doi: 10.1161/01.CIR.0000138192.65015.45
(Circulation. 2004;110:II-85 – II-90.)
© 2004 American Heart Association, Inc.
Surgery for Valvular Heart Disease |
Mechanism of Recurrent Ischemic Mitral Regurgitation After Annuloplasty
Continued LV Remodeling as a Moving Target
From the Cardiac Ultrasound Laboratory (J.H., L.P., R.A.L.), Massachusetts General Hospital, Boston; and the International Heart Institute of Montana and University of Montana (S.A.T., B.G.H., B.A.B., C.M.D.), Missoula.
Correspondence to Judy Hung, MD, Cardiac Ultrasound Laboratory-VBK 508, Massachusetts General Hospital, Boston, MA 02114. E-mail Jhung{at}partners.org
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Abstract |
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Background— Patients who undergo ring annuloplasty for ischemic mitral regurgitation (MR) often have persistent or recurrent MR. This may relate to persistent leaflet tethering from left ventricle (LV) dilatation that is not relieved by ring annuloplasty. Therefore, the purpose of this study was to test the hypothesis that recurrent MR in patients after ring annuloplasty relates to continued LV remodeling.
Methods and Results— Serial echoes were reviewed in 30 patients (aged 72±11 years) who showed recurrent MR late (47±27 months) versus early (3.8±5.8 months) after ring annuloplasty for ischemic MR during coronary artery bypass grafting without interval infarction. Patients with intrinsic mitral valve disease were excluded. Echocardiographic measures of MR (vena contracta and jet area/left atrial area) and LV remodeling (LV dimensions, volumes, and sphericity) were assessed at each stage. The degree of MR increased from mild to moderate, on average, from early to late postoperative stages, without significant change in LV ejection fraction. Changes in MR paralleled increases in LV volumes and sphericity index at end-systole and end-diastole. The only independent predictor of late postoperative MR was LV sphericity index at end-systole.
Conclusions— Recurrent MR late after ring annuloplasty is associated with continued LV remodeling, emphasizing its dynamic relation to the LV.
Key Words: mitral regurgitation • ring annuloplasty • left ventricle remodeling
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Introduction |
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Ischemic mitral regurgitation (MR) results from remodeling of the ischemic left ventricle (LV), leading to displacement of the papillary muscles, annular dilatation, and therefore tethering of the mitral leaflets. This restricts mitral leaflet closure, preventing proper coaptation at the annulus.1–13
A standard therapeutic approach to relieve ischemic MR is a ring annuloplasty,14–19 which reduces mitral annular area by bringing the dilated posterior annulus anteriorly to reduce the anterior–posterior dimension and bring the leaflets into apposition. However, the long-term efficacy of ring annuloplasty is unclear. Recent studies in several centers have demonstrated that MR can persist or recur after ring annuloplasty, consistent with clinical observations.20–24 Given the fundamental mechanism of mitral leaflet tethering, ring annuloplasty addresses only the annular end and does not directly address tethering by the remodeled ventricle. Remodeling is progressive,25–30 so that initial annular compensation for ventricular dilatation may not be durable. Therefore, the purpose of our study was to test the hypothesis that recurrent MR after ring annuloplasty relates to continued LV remodeling.
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Methods |
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To explore the mechanism underlying persistent or recurrent MR after ring annuloplasty, we specifically targeted patients with persistent or recurrent MR after ring annuloplasty and CABG. The study population consisted of patients undergoing coronary artery bypass and mitral ring annuloplasty for moderate to severe MR at 2 institutions, International Heart Institute of Montana, University of Montana, Missoula, and Massachusetts General Hospital, Boston, for a 2-year period from 1996 to 1998. Rigorous criteria were applied to exclude patients with intrinsic mitral valve disease to select for a relatively homogeneous patient population with ischemic MR. Patients with mitral valve thickening, prolapse, annular calcification, vegetation, fenestration, and rheumatic mitral valve changes were excluded. Patients with echocardiograms inadequate for quantitative analysis were also excluded.
