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J Thorac Cardiovasc Surg 2008;136:442-447
© 2008 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Determinants of early decline in ejection fraction after surgical correction of mitral regurgitation

^a Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minn
^b Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minn

Received for publication July 16, 2007; revisions received October 11, 2007; accepted for publication October 22, 2007.

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

	Abstract

Top Abstract Introduction Materials and Methods Results Discussion Conclusions References

 
Objective: We sought to echocardiographically examine the early changes in left ventricular size and function after mitral valve repair or replacement for mitral regurgitation caused by leaflet prolapse.

Methods: Preoperative and early postoperative echocardiograms of 861 patients with mitral regurgitation caused by leaflet prolapse who underwent mitral valve repair or replacement (with or without coronary revascularization) were studied. Among the patients, 625 (73%) were men and 779 (90%) had mitral valve repair.

Results: The rate of valve repair increased from 78% in the first decade of the study to 92% in the second decade. At early echocardiography (mean, 5 days postoperatively), we observed significant decreases in left ventricular ejection fraction (mean, –8.8) and left ventricular end-diastolic dimension (mean, –7.5). The magnitude of the early decline in ejection fraction was similar in patients who had mitral valve repair and replacement. The decrease in postoperative ejection fraction was independently associated with a lower preoperative ejection fraction, the presence of atrial fibrillation, advanced New York Heart Association functional class, greater left ventricular end-diastolic and end-systolic dimensions, and larger left atrial size.

Conclusion: Surgical correction of mitral regurgitation results in an early decrease in ejection fraction, particularly in symptomatic patients with increased left heart dimensions.

	Introduction

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Surgical correction of mitral regurgitation may lead to an early postoperative decline in left ventricular ejection fraction,^1-3 but studies addressing this phenomenon are limited to echocardiographic data obtained several weeks to years⁴ postoperatively. Few data characterize the changes in cardiac size and function in the early postoperative period. Furthermore, there is uncertainty about the magnitude of these changes and how soon they occur after mitral valve surgery,^5,6 together with the predisposing clinical and hemodynamic variables. Also, many of the reports from studies of ejection fraction change after mitral valve surgery have used data collected from patients who had mitral valve replacement. Whether a similar decrease occurs after mitral valve repair is controversial.^1,4,7-12 Finally, it has been suggested that maintenance of chordal continuity between the left ventricular wall and the leaflets during mitral valve replacement is essential to attenuate this decrease^13-15 or even increase postoperative ejection fraction.

The objective of this study was to examine the changes in left ventricular size and function that occur early after mitral valve surgery for correction of mitral regurgitation caused by leaflet prolapse.

	Materials and Methods

Top Abstract Introduction Materials and Methods Results Discussion Conclusions References

 
We reviewed the clinical and echocardiographic data of patients who underwent primary surgical correction (repair or replacement) for mitral regurgitation caused by leaflet prolapse. The study was approved by the Mayo Clinic Institutional Review Board. The primary inclusion criterion was the availability of measurements of left ventricular ejection fraction preoperatively (within 6 months of surgery) and early postoperatively. We included patients who had concomitant coronary artery bypass graft surgery or closure of a secundum atrial septal defect or patent foramen ovale. The study population included patients with mitral disease caused by fibroelastic deficiency and patients with myxomatous degeneration. We excluded patients who declined involvement in clinical research, who had previous mitral valve surgery or concomitant cardiac procedures, and who had a primary diagnosis of mitral regurgitation caused by congenital or ischemic heart disease or by other forms of cardiomyopathy. Also excluded were patients with significant mitral valve stenosis and patients with endocarditis causing leaflet destruction or subvalvar abscess at the time of primary mitral valve repair.

Between January 1, 1980, and December 31, 2000, a total of 2219 patients underwent surgical correction of mitral regurgitation at Mayo Clinic in Rochester, Minnesota. Among these patients, 861 met the study criteria. The mean (± standard deviation) period between surgery and postoperative echocardiography was 5 ± 1.8 days. Of the 861 patients, 779 underwent mitral valve repair and 82 underwent mitral valve replacement.

Surgical Procedure
During the 20-year study period, the indications for operation and the surgical methods evolved. During the second decade of the study, a strategy of earlier mitral valve repair for mitral regurgitation caused by leaflet prolapse was adopted on the basis of quantitative echocardiographic criteria.¹⁶ The lesion for which patients most frequently underwent surgical correction of mitral regurgitation at Mayo Clinic was isolated posterior leaflet prolapse of the middle scallop, caused by chordal elongation or chordal rupture. The most common repair that was performed was triangular partial resection and suture repair of the involved portion of the posterior leaflet, supplemented by a standard length (63 mm) of flexible posterior annuloplasty band.^17,18 In the first decade of the study, anterior leaflet prolapse was corrected by various techniques, including chordal shortening, chordal transfer, and commissural annuloplasty. In the current era (1990s and beyond), we have preferred the insertion of artificial neochordae (expanded polytetrafluorethylene; Gore-Tex; WL Gore & Associates, Flagstaff, Ariz) for repair of anterior leaflet prolapse.^19,20

Among the 82 patients who underwent mitral valve replacement, 46 (56%) received a mechanical valve and 36 (44%) received a bioprosthesis. During valve replacement, chordal preservation of the posterior leaflet was documented in 77 patients (94%).

