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Ann Thorac Surg 2003;76:1549-1555
© 2003 The Society of Thoracic Surgeons


Original article: cardiovascular

Annular remodeling in chronic ischemic mitral regurgitation: ring selection implications

Frederick A. Tibayan, MDa, Filiberto Rodriguez, MDa, Frank Langer, MDa, Mary K. Zasio, BSa, Lynn Bailey, ASb, David Liang, MD, PhDb, George T. Daughters, MSa,c, Neil B. Ingels, Jr, PhDa,c, D. Craig Miller, MDa*

a Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, California, USA
b Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA
c Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, Palo Alto, California, USA

* Address reprint requests to Dr Miller, Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247, USA.
e-mail: dcm{at}stanford.edu

Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
BACKGROUND: More precise understanding of annular remodeling in the evolution of chronic ischemic mitral regurgitation is needed to provide a more rational basis for optimal annuloplasty ring sizing and selection as well as the design of new reparative techniques. Three-dimensional in vivo data describing these geometric perturbations however are lacking. Using an ovine model of chronic myocardial infarction we determined the three-dimensional distortions of the mitral annulus associated with the development of chronic ischemic mitral regurgitation.

METHODS: Ten sheep underwent placement of radiopaque markers on the left ventricle and mitral annulus as well as placement of snares around the second and third obtuse marginal coronary arteries. After 8 days biplane cinefluoroscopy provided three-dimensional marker data and snare occlusion created an inferior infarction. After 7 more weeks the animals were studied again.

RESULTS: Severity of mitral regurgitation increased (0.6 ± 0.5 to 2.5 ± 0.7). Septal-lateral (2.99 ± 0.20 cm to 3.64 ± 0.35 cm, maximum dimension) and commissure-commissure (3.71 ± 0.32 cm to 4.40 ± 0.30 cm) mitral annular diameters and the lengths of the muscular (7.77 ± 0.39 cm to 9.51 ± 0.72 cm) and fibrous annular perimeters (3.36 ± 0.37 cm to 3.85 ± 0.39 cm, p < 0.0001 for all) increased while the height of the annular "saddle horn" above a best-fit plane fell (0.73 ± 0.52 cm to 0.57 ± 0.42 cm, minimum dimension, p = 0.01).

CONCLUSIONS: These three-dimensional in vivo data reflect annular remodeling in chronic ischemic mitral regurgitation and suggest that mitral repair in this context should be aimed at preventing further lengthening of the intertrigonal distance, reducing the septal-lateral annular diameter to reestablish adequate leaflet coaptation, and restoring the saddle shape of the annulus.


    Introduction
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
Altered annular geometry often contributes to leaflet malcoaptation in chronic ischemic mitral regurgitation (CIMR) [1,2]. Ring annuloplasty is the preferred treatment for CIMR but as many as 30% of patients after ring annuloplasty have residual or recurrent mitral regurgitation (MR) [3], which portends poor survival independent of underlying left ventricular (LV) systolic dysfunction [4]. More precise understanding of annular remodeling in CIMR is needed to provide a more rational basis for optimal annuloplasty ring sizing and selection of type of ring as well as the design of new reparative surgical techniques. Three-dimensional in vivo data describing these geometric perturbations however are not known. Using an ovine experimental model of chronic LV infarction we determined the three-dimensional distortions of the mitral annulus associated with CIMR.