Echocardiographic Analysis
Echocardiograms were analyzed offline on a Philips 7500 SONOS machine (Philips Medical Systems). Quantitation of MR was performed at the preoperative, intra-operative, early postoperative, and late postoperative stages. Analysis of LV remodeling changes was performed at preoperative, early postoperative, and late postoperative stages.
Quantification of MR
MR was quantified by vena contracta and the maximal jet area-to-left atrial of area ratio.31–35 The width of the vena contracta or the narrowest jet origin was measured in a long-axis view perpendicular to the coaptation line, typically the parasternal or apical long-axis views. The maximal jet area-to-left atrial area ratio was measured in the parasternal and apical view. An average was taken of 3 cardiac cycles for each MR measurement.
LV Volumes
LV volumes were calculated using the biplane Simpson method from the apical 4- and 2-chamber views.36
LV Sphericity Index
To assess changes in LV shape, the sphericity index was calculated at end-diastole and end-systole as the volume of the LV divided by the volume of a sphere with a diameter equal to the LV longest axis (measured in the apical view). As this ratio increases and approaches 1, the ventricle becomes more spherical.3–5 The sphericity index is a surrogate measure of the degree of leaflet tethering because the more spherical the LV becomes, the greater the degree of papillary muscle displacement that exerts tethering on the leaflets.3–5,11
Papillary Muscle Displacement Distance Outside the Annular Ring
Papillary muscles normally exert forces perpendicular to the leaflet surfaces to oppose left ventricular forces.37 However, if the papillary muscles are displaced in a posterior and/or lateral direction, they will apply distracting forces that prevent normal leaflet coaptation.10 The projected papillary muscle displacement (PM-Dis) outside of the annular ring is a measure of the degree of displacement that can generate distraction forces by the papillary muscles. To measure this projected papillary displacement, a perpendicular line is drawn from the tip of the papillary muscle to the mitral annular line in a long-axis view. The distance of this projection to the mitral ring itself is the PM-Dis (Figure 1).
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Statistical Analysis
Repeated measures ANOVA was performed to determine differences among stages (preoperative, early postoperative, and late postoperative), with significance at P<0.05. To study the progression of MR in different patients, quantitative measures of MR were normalized for the preoperative degree of MR at baseline for the multiple linear regression analysis. The determinants of MR at the late postoperative stage were explored by multiple linear regression analysis in a step-wise manner, entering LV end-diastolic and end-systolic volumes, LV ejection fraction, sphericity index at end-diastole and end-systole, ring type, ring size, and early postoperative MR. Differences in late postoperative MR, normalized to initial MR (both maximal jet area-to-left atrial area ratio and vena contracta) were compared among ring types (complete semi-rigid, complete flexible, and incomplete flexible) by ANOVA. All statistical analysis was performed on SAS 6.12.
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Results |
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Patient Characteristics
The study population consisted of 30 patients (18 males and 12 females) with a mean age of 72±11 years. All underwent coronary artery bypass and mitral ring annuloplasty for moderate or severe MR. All patients had complete revascularization. Preoperative echocardiograms were performed at an average of 0.7±1 month, early postoperative echocardiograms were performed at an average of 3.8±5.8 months, and the later postoperative echocardiograms were performed at an average of 47±27 months. After bypass surgery and ring annuloplasty, no patient had a subsequent myocardial infarction or required additional revascularization.
Patients were managed medically after bypass surgery with standard heart failure medications including beta-blockers, angiotensin-converting enzyme inhibitors, and diuretics. The average ring size was 30±2 mm (range 26 to 34 mm). Forty percent were Carpentier-Edwards Physio rings, 33% were Duran-Medtronic Flexible rings, 14% Cosgrove rings, and 13% were St. Jude Medical Seguin rings.