Statistical Analysis
Group statistics were expressed as the mean ± 1 standard deviation. Categoric variables were compared between the groups using the chi-square test for independence. Two-sample t tests or Wilcoxon rank-sum tests were used to compare continuous variables between the groups. Univariate and multivariate predictors of predismissal ejection fraction were determined using linear regression models. Multivariate models were constructed in 2 stages. In the first stage, only clinical variables and preoperative ejection fraction were included as possible predictors, and a stepwise selection technique was used to construct the final model. In the second stage, the importance of echocardiographic variables was analyzed; this analysis was necessary to account for the inability to collect all measurements from each study. Each of the second-stage variables was forced into the final clinical model to determine importance. P values of less than .05 were considered significant.

	Results

Top Abstract Introduction Materials and Methods Results Discussion Conclusions References

 
Baseline characteristics are shown in Table 1 for all 861 patients and the 2 treatment groups (mitral valve repair and mitral valve replacement). Compared with patients who had mitral valve replacement, the patients who underwent mitral valve repair were younger, had a lower incidence of preoperative atrial fibrillation, and were more likely male. The repair group was also slightly less symptomatic and less likely to have significant coronary artery disease but more likely to have isolated posterior leaflet prolapse. Preoperative ejection fraction and left heart dimensions were similar between the 2 groups.

	Discussion

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This series analyzed a relatively homogeneous population of patients who had surgical correction of mitral regurgitation solely caused by isolated degenerative mitral leaflet prolapse. Although other studies have also reported that ejection fraction is diminished after correction of mitral regurgitation, there has been considerable variability in the timing of the studies that documented the change in left ventricular ejection fraction. Also, there has been debate on whether the postoperative decrease in left ventricular ejection fraction is influenced by the type of procedure performed.^7-11 In our study, the mean interval between operation and echocardiography before dismissal was 5 days. Ren and colleagues⁸ analyzed intraoperative echocardiograms in 50 patients and found that ejection fraction was better preserved after mitral valve repair than after mitral valve replacement. However, if the assumption is made that forward stroke volume remained constant before and after surgery, the reported change in left ventricular end-diastolic and end-systolic volumes suggests that preoperative mitral regurgitation in patients who had mitral valve repair was not severe (ie, >60 mL/beat), which may partially explain the difference between our two studies. In addition, our assessment of ventricular function occurred at a mean of 5 days after surgery, and normalization of hemodynamic and neurohumoral imbalances may have occurred since the time of operation. Le Tourneau and colleagues⁷ studied patients who underwent mitral valve repair or mitral valve replacement for myxomatous or rheumatic heart disease at a mean of 216 days after surgery and found that left ventricular ejection fraction was preserved by repair but not by replacement. Corin and colleagues⁹ reported similar findings at a mean of 22 months after surgery.

Several other studies have reported that mitral valve replacement is associated with a decrease in left ventricular ejection fraction of approximately 10 units postoperatively^7-11 and suggested that the magnitude of this decrease might be attenuated by chordae-sparing valve replacement.^13-15,21 Goldman and colleagues¹¹ suggested that intraoperative left ventricular ejection fraction remained stable after mitral valve repair. Harpole and colleagues²² suggested that partial resection of the subvalvar apparatus during mitral replacement did not significantly diminish early left ventricular function. In our study, the decrease in left ventricular ejection fraction after mitral valve replacement for mitral regurgitation was similar to that reported by other investigators despite the fact that chordal preservation was documented in 94% of patients, and a similar decrease was seen after mitral valve repair.

Our data suggest that considerable early reverse cardiac remodeling occurs early after correction of mitral regurgitation ( Figure 1). We observed, as have others,²³ that LVEDD significantly decreased early after correction of mitral regurgitation, whereas LVESD remained relatively unchanged.^5,24 Other investigators have also shown that left atrial dimension decreased early after mitral valve surgery,^25-27 as we found. We have no mechanistic data in this study to indicate whether cellular or molecular alterations accompany early reverse geometric remodeling. However, other investigators have suggested that these changes may occur.²⁸ This question will be the subject of future investigations.

View larger version (34K): [in this window] [in a new window]   Figure 1. Early ventricular remodeling. Diagrammatic representation of early changes in left ventricular (LV) volume and ejection fraction (EF) after surgical correction of severe chronic mitral regurgitation (MR). A, Normal heart ejecting typical stroke volume of 60 mL. LV end-diastolic volume (LVEDV) of 100 mL and LV end-systolic volume (LVESV) of 40 mL generate an observed EF of 60%. LVEDD of normal heart (solid line). B, Severe chronic MR leads to increase in left heart dilatation and LV capacity to maintain forward stroke volume of 60 mL per beat while losing an additional 60 mL per beat into left atrium. Increases in LVEDV to 180 mL and LVESV to 60 mL lead to apparent preservation of EF at 66%. LVEDD with increased dimension (dotted line) caused by severe chronic MR (LVEDD + x). C, Early after correction of MR (leaflet repair plus posterior annuloplasty band), atrial runoff is eliminated. To maintain normal forward stroke volume of 60 mL per beat, LVEDV decreases while LVESV remains constant. Because LVEDV is still increased compared with normal volume, EF declines to limit stroke volume. LVEDD + x (dashed line) that has been decreased because of early postoperative remodeling (LVEDD + x – y). (Used with permission of Mayo Foundation for Medical Education and Research.) LVEDV, Left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; EF, ejection fraction.

