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Ann Thorac Surg 2007;84:553-559
© 2007 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Regional and Global Patterns of Annular Remodeling in Ischemic Mitral Regurgitation

^a Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
^b Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Accepted for publication April 2, 2007.

^_* Address correspondence to Dr Gorman, University of Pennsylvania School of Medicine, 313 Stemmler Hall, 36th and Hamilton Walk, Philadelphia, PA 19104-4283 (Email: gormanr{at}uphs.upenn.edu).

	Abstract

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background: The mammalian mitral annulus is saddle shaped. Experimental studies have shown that loss of saddle shape occurs in ischemic mitral regurgitation. However, neither the temporal pattern of global annular remodeling nor the geometric pattern of regional annular remodeling has been described. We sought to characterize these changes using real-time three-dimensional echocardiography in an ovine model.

Methods: Ten sheep underwent real-time three-dimensional echocardiography at baseline and 1 hour and 8 weeks after posterobasal myocardial infarction. Multiple mitral annular geometric indexes were measured at each time point to assess regional and global annular remodeling.

Results: One hour after infarction, global annular height decreased from 5.8 ± 0.5 mm to 4.0 ± 0.4 mm (p < 0.001) while intercommissural width increased from 29.0 ± 1.3 mm to 35.7 ± 1.7 mm (p = 0.023), resulting in a decrease in the global annular height to commissural width ratio from 20.0% ± 1.6% to 11.2% ± 0.9% (p < 0.001). Eight weeks after infarction, global annular height decreased to 3.9 ± 0.2 mm (p < 0.05) while intercommissural width increased to 40.7 ± 1.5 mm (p < 0.001), resulting in an additional decrease in the global annular height to commissural width ratio to 9.4% ± 0.4% (p < 0.001). Although annular remodeling involved the entire mitral annulus, there was regional heterogeneity in its extent.

Conclusions: Significant global annular flattening and dilatation occur during the development of ischemic mitral regurgitation in an ovine model. Regional annular remodeling is heterogeneous and is not limited the posterior commissure or the posterior annulus.

	Introduction

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The mitral valve annulus has a distinctly nonplanar saddle shape in all mammalian species studied to date [1, 2]. A recent theoretical finite element analysis has shown that this unique three-dimensional (3D) annular shape imposes leaflet curvature that, in combination with leaflet billowing, likely acts to reduce stress on all components of the mitral valvular apparatus during systole [2]. There is growing interest in understanding how the preservation or restoration of this unique annular shape contributes to normal valvular and ventricular function as well as its importance for improving the effectiveness and durability of mitral valve repair procedures [3].

Previously, our group has used sonomicrometry array localization to assess the changes in annular geometry that occur in an ovine model of acute ischemic mitral regurgitation [4]. In that report, we demonstrated significant global annular flattening immediately after myocardial infarction in conjunction with the development of ischemic mitral regurgitation. In this study, we expand on our previous work by describing regional annular geometry in quantitative terms and by assessing the changes that occur in annular geometry during long-term infarction-induced ventricular remodeling leading to chronic ischemic mitral regurgitation. Again, we use a well-established ovine model of ischemic mitral regurgitation. However, in this experiment we have employed real-time three-dimensional echocardiography (rt-3DE) to assess both regional and global indexes of mitral annular geometry longitudinally in time as chronic ischemic mitral regurgitation develops.

Our goal is therefore two-fold: (1) we seek to characterize the nature of both regional and global annular remodeling during the development of ischemic mitral regurgitation with a spatial resolution not previously possible and (2) to introduce rt-3DE as a clinically relevant, noninvasive, and powerful imaging modality for interrogating the mitral valve in three-dimensional space.

	Material and Methods

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Surgical Protocol
The study protocol was reviewed and approved by the University of Pennsylvania School of Medicine Institutional Animal Care and Use Committee. In compliance with guidelines for humane care (National Institutes of Health publication 85-23, revised 1996), 10 male sheep were pretreated with buprenorphine (2 µg/kg) and then induced with sodium thiopental (10 to 15 mg/kg intravenously), intubated, and anesthetized with isofluorane (1.5% to 2.0%) and oxygen (Narkomed; North American Drager, Telford, PA). All animals received glycopyrrolate (0.02 mg/kg intravenously) and cefazolin (1.0 g intravenously). The electrocardiogram, arterial blood pressure, and pulmonary artery pressure were monitored throughout the procedure. A left thoracotomy was performed, and baseline echocardiographic data were acquired. A posterobasal myocardial infarction was then performed by ligating all branches of circumflex coronary artery between the posterior ventricular vein and the posterior coronary artery. Image acquisition was repeated 1 hour after infarction. Eight weeks after myocardial infarction, the sheep were again anesthetized, monitored, and studied as described. After final image acquisition, the animals were euthanized. Heart rate, arterial blood pressure, central venous pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure were recorded at the time of image acquisition in each case.