Change in MR
At the preoperative stage, the average vena contracta width was 0.72±0.30 cm, corresponding to moderate to severe MR.34,35 At the intra-operative stage, immediately after bypass and ring annuloplasty, the average MR degree decreased to mild (vena contracta 0.24±0.24 cm). Frequently at the end of the operation, the MR was undetectable.24 At the early postoperative stage, the VC had increased to 0.35±0.31 cm, and at the time of the late postoperative stage, the average VC had increased to 0.50±0.37 cm (Figure 2). At the early postoperative stage, the majority of patients had only mild MR (70%), with only 30% having moderate or severe MR. However, at the time of the late postoperative stage, these proportions were reversed, with only 28% having mild MR and 72% have moderate or severe MR (Table 1). A similar pattern was found with MR quantification by jet area/left atrial area ratio (Figure 2).
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Changes in LV Volumes and Sphericity
The changes in MR were paralleled by changes in LV volumes (Figure 3) without concomitant change in LVEF (Figure 4). There was initial reduction in LV volumes at the early postoperative stage, followed by a significant increase at the late postoperative stage (Figure 3). Changes in sphericity index mirrored those of MR and LV volumes. There was an initial reduction in sphericity index both at end-diastole and end-systole in the early postoperative stage with a late increase, exceeding the preoperative value, consistent with further remodeling after ring annuloplasty (Figure 5). Table 2 summarizes the MR, LV volume, and LV sphericity changes. Figure 6 shows an example of the changes in LV volume and shape that occurred in a patient. At the early postoperative stage, the LV, although dilated with a left ventricular dimension of 58 mm, retains its bullet shape. At this early stage, the patient has little leaflet tethering and only mild MR (Figure 6A and 6B). However, at the late postoperative stage, the LV has further dilated (left ventricular dimension=73 mm) and become more spherical, resulting in increased tethering of the mitral leaflets. The posterior leaflet has become restricted and tethered toward the posterior papillary muscle region as the wall underlying that papillary muscle bulges further posteriorly and outward (Figure 6C). This increased tethering has resulted in moderate MR (Figure 6D).
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The increases in sphericity index at the late postoperative stage reflect increased tethering on the mitral valve and greater displacement of the papillary muscles. Ring annuloplasty can potentially exacerbate papillary muscle displacement by increasing the distance from the papillary muscle to the mitral annulus (Figure 1). This projected PM-Dis increased from the early to the late postoperative stage, consistent with increased displacement of the papillary muscle outside the mitral annulus (Figure 1A).
Stepwise multiple linear regression analysis demonstrated that late postoperative end-systolic sphericity index was the only predictor of late postoperative MR (P=0.004, R2=0.41 for vena contracta and P=0.002, R2=0.43 for jet area/left atrial area ratio). Ring size and type of ring were not predictors of late postoperative MR in this model. ANOVA showed no significant difference in late postoperative MR among ring types (complete semi-rigid, complete, or incomplete flexible rings; P=0.11 for maximal jet area/left atrial area ratio, P=0.15 for vena contracta), although there are limited numbers within each subgroup.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionSummaryReferences |
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This study shows that recurrence of MR after ring annuloplasty is associated with continued LV remodeling, as demonstrated by increases in LV volumes and sphericity, which parallel the increases in MR after ring annuloplasty. Multiple linear regression analysis demonstrated that end-systolic sphericity index, which reflects global LV shape and volume, predicted late postoperative MR. Of note is that MR progression occurred from an early postoperative study acquired several months, on average, after the surgery, and therefore is not subject to the altered loading conditions widely recognized as reducing apparent MR severity intraoperatively.38
Mechanistic Insights
These results highlight the limitations of ring annuloplasty as sole therapy, because it reduces tethering only at the annular and not at the ventricular end. Progressive ventricular remodeling in ischemic heart disease can therefore increase tethering and worsen MR despite initial reduction. The ability of ring annuloplasty to compensate for ventricular tethering can then be overwhelmed by further ventricular remodeling.