Further, we found that greater degrees of left heart dilatation (ie, LVEDD, LVESD, and left atrial size) were associated with lower postoperative left ventricular ejection fraction. Prior investigations have also established that left ventricular enlargement is associated with both diminished ejection fraction^4,5,23 and poorer long-term survival.^1,4,12,30 However, the current study is the first documentation of the early postoperative change in ejection fraction in a population of patients with mitral regurgitation caused by isolated leaflet prolapse. The independence of left ventricular systolic and diastolic dimensions and left atrial size in predicting postoperative ejection fraction is interesting and requires further study.

On the basis of the data we have collected in this study, we cannot comment specifically as to whether left ventricular contractility is also affected by these clinical factors, recognizing that contractility correlates poorly with static ejection fraction measurements. Several historic reports have addressed contractile function after surgery, however Kouchoukos³¹ found that the elimination of severe chronic, simulated mitral regurgitation led to an increase in left ventricular afterload and elevated end-diastolic pressure in dogs. He suggested that similar changes after the elimination of chronic mitral regurgitation in humans may predispose patients with impaired preoperative left ventricular contractility to cardiac dysfunction postoperatively. Rankin and colleagues³² further developed this concept, proposing that the acute increase in afterload after the surgical procedure may be responsible for impaired postoperative ventricular function in patients with a "chronically depressed left ventricle." Spratt and colleagues³³ suggested that the decrease in cardiac output after surgical correction of mitral regurgitation might not be fully explained by the increase in afterload, proposing that myocardial fibrosis and intraoperative injury might also be important. Starling⁶ demonstrated that left ventricular contractility (measured by left ventricular chamber elastance) may actually increase despite a decrease in ejection fraction after correction of mitral regurgitation. He concluded that early mitral valve repair before ejection fraction decline or left ventricular dilation is important to allow improvement in contractility after surgery.

We propose that the early postoperative decline in ejection fraction may be explained as a volumetric adjustment to the elimination of mitral regurgitation in patients with left ventricular dilatation. With severe chronic mitral regurgitation, ventricular enlargement compensates for regurgitant volume into the left atrium; left ventricular capacity increases, expanding LVEDD and LVESD while maintaining normal left ventricular ejection fraction. Soon after the surgical correction of mitral regurgitation and the elimination of regurgitant volume, increased efficiency of antegrade cardiac pumping could as much as double the stroke volume if ejection fraction was preserved and cardiac volumes were unchanged. To maintain near-normal forward aortic stroke volume, left ventricular diastolic volume decreases, but not enough to preserve left ventricular ejection fraction in the early postoperative period.

Limitations
Our study has the typical limitations associated with retrospective reviews. Patients in this study were selected because of the availability of early postoperative echocardiograms. Those patients who did not survive to have postoperative echocardiography are obviously missing from the series.

Clinical Implications
Our data suggest that the early change in left ventricular ejection fraction after surgical correction of mitral regurgitation can be explained by compensatory alterations in left ventricular volume and dimension. The fear that surgery might result in a prohibitively large decline in ejection fraction postoperatively should not be used as justification to deny patients an operation. Rather, it is likely that patients who undergo early surgical correction of mitral regurgitation with favorable clinical and echocardiographic characteristics are more likely to have optimal recovery of normal left ventricular geometry and function in the early postoperative period.

	Conclusions

Top Abstract Introduction Materials and Methods Results Discussion Conclusions References

 
Left ventricular ejection fraction decreases early after correction of mitral regurgitation caused by leaflet prolapse, and this decrease occurs to a similar extent in patients who have mitral valve repair or mitral valve replacement. Preoperative predictors of a decrease in ejection fraction after correction of mitral regurgitation include 1) significant symptoms or atrial fibrillation and 2) larger left heart dimensions (ie, LVESD, LVEDD, and left atrial size).

Editing, proofreading, and reference verification were provided by the Section of Scientific Publications, Mayo Clinic.

	Footnotes

 
Dr Sarano reports consulting, lecture fees, and grant support from Edwards Lifesciences.

	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 Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Rakesh M. Suri Hartzell V. Schaff Joseph A. Dearani Thoralf M. Sundt, III Richard C. Daly Charles J. Mullany Thomas A. Orszulak Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Suri, R. M. Articles by Orszulak, T. A. Search for Related Content PubMed Articles by Suri, R. M. Articles by Orszulak, T. A. Related Collections Cardiac - other Valve disease