Echocardiographic Protocol
Epicardial real-time three-dimensional echocardiography was performed through a left thoracotomy immediately before and 1 hour after myocardial infarction in all subjects. Transdiaphragmatic rt-3DE was performed through a limited upper midline laparotomy at 8-week follow-up. In each case, full-volume images were acquired by a single operator using a Sonos 7500 (Philips Medical Systems, Andover, Massachusetts) platform equipped with a 2 to 4 MHz phased array probe and an X4 matrix-array handheld transducer. The degree of mitral regurgitation was determined semiquantitatively by assessing the area of the regurgitant jet as a percentage of left atrial area in the apical four-chamber view. The following grading was used: grade 1, less than 20%; grade 2, 20% to 40%; grade 3, 40% to 60%; and grade 4, greater than 60% [5]. Gated images were acquired over eight cardiac cycles. Real-time 3DE data sets were exported to a dedicated workstation (Dell Optiplex GX 270; Dell, Round Rock, Texas) for image manipulation and analysis.

Image Analysis
Image analysis of full-volume data sets was performed using QLab 3D Advanced Quantification Software (Philips Medical Systems). For each data set, left ventricle (LV) cavity volumes were measured as follows: endocardial contours were manually traced in both end-diastolic and end-systolic frames. The endocardial contours of the remaining frames were traced in sequence by means of automated contour detection. Left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were derived from the resultant global time-volume curve for each data set. The corresponding stroke volume and ejection fraction were calculated.

Geometric analysis of the mitral valve using each full-volume data set was then performed using Tomtec Cardio-View (Tomtec Imaging Systems, Munich, Germany). All calculations were performed at end systole, which was defined as the first frame demonstrating closure of the aortic valve. Cardio-View allows the interactive manipulation—including rotation, translation, surface rendering, and measurement—of fully 3D ultrasound data sets. A rotational template consisting of 18 long-axis cross-sectional planes separated by 10-degree increments was placed at the geometric center of the mitral valve orifice, aligned with the axis of the mitral orifice, and superimposed on the 3D echocardiogram. (Fig 1A). The two annular points intersecting each of the 18 long-axis rotational planes were then identified by orthogonal visualization of each plane; the two points were marked interactively in Cardio-View (Fig 1B).

View larger version (97K): [in this window] [in a new window]   Fig 1. (A) A view of the mitral valve where the selected short-axis plane coincides with the plane of the mitral valve. The aorta (Ao) and mitral valve orifice (MVO) are indicated. A rotational template consisting of 18 long-axis planes evenly spaced at 10-degree increments and centered at the geometric center of the mitral valve has been constructed. (B) A single long-axis view (0 degrees on the rotational template of [A]) of the heart. The left ventricle (LV), anterior (AL) and posterior (PL) mitral valve leaflets, left atrium (LA), left ventricular outflow track (LVOT), aortic valve (AoV), and the aorta (Ao) have been illustrated. Anterior (AA) and posterior (PA) annular points have been marked. Note that in this orientation, the negative z-axis (for purposes of annular height calculations) extends toward the apex while the positive z-axis extends toward the left atrium.

The Cartesian coordinates for each point in a given annular model were converted to cylindrical coordinates (r, , z), defined and oriented such that larger positive z’s represent points positioned atrially, and larger negative z’s represent points positioned closer to the LV apex. The data set was then translated in the z-direction and rotated around the mitral valve axis (-direction) so that the data point containing z_max (which corresponded to the midpoint of the anterior annulus in all cases) was located at = 0 rad, and the data point containing z_min was located at z = 0 mm. Values of _n and z_n for each point in a given data set were then recalculated in this fixed frame of reference.