This limitation is reflected by the increases in the projected papillary muscle displacement outside the annular ring (PM-Dis) from early to late postoperative stages. This displacement outside the annular ring has the potential to produce forces that distract the leaflets from effective coaptation.10,37 The papillary muscles are normally aligned directly over the mitral annular area to exert a perpendicular force on the mitral leaflets, producing normal coaptation.37 With ischemic LV distortion and lateral and/or posterior papillary muscle displacement, the papillary muscles now exert forces in an oblique direction, resulting in increased tethering and ineffective coaptation. Whether the papillary muscle is "in or out" of the mitral ring plane as assessed in standard 2-dimensional echocardiographic views may provide a rapid visual estimation of the degree of tethering.
Clinical Implications
Although successful acutely, ring annuloplasty did not prevent the recurrence of MR in these patients, especially when there was further ventricular remodeling. In fact, the majority of patients had mild MR at the time of the early postoperative study. Mild MR therefore may not be benign in this patient population if it contributes to continued remodeling, resulting in a vicious cycle in which MR begets more MR. There was no correlation between ring size or type and development of MR at the late postoperative stage in this study. However, in this study, markedly undersized rings were not placed, and the usefulness of restrictive or undersized ring annuloplasty warrants further investigation.39–41
One point of caution with annular ring reduction is demonstrated in Figure 1. Reducing annular size can potentially shift the posterior annulus farther anteriorly, increasing its displacement relative to the papillary muscles, which may actually, in principle, exacerbate tethering. This concern is highlighted by the common observation in patients with annular ring reduction that the posterior leaflet, under increased tethering, becomes nearly rigid, converting the valve effectively into a unicuspid valve with a restricted anterior leaflet as well.42
In addition to the use of rings, which may be undersized to compensate for persistent tethering, methods that reinforce the mitral annulus in the septal–lateral (anterior–posterior) dimensions43–45 also merit further exploration. The development and evaluation of therapies that directly address tethering may provide a more efficacious treatment for ischemic MR, either independently or more comprehensively in conjunction with ring annuloplasty.46–48
Limitations
This is a mechanistic study designed specifically to examine the mechanism underlying recurrent MR after ring annuloplasty and was not designed to address the overall frequency of recurrent MR. Tahta et al24 in a large single-center surgical series have reported an incidence of 
30% of recurrent moderate or greater MR over a 3-year follow-up period, with other smaller studies reporting higher frequencies of recurrent MR (moderate or greater) after ring annuloplasty.20,22,23 Future work is indicated to determine whether LV remodeling is attenuated in patients whose repair is successful long-term. In addition, this study did not address undersizing of rings or the 3-dimensional saddle shape of the mitral annulus. It is possible that use of a ring that better mimics the saddle shape of the annulus may better reduce the distance between papillary muscles and the medial and lateral edges of the annulus.
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Summary |
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Recurrent MR after ring annuloplasty relates to continued LV remodeling. Approaches that also alleviate ventricular remodeling could therefore potentially be part of a more comprehensive and effective management strategy for patients with ischemic MR.
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Acknowledgments |
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This study was supported by National Institute of Health grants K23 HL04504 (to Dr. Hung) and RO1 HL38176 and K24 HL67434 (to Dr. Levine) and by an American Society of Echocardiography grant-in-aid (to Dr. Hung).
This study was supported by National Institute of Health grants K23 HL04504 (to Dr. Hung) and RO1 HL38176 and K24 HL67434 (to Dr. Levine), and by an American Society of Echocardiography grant-in-aid (to Dr. Hung). We thank Gloria L. Healy for her expert technical assistance, and Lars C. Erickson, MD, MPH for his statistical expertise.
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References |
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1. Ogawa S, Hubbard FE, Mardelli TJ, Dreifus LS. Cross-sectional echocardiographic spectrum of papillary muscle dysfunction. Am Heart J. 1979; 97: 312–321.[CrossRef][Medline] [Order article via Infotrieve]
2. Godley RW, Wann S, Rogers EW, Feigenbaum H, Weyman AE. Incomplete mitral leaflet closure in patients with papillary muscle dysfunction. Circulation. 1981; 63: 565–571.