    Material and methods
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
Surgical preparation
Thirty-six Dorsett hybrid sheep (71 ± 5 kg) were premedicated with ketamine (25 mg/kg intramuscularly) and anesthesia was induced with sodium thiopental (6.8 mg/kg intravenously [IV]) and maintained with inhalational isoflurane (1% to 2.5%). Through a left thoracotomy, eight tantalum myocardial markers (nos. 2 to 9, Fig 1) were inserted in the LV epicardial layer along four equally spaced longitudinal meridians, with one marker at the LV apex (no. 1, Fig 1). Polypropylene 2-0 sutures were passed around the second and third obtuse marginal branches of the left circumflex coronary artery and loosely snared using the method of Llaneras and associates [5]. After establishment of cardiopulmonary bypass, eight tantalum markers were sutured around the circumference of the MA (one near each commissure [nos. 16 and 20], and three along the septal [nos. 15, 21, 22] and lateral [nos. 17, 18, 19] annulus; see Fig 1). A micromanometer pressure transducer (PA4.5-X6; Konigsberg Instruments, Pasadena, CA) was placed in the LV chamber through the apex. Ten animals died postoperatively primarily due to respiratory failure.



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Fig 1. Schematic of marker array showing markers on the left ventricle and around the mitral annulus.

 
Experimental protocol
After 8 ± 2 days, the animals were taken to the cardiac catheterization laboratory, sedated with ketamine (1 to 4 mg · kg-1 · h-1 IV infusion) and diazepam (5 mg IV), intubated, mechanically ventilated, and maintained with inhalational isoflurane (1% to 2.5%). Transesophageal echocardiography and coronary angiography were performed and baseline videofluoroscopic marker and hemodynamic data acquired. After premedication with lidocaine (100 mg IV), bretylium (75 mg IV), and magnesium (3 g IV), the coronary artery snares were tightened and complete occlusion of the selected vessels verified by angiography. An epinephrine drip was titrated to maintain a coronary perfusion pressure (aortic diastolic pressure minus LV diastolic pressure) greater than 60 mm Hg. Ventricular arrhythmias were treated with lidocaine (50 to 100 mg IV) and amiodarone (50 to 150 mg IV), as needed. Nine sheep died after vessel occlusion owing to refractory ventricular fibrillation. The sheep were observed for clinical signs of heart failure (tachypnea, lethargy, anorexia), and serial transthoracic echocardiography was performed to detect LV dilatation and MR.

After 7 ± 1 weeks, the animals returned to the cardiac catheterization laboratory for recording of hemodynamic, transesophageal echocardiography (TEE), and marker data. The MR was graded based on TEE color Doppler regurgitant jet extent and width as none (0), trace (+0.5), mild (+1), moderate (+2), moderate-severe (+3), or severe (+4) by an experienced echocardiographer (DL). Of the 17 remaining animals, 7 had only trace-mild MR after 7 weeks. The 10 animals in which moderate or worse MR developed formed the final study group.

All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by the National Institutes of Health (DHEW NIHG publication 85-23, revised 1985). This study was approved by the Stanford University Medical School Laboratory Research Animal Review committee and conducted according to Stanford University policy.

Data acquisition
Images were acquired with the animal in the right lateral decubitus position with a biplane videofluoroscopy system (Philips Medical Systems, North America Company, Pleasanton, CA). Data from two radiographic views were digitized and merged to yield three-dimensional coordinates for each of the radiopaque markers every 16.7 ms using custom-designed software. Ascending aortic pressure, LV pressure, and electrocardiography (ECG) voltage signals were recorded simultaneously during marker data acquisition.

Data analysis
For hemodynamics and cardiac cycle timing, variables from three consecutive steady-state beats before infarction were averaged and defined as "baseline" data for each animal. Similarly three beats at the follow-up study were averaged and termed "chronic." End systole (ES) was defined as the time of the videofluoroscopic frame containing the point of peak negative rate of LV pressure fall (-dP/dt), and end diastole (ED) as the videofluoroscopic frame containing the peak of the ECG R wave. Instantaneous LV volume for each frame, namely every 16.7 ms, was calculated from the positions of the epicardial LV and annular markers using a space-filling multiple tetrahedral volume method [6].