The regional annular height (AH_n) of each point in a given data set was defined as z_n-z_min. The global annular height (AH_g) for a given data set was then defined as z_max- z_min. Septolateral diameter for a given data set was defined as the distance, in three-dimensional space, separating the two data points located at = 0 and (radians). The intercommissural width (CW) for a given data set was defined as the distance, in three-dimensional space, separating the data point with the lowest z_n between = 0 and = from the data point with the lowest z_n between = and = 2. Mitral annular area was defined as the area enclosed by the two-dimensional projection of a given annular data set onto its corresponding least squares plane. The spatial relationships of these geometric indexes are illustrated in Figure 2.

View larger version (14K): [in this window] [in a new window]   Fig 2. Shown are (A) oblique, (B) intercommissural, and (C) transvalvular views of a single real-time three-dimensional echocardiography–derived mitral annular model. Each of the 36 annular data points (white spheres) has been included. The least square plane has been superimposed on the annulus in each view. (A) The midanterior annulus (Mid-AA), anterior commissure (AC), posterior commissure (PC), and midposterior annulus (Mid-PA) have been labeled, illustrating both the manner in which zn is measured for a given data point and the manner in which the values of global annular height (AHg) and regional annular height (AHn) are subsequently determined. (B) The manner in which septolateral diameter (SL) is determined for a given data set is illustrated. (C) The manner in which intercommissural width is determined for a given data set is illustrated. Note the characteristic "D" shape of the annulus.

Comparison between values at baseline, 1 hour after myocardial infarction, and 8 weeks after myocardial infarction were made with Student’s t test for paired observations. All statistical analysis was performed using Statistical Package for the Social Sciences (SPSS, Chicago, Illinois). The level of significance selected for all variables was p less than 0.05. All data are reported as mean ± SEM.

	Results

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
To ensure that mitral leaflet loading conditions, which influence annular geometry [6], were similar at each data acquisition time point, statistical comparisons were performed for all hemodynamic determinants at each data acquisition point. These comparisons are summarized in Table 1. There were no statistically significant differences between time points for any determinant. Therefore, leaflet loading conditions were likely similar at all data acquisition points. None of the animals had significant mitral regurgitation at baseline. All animals had early (1 to 2+) and late (3+) ischemic mitral regurgitation.

Annular height decreased from 5.8 ± 0.5 mm at baseline to 4.0 ± 0.4 mm 1 hour after infarction (p = 3.7 x 10^–4) and to 3.9 ± 0.2 mm 8 weeks after infarction (p = 3.9 x 10^-3) while AH_gCWR decreased from 20.0% ± 1.6% at baseline to 11.2% ± 0.9% and then to 9.4% ± 0.4% over the same intervals (p = 7.0 x 10^–4, p = 1.4 x 10^–4).

Mean AH_nCWR ± SEM is plotted as a function of rotational position for the 10-subject cohort at baseline, 1 hour after infarction, and 8 weeks after infarction in Figure 3. At baseline, the value of AH_nCWR at the midpoint of the anterior annulus (20.0% ± 1.5%) was more than twice that at the midpoint of the posterior annulus (9.6% ± 1.1%), which was defined as that point on the mitral annulus corresponding to = . The value of AH_nCWR (3.7% ± 0.6%) at the posterior commissure, which occurred at 5.3 rad, was also lower than that of the anterior commissure (4.7% ± 1.2%) which occurred at 0.8 rad.

View larger version (29K): [in this window] [in a new window]   Fig 3. Mean regional annular height to commissural width ratio (AHnCWR) ± SEM (dotted lines) is plotted as a function of rotational position for the 10-subject cohort at baseline (black line), 1 hour after myocardial infarction (dark gray line), and 8 weeks after myocardial infarction (light gray line). For each data set, the midpoint of the anterior annulus was defined as 0 rad. The positions of the midanterior annulus (Mid-AA), the midposterior annulus (Mid-PA), the anterior commissure (AC), and the posterior commissure (PC) are indicated. Note that the rotational positions of the lowest points on the mitral annulus shift toward the posterior annulus as remodeling occurs.