3. Kono T, Sabbah HN, Stein PD, Brymer JF, Khaja F. Left ventricular shape as a determinant of functional mitral regurgitation in patients with severe heart failure secondary to either coronary artery disease or idiopathic dilated cardiomyopathy. Am J Cardiol. 1991; 68: 355–359.[CrossRef][Medline] [Order article via Infotrieve]
4. Sabbah HN, Kono T, Rosman H, Jafri S, Stein PD, Godstein S. Left ventricular shape: a factor in the etiology of functional mitral regurgitation in heart failure. Am Heart J. 1992; 123: 961–966.[CrossRef][Medline] [Order article via Infotrieve]
5. Kono T, Sabbah NH, Rosman H, et al. Left ventricular shape is the primary determinant of functional mitral regurgitation in heart failure. J Am Coll Cardiol. 1992; 20: 1594–1598.[Abstract]
6. Kisanuki A, Otsuji Y, Kuroiwa R, et al. Two-dimensional echocardiographic assessment of papillary muscle contractility in patients with prior myocardial infarction. J Am Coll Cardiol. 1993; 21: 932–938.[Abstract]
7. Gorman RC, McCaughan JS, Ratcliffe MB, et al. Pathogenesis of acute ischemic mitral regurgitation in three dimensions. J Thorac Cardiovasc Surg. 1995; 109: 684–693.
8. Komeda M, Glasson JR, Bolger AF, Daughters GT, Maclsaac A, Osterle SN, Ingels NB Jr, Miller DC. Geometric determinants of ischemic mitral regurgitation. Circulation. 1997; 96 (suppl II): II-128–II-133.
9. Yiu SF, Sarano ME, Tribouilloy C, Seward J, Tajik J. Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction. A quantitative clinical study. Circulation. 2000; 102: 1400–1406.
10. He S, Fontaine A, Schwammental E, Yoganathan A, Levine RA. Integrated mechanism for functional mitral regurgitation. Leaflet restriction versus coapting force: in vitro studies. Circulation. 1997; 96: 1826–1834.
11. Otsuji Y, Handschumacher MD, Schwammenthal E, et al. Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation. Direct in vivo demonstration of altered leaflet tethering geometry. Circulation. 1997; 96: 1999–2008.
12. Otsuji Y, Handschumacher MD, Liel-Cohen N, Tanabe H, Jiang L, Schwammenthal E, Guerrero JL, Nicholls LA, Vlahakes GJ, Levine RA. Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: Three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation. J Am Coll Cardiol. 2001; 37: 641–648.
13. Messas E, Guerrero JL, Handschumacher MD, Chow C-M, Sullivan S, Schwammenthal E, Levine RA. Paradoxic decrease in ischemic mitral regurgitation with papillary muscle dysfunction: insights from three-dimensional and contrast echocardiography with strain rate measurement. Circulation. 2001; 104: 1952–1957.
14. Carpentier A. Cardiac valve surgery - the "French correction." J Thorac cardiovasc Surg. 1983; 86: 323–337.[Medline] [Order article via Infotrieve]
15. Jebara VA, Dervanian P, Acar C, Grare P, Mihaileanu S, Chauvaud S, Fabiani JN, Deloche A, Carpentier A. Mitral valve repair using Carpentier techniques in patients more than 70 years old. Early and late results. Circulation. 1992; 86 (5 Suppl): II53–II59.
16. Spencer FC, Galloway AC, Grossi EA, Ribakove GH, Delianides J, Baumann FG, Colvin SB. Recent developments and evolving techniques of mitral valve reconstruction. Ann Thorac Surg. 1998; 65: 307–313.
17. Grossi EA, Goldberg JD, LaPietra A, Ye X, Zakow P, Sussman M, Delianides J, Culliford AT, Esposito RA, Ribakove GH, Galloway AC, Colvin SB. Ischemic mitral valve reconstruction and replacement: comparison of long-term survival and complications. J Thorac Cardiovasc Surg. 2001; 122: 1107–1124.