Mitral annular geometry
Mitral annular area (MAA) in three-dimensional space was calculated for each frame throughout the cardiac cycle as the sum of the areas of eight triangles formed by consecutive adjacent marker pairs on the annulus and the annular centroid defined from markers no. 15 to 22 (Fig 1). The septal-lateral (S-L) diameter of the annulus was calculated as the distance in three-dimensional space between the two markers placed in the middle of the septal (clinically termed "anterior") and lateral ("posterior") mitral annulus, respectively (nos. 22 and 18, Fig 1). The commissure-commissure (C-C) diameter was calculated as the distance in three-dimensional space between the two annular commissural markers (nos. 16 and 20, Fig 1). Height of the midseptal annulus (no. 22, or "saddle horn") was defined as the distance of marker no. 22 above a best-fit plane to the markers of the muscular annulus (nos. 16 to 20). The perimeter of the fibrous annulus was defined as the sum of distances between the markers from trigone to trigone (nos. 21 to 22 and nos. 22 to 15). The perimeter of the muscular annulus was defined as the sum of the distances between the markers along the muscular annulus (nos. 15 to 16, nos. 16 to 17, nos. 17 to 18, nos. 18 to 19, nos. 19 to 20, and nos. 20 to 21).

Statistical analysis
All data are reported as mean plus or minus 1 standard deviation (±1 SD) unless otherwise noted. Comparisons between baseline and CIMR conditions were made using Student's t test for paired observations.


    Results
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
Table 1 summarizes group mean hemodynamic data at baseline and after CIMR. Maximum LV dP/dt and maximum LVP decreased with CIMR while EDV, LVEDP, and the severity of MR increased. Table 2 and Figure 2 summarize mitral annular geometry throughout the cardiac cycle before and after the development of CIMR. Dilatation in the C-C annular dimension (18% increase from baseline minimum, 19% from baseline maximum) was roughly proportional to the degree of S-L dilation (16% and 22%, respectively). Mitral annular area also increased significantly. Surprisingly the length of the fibrous annulus increased significantly after only 7 weeks of CIMR (Fig 2). Moreover lengthening of the fibrous annulus (14% from baseline minimum, 15% from baseline maximum) was comparable with that of the muscular annulus (18% and 22%; Fig 2). Minimum and maximum height of the saddle horn decreased.


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Table 1. Hemodynamics

 

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Table 2. Annular Geometry

 


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Fig 2. Annular dimensions (mean ± standard error) versus time with data centered on end diastole (ED). For orientation, a bar is shown at the top to indicate the mean duration of systole. (Squares = baseline; circles = chronic ischemic mitral regurgitation.)

 

    Comment
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
The key findings of this study have important implications on our understanding of the pathogenesis of CIMR and its potential surgical treatment. First, the fibrous annulus dilates almost as much as the muscular mitral annulus. Second, the mitral annulus dilates proportionally in the S-L and C-C directions. And third, the annulus "flattens" (the height of the saddle horn above the muscular annulus fell).

Fibrous annular dilatation
Many techniques of mitral valve repair are based on the assumption that the intertrigonal distance as part of the fibrous skeleton of the heart does not dilate [7]. This tenet is the rationale for annuloplasty methods using rings [8], suture [9], or other materials [10] that reduce only the posterior annulus, leaving the intertrigonal portion of the anterior annulus untouched. The intertrigonal distance is also used by some as a guide for annuloplasty ring sizing [11]. This in vivo study of the three-dimensional dimensions of the mitral annulus demonstrates that the intertrigonal distance does in fact dilate in the setting of CIMR (4 to 5 mm, 14% to 15%), and this dilatation of the fibrous portion was comparable with the relative changes of the muscular annulus (1.4 to 1.7 cm, 18% to 22%). Dilatation of the fibrous annulus, which has been recently reported in humans with cardiomyopathy of ischemic and idiopathic etiologies [12], may have important implications on ring sizing in functional mitral regurgitation, for example choosing a ring size based on a dilated intertrigonal distance may result in too large a ring being selected. Bolling and associates [13] advocate the use of a markedly undersized annuloplasty ring in patients with ischemic cardiomyopathy (and currently Bolling favors a stiff, complete type of ring), and common surgical practice is to downsize the ring by two or more sizes. Our current observations provide some rationale for why a ring should be undersized in cases of CIMR.