Eight weeks after infarction, the value of AH_nCWR at the midpoint of the anterior annulus had decreased to 9.4% ± 0.4% while that at the midpoint of the posterior annulus was minimally changed at 6.7 ± 0.6 mm. The value of AH_nCWR at the posterior commissure, the rotational position of which had shifted to 4.5 rad, had increased to 3.2% ± 0.7%, while that at the anterior commissure, the rotational position of which had shifted to 1.8 rad, had increased to 3.0% ± 0.6%. While the value of AH_nCWR at the midpoint of the posterior annulus did not change during this interval, the remainder of posterior annulus (between 1.8 and 4.5 rad) underwent substantial flattening (Fig 3).

To illustrate the characteristic global and regional geometric changes that accompany the development of chronic ischemic mitral regurgitation, rt-3DE-derived 3D renderings of an ovine mitral annulus at baseline and both 1 hour and 8 weeks after myocardial infarction have been included (Fig 4). Both annular dilatation and flattening, as well as commissural rotation (toward the midposterior annulus) can be appreciated.

View larger version (31K): [in this window] [in a new window]   Fig 4. The three-dimensional geometry of a single ovine mitral annulus is shown (A) at baseline, (B) 1 hour after myocardial infarction, and (C) 8 weeks after myocardial infarction. At baseline, global annular height (AHg), intercommissural width (CW), septolateral diameter (SL), and global annular height to commissural width ratio (AHgCWR) were 8.0 mm, 28.2 mm, 31.1 mm, and 27.8%, respectively. One hour after myocardial infarction, AHg and AHgCWR had decreased to 3.9 mm and 10.2% respectively, while CW and SL had increased to 38.4 mm and 33.7 mm. Eight weeks after myocardial infarction, AHg and AHgCWR had decreased to 3.3 mm and 7.9% respectively, while CW and SL had increased to 41.9 mm and 35.2 mm. The positions of the midanterior annulus (Mid-AA), the midposterior annulus (Mid-PA), the anterior commissure (AC), and the posterior commissure (PC) are indicated.

	Comment

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

The effect of infarction induced ventricular remodeling on mitral annular shape has been studied only incompletely to date. In a recent report, we applied sonomicrometry array localization [7, 8] to an ovine model of acute ischemic mitral regurgitation to assess the effect of a posterobasal infarction on 3D annular geometry immediately after infarction [4]. In that study, we demonstrated immediate decrease in the global annular height to commissural width ratio that resulted primarily from a loss of annular height and to a much lesser extent, annular dilatation. In the current study, we sought to confirm these early postinfarction findings using rt-3DE and to achieve a detailed understanding of the changes that occur in 3D annular geometry as ventricular remodeling progresses and chronic ischemic mitral regurgitation develops. Given our work [9] in the acute setting and that of others [10], which has applied marker imaging techniques to the characterization of chronic ischemic mitral regurgitation in a similar ovine model, we hypothesized that the global annular height to commissural width ratio would decrease early after myocardial infarction and continue to do so progressively in concert with annular dilatation and LV remodeling. Using rt-3DE, we have confirmed this hypothesis. Additionally, we have characterized both the time course over which postinfarction annular remodeling occurs and the relative contributions of annular flattening, commissural widening, and septolateral widening to this process. One hour after infarction, LV end-diastolic and end-systolic volumes increased by 37.6% and 60.5%, respectively. Concomitant annular distortion was reflected by a 31.0% decrease in global annular height and an increase in intercommissural width of 23.1%, resulting in a 44.0% decrease in the global annular height to commissural width ratio—this pattern of acute annular distortion is very similar to that described previously through the use of sonomicrometry array localization [4, 9]. Mitral annular area increased by 13.6% while the septolateral diameter increased by 7.1%, suggesting that the observed increase in mitral annular area during this interval was primarily driven by intercommissural widening.