18. Badhwar V, Bolling SF. Mitral valve surgery in the patient with left ventricular dysfunction. Semin Thorac Cardiovasc Surg. 2002; 14: 133–136.[CrossRef][Medline] [Order article via Infotrieve]
19. Szalay ZA, Civelek A, Hohe S, Brunner-LaRocca HP, Klovekorn WP, Knez I, Vogt PR, Bauer EP. Mitral annuloplasty in patients with ischemic versus dilated cardiomyopathy. Eur J Cardiothorac Surg. 2003; 23: 567–572.
20. Liel-Cohen N, Otsuji Y, Vlahakes GJ, Akins CW, Levine RA. Functional ischemic mitral regurgitation can persist despite ring annuloplasty: mechanistic insights. Circulation. 1997; 96: I–540.
21. Hung J, Handschumacher MD, Rudski L, Chow CM, Guerrero JL Levine RA. Persistence of ischemic mitral regurgitation despite annular ring reduction: mechanistic insights from 3D echocardiography. Circulation. 1999; 100: I–73.
22. Calafiore AM, Gallina S, DiMauro M, Gaeta F, Iaco AL, D’Allesandro S, Mazzei V, Di Giammarco G. Mitral valve procedure in dilated cardiomyopathy: repair or replacement. Ann Thorac Surg. 2001; 71: 1146–1152.
23. Lachmann J, Shirani J, Plestis KA, Frater RW, LeJemtel TH. Mitral ring annuloplasty: an incomplete correction of functional mitral regurgitation associated with left ventricular remodeling. Curr Cardiol Rep. 2001; 3: 241–246.[Medline] [Order article via Infotrieve]
24. Tahta SA, Oury JH, Maxwell JM, Hiro SP, Duran CM. Outcome after mitral valve repair for functional ischemic mitral regurgitation. J Heart Valve Dis. 2002; 11: 11.[Medline] [Order article via Infotrieve]
25. Kurrelmeyer K, Kalra D, Bozkurt B, Wang F, Dibbs Z, Seta Y, Baumgarten G, Engle D, Sivasubramanian N, Mann DL. Cardiac remodeling as a consequence and cause of progressive heart failure. Clin Cardiol. 1998; 21 (12 Suppl 1): I14—I19.[Medline] [Order article via Infotrieve]
26. Spinale FG. Novel approaches to retard ventricular remodeling in heart failure. Eur J Heart Fail. 1999; 1: 17–23.
27. Garrido MJ, Oz MC. New surgical treatments for heart failure. Curr Cardiol Rep. 2002; 4: 233–237.[Medline] [Order article via Infotrieve]
28. Moainie SL, Guy TS, Gorman JH 3rd, Plappert T, Jackson BM, St John-Sutton MG, Edmunds LH Jr, Gorman RC. Infarct restraint attenuates remodeling and reduces chronic ischemic mitral regurgitation after postero-lateral infarction. Ann Thorac Surg. 2002; 74: 444–449.
29. Hein S, Arnon E, Kostin S, Schonburg M, Elsasser A, Polyakova V, Bauer EP, Klovekorn WP, Schaper J. Progression from compensated hypertrophy to failure in the pressure-overloaded human heart: structural deterioration and compensatory mechanisms. Circulation. 2003; 107: 984–991.
30. Udelson JE, Patten RD, Konstam MA. New concepts in post-infarction ventricular remodeling. Rev Cardiovasc Med. 2003; 4 (Suppl3): S3–S12.
31. Helmcke F, Nanda NC, Hsiung MC, Soto B, Adey CK, Goyal RG, Gatewood RP Jr. Color Doppler assessment of mitral regurgitation with orthogonal planes. Circulation. 1987; 75: 175–183.
32. Tribouilloy C, Shen WF, Quere JP, et al. Assessment of severity of mitral regurgitation by measuring regurgitant jet width at its origin with transesophageal Doppler color flow imaging. Circulation. 1992; 85: 1248–1253.
