in the upcoming STS [Society of Thoracic Surgeons] meeting using coronary bypass patients as the reference, but showing virtually the same thing. So have you looked at risk-adjusted data to see how much of the problem is related to the elderly and sick baseline profiles of ischemic MR patients?
Second, there seems to have been an excessive recurrence rate with flexible rings in a lot of studies, like the Duran ring [Medtronic, Minneapolis, MN], and perhaps full rigid rings are associated with better outcomes by more closely approximating the anterior-posterior valvar dimension, as the Stanford group would suggest. In fact, in the Glower study the reoperation rate was only 2%, and moderate recurrence was 9% over 8 years with full rings. Thus, did there seem to be any association between flexible rings and recurrent MR?
Third, the 9% of patients experiencing recurrence in Glower's study uniformly had evidence of preoperative leaflet tethering or very poor LV function predisposing to tethering. In those patients I currently am adding a posterior leaflet pericardial gusset to the ring annuloplasty, but as discussed in the Virginia paper, other ancillary procedures also may be effective. At this point in time what are you doing to compensate for potential leaflet tethering in these patients at the time of repair?
And finally, IMR patients are more susceptible to postoperative complications that contribute significant to mortality, complications like the 13% incidence of pneumonia in your series. We now are focusing on immune dysfunction as a cause of complications in these patients, and it was an epiphany to find that many have very low immunoglobulin G levels postoperatively associated with and perhaps contributing to pulmonary dysfunction/multiorgan failure syndrome. As we published 2 years ago (J Heart Valve Dis 2005;14:783–91), administering intravenous immunoglobulin postoperatively in this setting has been very effective in reversing multiorgan failure, and our operative mortality now may be approaching zero. So perioperative care is very important in these critically ill patients, and are there other innovations coming from Marin Kollef's institution to prevent ventilator-acquired pneumonia and minimize postoperative complications?
Again, congratulations on an excellent paper, and I would like to thank the Association for the privilege of discussing it.
DR CRABTREE: Dr Rankin, thank you very much for those comments and questions. We have compared ischemics and nonischemics, and for the sake of time, I didn't have the opportunity to present that data today. We had a cohort of about 540 patients who underwent repair of MR for nonischemic causes, and consistent with your previously published results, there was a significant difference in both operative and late mortality that was related to relatively higher preoperative comorbidity in the ischemic group. The ischemic patients were much older, had more comorbidities, worse heart function, and more severe heart failure symptoms preoperatively. So I agree with you that a direct comparison of degenerative MR to ischemic MR without risk adjustment is essentially like comparing apples to oranges. This comparison, however, was not the focus of our paper. There has been a concern that maybe our cardiology colleagues have somehow had a bias against referring patients with MR related to ischemia compared with nonischemic causes of MR because of the mortality associated with the ischemic patients. I don't know how much of that is really happening, but the mortality differential has more to do with higher preoperative comorbidity and severity of illness in the ischemic group rather than some intrinsic component of the mitral valve in the ischemics.
In terms of the reoperation rate comparing ischemics and nonischemics, our reoperation rate in the ischemic patients was around 1% to 2%. I think this is a difficult thing to compare between ischemics and nonischemics, because they are completely different populations. The 60-year-old that undergoes repair for degenerative disease and develops recurrent MR from presumed failure of the repair is certainly different than the 70-year-old with ischemic MR with multivessel coronary artery disease and LV dysfunction. The patterns of failure are different for ischemic MR and are often related to ventricular dysfunction rather than a failure of repair. Such progression of LV dysfunction in addition to the higher comorbidity index in these patients also changes the threshold for reoperation compared with the nonischemic group.
Our group has really not been enthusiastic about adding subvalvular procedures to annuloplasty in the ischemic patients. I know the Toronto group recently published a small series on chordal cutting. I know Dr Kron's recent paper from UVA [University of Virginia] to which you were referring performed papillary muscle translocation in about 29% of patients with ischemic MR with good overall results. We remain skeptical about these subvalvular techniques given the limited data and the fact that these still seem to be valvular treatments for a ventricular problem.
Regarding postoperative complications, I am particularly concerned with our 6.6% stroke rate and the dramatic mortality associated within this subgroup. I think patient selection and more frequent utilization of epiaortic echocardiography as we progress with our experience may play a role in decreasing that. Certainly it would help our overall mortality as well.
DR KIT V. AROM (Bangkok, Thailand): I enjoyed your paper very much and would like to make couple of comments and ask few questions. I realize that this is a retrospective review, and the results may not represent the current treatment method for ischemic MR, but could possibly suggest that the operative technique used in this study may not be an appropriate one.
Your mortality rate of nearly 50% at 2.8 years is almost equal to the death rate of chronic ischemic mitral valve treated with medical means. As ischemic mitral valve disease is an imbalance of the entire mitral valve–ventricular complex, including the valve, valvular apparatus, and left ventricular wall, the long–term benefit of surgical correction of ischemic mitral valve therefore depends on whether myocardial dysfunction can be reversed and/or the mitral valve–ventricular complex could be corrected and improved by surgical means. The procedure you used in this presentation does not seem to correct the problem.
I have three questions: First, were the people you operated on acute or chronic mitral regurgitation? Second, did you look at the viability of the myocardium prior to surgery? Third, in your multivariate analysis did you or did you not include the severity of coronary artery disease and regional wall motion score? I believe these two variables could be even more important in predicting mortality than even age and diabetes.
DR CRABTREE: What was the last question? I am sorry I could not hear you very well.
DR AROM: Did you include the severity of coronary artery disease and regional wall motion score in your multivariate analysis?
DR CRABTREE: The majority of patients had chronic ischemic MR although some had acute MR related to wall motion abnormalities. We did not include patients with acute chordal rupture or papillary muscle rupture.
I agree with you that the severity of coronary disease is an important prognostic factor as well. Approximately 45% of ischemic patients had 3-vessel disease, while 74% had a previous MI. We did not, however, further stratify patients based on the degree of stenoses or on the quality of targets and runoff. This would be interesting to look at in the future.
I also agree with you that myocardial viability is a critical component of predicting who will most likely benefit from MV repair. Unfortunately, viability studies were performed infrequently and we do not have adequate data on this for analysis.
Other groups have shown that preoperative viability assessment and progression of LV dysfunction both regionally and globally impact the outcome of patients with ischemic MR. This again emphasizes that this is a ventricular disease rather than a valvular disease. Preoperative left ventricular dimension, for instance, may guide the decision to perform ventricular reconstruction in some of these patients. I think attention to the ventricle similar to NYU's [New York University] utilization of the Coapsys [Myocor Inc, Maple Grove, MN] device and I believe one of the very good papers from the Netherlands using the CorCap [Acorn Cardiovascular, St Paul, MN] device in patients with a very large preoperative left ventricular dimension are important steps. So I think this is the direction that we should be going in patients with ischemic MR.
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