As remodeling progressed over an 8-week period and ischemic mitral regurgitation became more severe, LV end-diastolic and end-systolic volumes increased by an additional 44.3% and 85.5%, respectively. Mitral annular remodeling was reflected by an additional 9.0% decrease in the global annular height to intercommissural width ratio when compared with baseline. While intercommissural width increased by an additional 17.2%, annular height remained essentially unchanged, decreasing by only 1.8% compared with baseline—indicating that while acute annular planarization is driven by both annular flattening and annular dilation, progressive annular planarization in the context of chronic ischemic mitral regurgitation is principally driven by the latter. The septolateral diameter increased an additional 8.5% over its baseline value and mitral annular area increased an additional 16%. The large increase in intercommissural width was likely due, in part, to the manner in which the positions of the commissures were identified—as previously described, the commissures were defined mathematically as the lowest points along prescribed regions of the annulus. Using this definition, the mean rotational position of both commissures moved toward the posterior annulus, both acutely and during the 8-week follow-up interval. This rotation was particularly pronounced at the 8-week time point. This finding may reflect a pattern of geometric distortion in which the commissures are no longer the lowest points on the annulus. Therefore, our calculated values 8 weeks after infarction likely overestimated the intercommissural width and may have more closely approximated the maximum diameter of the mitral annulus. Since our calculated global annular heights were also based on the position of the lowest point on the annulus (as opposed to the true position of either commissure), these values also likely overestimated global annular height after infarction. To address this potential shortcoming—which is inherent to all techniques that rely on the visual identification of critical landmarks—we have recently begun to study the geometric changes that occur in this model using sonomicrometry array localization and rt-3DE in parallel.

Using sophisticated marker angiographic imaging techniques, Tibayan and colleagues [10] have demonstrated a comparable pattern of annular remodeling over a 7-week period after myocardial infarction in a similar ovine model. However, acute changes in annular geometry immediately after infarction were not characterized in their study. Although these authors did not specifically calculate an index of annular shape, their data support the conclusion that both annular flattening and annular dilatation, as reflected by intercommissural and septolateral widening, develop after posterobasal infarctions that result in chronic ischemic mitral regurgitation in sheep.

Whereas previous studies of annular remodeling have largely focused on indexes of global annular geometry [9, 10], the present study characterizes annular remodeling at a regional level. As illustrated in Figure 3, remodeling is not limited to the posteromedial annulus. Although more pronounced across the posterior annulus, diffuse annular flattening was observed in this model of chronic ischemic mitral regurgitation.

Watanabe and colleagues [11] have demonstrated that the magnitude of global annular remodeling observed in a given subject is influenced by the associated spatial distribution of myocardial ischemia. However, relative patterns of regional annular remodeling were not examined. We believe that in addition to influencing the magnitude of global annular remodeling, different valvular and subvalvular pathologies may also promote geometrically distinct patterns of regional annular remodeling. Consequently, the capacity to describe regional annular geometry in quantitative terms is essential to improving both our collective understanding of annular dynamics and corrective procedures intended to restore normal geometry.

Several recent studies suggest that the dramatic degree of annular flattening demonstrated in the ovine model also occurs in patients with ischemic mitral regurgitation or functional mitral regurgitation of nonischemic etiology. Kaplan and colleagues [12], using less sophisticated, early stage rotational probe 3D echocardiographic technology, first demonstrated that clinical functional mitral regurgitation, like experimental ischemic mitral regurgitation, was associated with both an increase in intercommissural distance and a decrease in annular height. Although these authors did not specifically report the AHCWR, their tabulated data allow its calculation in retrospect. In normal patients, the AHCWR was 22% at end systole, and in the functional mitral regurgitation group, this value decreased to 18%. Their initial findings have been confirmed both by Watanabe and colleagues [11] using rt-3DE and by Kaji and colleagues [13] using 3D cardiac magnetic resonance imaging. In both cases, annular height in patients with ischemic mitral regurgitation was reduced to a similar degree as that reported in the current study. In the former case, intercommissural width was not measured. Therefore, AHCWR cannot be calculated retrospectively. However, in the latter case, AHCWR was reported as 21% in controls and 12% in the ischemic mitral regurgitation cohort—both of which agree very well with the values of 20.0% and 9.4% reported here.

Importantly, this study also serves to establish rt-3DE as a powerful, readily applicable, clinical tool for studying large cohorts of patients with and without ischemic mitral regurgitation to definitively determine the effect of chronic LV remodeling on mitral annular shape. This imaging modality is a noninvasive, clinically available imaging modality that, we believe, will help to facilitate the translation of knowledge gained in laboratory experiments to the bedside and into the operating room. If it is indeed determined that annular flattening is an essential component of the ischemic mitral regurgitation phenotype, as now seems likely, it will next be necessary to determine how preservation or restoration of the normal saddle shape affects such critical structural and clinical variables as leaflet stress, geometry of the subvalvular apparatus, and repair durability as well as LV size, LV function, and survival. Continued study of the ovine ischemic mitral regurgitation models, normal volunteers, and patients with ischemic mitral regurgitation/functional mitral regurgitation using clinically relevant 3D imaging modalities such as rt-3DE and possibly magnetic resonance imaging and ultrafast computed tomography will be necessary to definitively determine if an annular saddle shape will be important as a therapeutic target of valvular repair strategies for ischemic mitral regurgitation/functional mitral regurgitation in the future.