33. Grayburn PA, Fehske W, Omran H, Brickner ME, Luderitz B. Multiplane transesophageal echocardiographic assessment of mitral regurgitation by Doppler color flow mapping of the vena contracta. Am J Cardiol. 1994; 74: 912–91734.[CrossRef][Medline] [Order article via Infotrieve]
34. Mele D, Vandervoot P, Palacios I, et al. Proximal jet size by Doppler Color Flow mapping predicts severity of mitral regurgitation. Clinical studies. Circulation. 1995; 91: 746–754.
35. Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA, Nihoyannopoulos P, Otto C, Quinones MA, Rakowski H, Stewart WJ, Waggoner A, Weissman NJ. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003; 16: 777–802.[CrossRef][Medline] [Order article via Infotrieve]
36. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. Am Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989; 2: 358–367.[Medline] [Order article via Infotrieve]
37. Perloff JD, Roberts WC. The mitral apparatus. Functional anatomy of mitral regurgitation. Circulation. 1972; 46: 227–239.
38. Aklog L, Filsoufi F, Flores KQ, Chen RH, Cohn LH, Nathan NS, Byrne JG, Adams DH. Does coronary artery bypass grafting alone correct moderate ischemic mitral regurgitation? Circulation. 2001; 104 (12Suppl1): I68–I75.
39. Bach DS, Bolling SF. Improvement following correction of secondary mitral regurgitation in end-stage cardiomyopathy with mitral annuloplasty. Am J Cardiol. 1996; 78: 966–969.[CrossRef][Medline] [Order article via Infotrieve]
40. Bolling SF, Pagani FD, Deeb GM, Bach DS. Intermediate-term outcome of mitral reconstruction in cardiomyopathy. J Thorac Cardiovasc Surg. 1998; 115: 381–388.
41. Bax JJ, Braun J, Somer S, Klautz R, Holman E, Versteegh M, Schalij M, Vanderwall E, Dion R. Restrictive annuloplasty and coronary revascularization in ischemic mitral regurgitation results in reverse left ventricular remodeling. Circulation. 2003; 108 (Suppl 1): II39–II42.
42. Green GR, Dagum P, Glasson JR, Nistal JF, Daughters GT, 2nd, Ingels NB Jr, Miller DC. Restricted posterior leaflet motion after mitral ring annuloplasty. Ann Thorac Surg. 1999; 68: 2100–2106.
43. Timek TA, Lai DT, Tibayan FA, Daughters GT, Liang D, Dagum P, Ingels NB Jr, Miller DC. Septal-lateral annular cinching (’SLAC) reduces mitral annular size without perturbing normal annular dynamics. J Heart Valve Dis. 2002; 11: 2–9.[Medline] [Order article via Infotrieve]
44. Timek TA, Nielsen SL, Lai DT, Tibayan FA, Liang D, Rodriguez F, Daughters GT, Ingels NB Jr, Miller DC. Edge-to-edge mitral valve repair without ring annuloplasty for acute ischemic mitral regurgitation. Circulation. 2003; 108 (Suppl 1): II122–II127.
45. Timek TA, Lai DT, Tibayan FA, Liang D, Rodriguez F, Langer F, Daughters GT, Ingels NB Jr, Miller C. Effect of para-commissural annular cinching on acute ischemic mitral regurgitation. Circulation. 2003; 108: 2180: IV475.
46. Messas E, Guerrero JL, Handschumacher MD, Conrad C, Chow C-M, Sullivan S, Yoganathan AP, Levine RA. Chordal cutting: a new therapeutic approach for ischemic mitral regurgitation. Circulation. 2001; 104: 1958–1963.
47. Hung J, Guerrero JL, Handschumacher MD, Supple G, Sullivan S, Levine RA. Reverse ventricular remodeling reduces ischemic mitral regurgitation: echo-guided device application in the beating heart. Circulation. 2002; 12: 2594–2600.
48. Trehan N, Mishra Y, Mittal S, Mehta Y. Off-pump mitral valve repair using the CoapsysTM device: early results in patients with functional mitral regurgitation. Circulation. 2003; 108: 2178: IV475.
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