A second aspect of valve repair in CIMR where the fibrous annulus may already be dilated is the choice of a complete or a partial annuloplasty ring. The 4 to 5 mm lengthening of the fibrous (anterior) annulus in just 7 weeks in these sheep, although probably greater than the lengthening seen in patients without ischemic cardiomyopathy, suggests that a complete ring would be better suited to the surgical repair of CIMR.

Septal-lateral and commissure-commissure proportional dilatation
Chronic ischemic MR was associated with annular dilatation in both the S-L and C-C dimensions throughout the cardiac cycle. In this study of CIMR, the extent of S-L and C-C dilatation were roughly proportional (about 16% and 22%, minimum and maximum, versus 18% and 19%, respectively), in contrast to a previous experimental study of dilated cardiomyopathy in which S-L dilatation predominated [14]. Overall annular dilation (assessed as annular area) is consistently associated with CIMR [1, 2, 15] but the role of annular dilatation in the pathogenesis of ischemic MR is still being debated. Some argue that leaflet tissue redundancy (1.5 to 2.2 times normal mitral annular area) protects against leaflet malcoaptation in isolated annular dilatation [16]. Indeed limited annular dilation, or dilatation primarily in the C-C dimension [1618], may not be sufficient to cause functional mitral regurgitation. On the other hand, Levine and associates [19] demonstrated that the mitral leaflets enclose a volume between the leaflet surface area and the annular plane during systole, much like an upside-down tent, and that this volume correlates with regurgitant volume in CIMR. The volume of this "tent" can increase by making the tent floor bigger (increased annular area) or by making the tent pole longer (increased apical leaflet restriction). Thus annular dilatation even in the C-C direction may exacerbate leaflet malcoaptation by exhausting the supply of redundant leaflet tissue. Furthermore, dilatation in the C-C direction may contribute to malcoaptation of the individual scallops of the posterior leaflet [20, 21].

Clinical and experimental evidence indicate a more prominent role for S-L mitral annular dilatation in functional mitral regurgitation. In finite element models such dilation cause delayed and decreased leaflet coaptation as well as increased leaflet stress [22]. In an ovine model of dilated cardiomyopathy marked S-L dilatation was associated with significant MR and type-I (nonrestricted, nonprolapsed) leaflet motion without prominent subvalvular LV remodeling [14]. Other studies have demonstrated that in acute ischemic MR S-L annular dilatation is the predominant mechanism of mitral incompetence [23, 24] and that reduction of S-L diameter alone is sufficient to restore satisfactory leaflet coaptation, even with a slight increase in C-C diameter [25]. These studies indicate that although both S-L and C-C annular diameters are increased in CIMR, mitral repair should focus primarily on achieving S-L annular reduction.

Annular flattening
The saddle shape of the mitral annulus has been confirmed by three-dimensional echocardiography [26], marker fluoroscopy [14], and sonomicrometry [27]. This saddle shape contributes to leaflet curvature, which theoretically reduces leaflet stress in finite element models [28]. In CIMR the height of the annular saddle horn, or midseptal annulus, above the plane of the lateral annulus is reduced (Table 2, Fig 2), which makes the annulus flatter and could potentially increase leaflet closing stresses. Most existing mitral valve ring annuloplasty methods focus on annular geometry in only two dimensions (the plane of the annulus) without attempting to maintain or restore the saddle shape. Most currently available complete annuloplasty rings (with the exception of the slightly raised anterior "hump" of the Carpentier-Edwards Physio ring; Edwards Lifesciences, Irvine, CA) are relatively planar when compared with the native mitral annulus. These ovine findings suggest that mitral repair for CIMR should aim to restore the physiologic saddle shape of the annulus, perhaps by means of a ring designed with a more prominent saddle horn. Such a design theoretically would decrease leaflet stress, which might in turn potentially reduce the incidence of long-term structural valve deterioration [28].