	Acknowledgments

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
This research was supported by National Institutes of Health Grants HL63954 (RCG) and HL73021 (JHG), and by The American Heart Association Postdoctoral Fellowship 0625455U (LPR).

	References

Top Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

1. Levine RA, Handschumacher, MD, Sanfilippo AJ, et al. Three-dimensional echocardiographic reconstruction of the mitral valve, with implications for the diagnosis of mitral valve prolapse Circulation 1989;80:589-598.[Abstract/Free Full Text]
2. Salgo IS, Gorman III JH, Gorman RC, et al. Effect of annular shape on leaflet curvature in reducing mitral leaflet stress Circulation 2002;106:711-717.[Abstract/Free Full Text]
3. Ryan LP, Salgo IS, Gorman RC, Gorman III JH. The emerging role of three-dimensional echocardiography in mitral valve repair Semin Thorac Cardiovasc Surg 2006;18:126-134.[Medline]
4. Gorman III JH, Jackson BM, Enomoto Y, Gorman RC. The effect of regional ischemia on mitral valve annular saddle shape Ann Thorac Surg 2004;77:544-548.[Abstract/Free Full Text]
5. Miyatake K, Izumi S, Okamoto M, et al. Semiquantitative grading of severity of mitral regurgitation by real-time two-dimensional Doppler flow imaging technique J Am Coll Cardiol 1986;7:82-88.[Abstract]
6. Parish LM, Jackson BM, Enomoto Y, Gorman RC, Gorman III JH. The dynamic anterior mitral annulus Ann Thorac Surg 2004;78:1248-1255.[Abstract/Free Full Text]
7. Gorman III JH, Gupta KB, Streicher JT, Gorman RC, Jackson BM, Edmunds Jr. LH. Dynamic 3-D imaging of the mitral valve using rapid sonomicrometry array localization J Thorac Cardiovasc Surg 1996;112:712-725.[Abstract/Free Full Text]
8. Ratcliffe MB, Gupta KB, Streicher JT, Savage EB, Bogen DK, Edmunds Jr. LH. Use of sonomicrometry and multidimensional scaling to determine the three-dimensional coordinates of multiple cardiac locations: feasibility and initial implementation IEEE Trans Biomed Eng 1995;42:587-598.[Medline]
9. Gorman III JH, Gorman RC, Jackson BM, Enomoto Y, St. John-Sutton MG, Edmunds LH. Annuloplasty ring selection for chronic ischemic mitral regurgitation: lessons from the ovine model Ann Thorac Surg 2003;76:1556-1563.[Abstract/Free Full Text]
10. Tibayan FA, Rodriguez F, Langer F, et al. Annular remodeling in chronic ischemic mitral regurgitation: ring selection implications Ann Thorac Surg 2003;76:1549-1555.[Abstract/Free Full Text]
11. Watanabe N, Ogasawara Y, Yamaura Y, et al. Mitral annulus flattens in ischemic mitral regurgitation: geometric differences between inferior and anterior myocardial infarctionA real-time 3-dimensional echocardiographic study. Circulation 2005;112(Suppl 1):458-462.
12. Kaplan SR, Bashein G, Sheehan FH, et al. Three-dimensional echocardiographic assessment of annular shape changes in the normal and regurgitant mitral valve Am Heart J 2000;139:378-387.[Medline]
13. Kaji S, Nasu M, Yamamuro A, et al. Annular geometry in patients with ischemic mitral regurgitationThree-dimensional magnetic resonance imaging study. Circulation 2005;112(Suppl 1):409-414.

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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): Joseph H. Gorman, III Robert C. Gorman Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ryan, L. P. Articles by Gorman, R. C. Search for Related Content PubMed PubMed Citation Articles by Ryan, L. P. Articles by Gorman, R. C. Related Collections Valve disease