The present findings extend those of previous studies using marker fluoroscopy or sonomicrometry to determine annular geometric distortions in acute ischemic MR that have demonstrated increased mitral annular area, S-L dilation [29, 30], and lengthening of the muscular annulus [29, 31]. These models of acute LV ischemia however did not detect C-C dilation [29, 30], lengthening of the fibrous annulus [29, 31], or reduced saddle horn height [31]. A comparison of annular geometric changes in acute IMR versus CIMR, summarized in Table 3, highlights the potential of the fibrous annulus to remodel over time, which may contribute to recurrent mitral regurgitation. This study was not designed to elucidate the mechanisms of dilation of the intertrigonal distance but we speculate that some combination of repetitive stress in a steadily dilating ventricle [32] and activation of matrix metalloproteinases (which have been implicated in remodeling associated with both mitral insufficiency [33] and ischemic heart failure [34]) contribute to the degradation and stretching of the fibrous skeleton.


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Table 3. Comparison of Annular Remodeling in Acute Versus Chronic Ischemic Mitral Regurgitation (IMR)

 
In summary CIMR was associated with proportional dilatation of the S-L and C-C annular diameters, lengthening of both the fibrous and muscular annular perimeters, and reduction in height of the mitral annulus. Such alterations in annular geometry may contribute to leaflet malcoaptation and increased leaflet closing stress. These three-dimensional in vivo data provide some rationale for the use of an undersized, complete annuloplasty ring that reduces the S-L annular dimension and restores the saddle shape of the annulus.

Limitations
This study used a model of ovine chronic inferior infarction that differs from the clinical entity in some respects. The sheep in this model had all undergone opening of the pericardium, cardiopulmonary bypass, and surgical manipulation of the mitral apparatus for marker placement. Also the animals were studied relatively early (7 weeks) after inferior myocardial infarction. Future studies with longer follow-up might show a greater degree of annular and LV remodeling.


    Acknowledgments
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
We appreciate the superb technical assistance provided by Carol W. Mead and Maggie Brophy. This work was supported by Grants HL-29589 and HL-67025 from the National Heart, Lung and Blood Institute (NHLBI). Doctors Tibayan, Rodriguez, and Langer are Carl and Leah McConnell Cardiovascular Surgical Research Fellows. Doctor Tibayan was supported by NHLBI Individual Research Service Award HL-67563. Doctor Rodriguez was supported by Grant HL67025–01S1 from the NHLBI and was a recipient of the American College of Surgeons Resident Research Scholarship Award.


    Footnotes
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
The Thoracic Surgery Directors Association (TSDA) Resident Research Award, sponsored by Medtronic, Inc, was established in 1990 to encourage resident research in cardiothoracic surgery. Abstracts submitted to The Society of Thoracic Surgeons (STS) Program Committee representing research performed by residents were forwarded to the TSDA to be considered for this award. The abstracts were reviewed by the TSDA Executive Committee, consisting of Edward D. Verrier, President, Douglas Mathisen, President-Elect, Jeffrey P. Gold, Secretary/Treasurer, and Richard Shemin and John Calhoon, Councillor-at-Large.

The twelfth TSDA Resident Research Award was given to Frederick A. Tibayan, MD, a cardiothoracic surgery resident, Stanford University School of Medicine, Stanford, CA. He received a monetary award of $2,500 and an engraved desktop award.

The TSDA, with support by Medtronic, Inc, makes this award annually, using the above selection procedure. The resident author of the selected study is recognized at the STS meeting.


    Discussion
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
DR L. HENRY EDMUNDS, JR (Philadelphia, PA): Our laboratory, now headed by the Gorman brothers, has performed similar studies of ischemic mitral regurgitation using the OM2,3 sheep model. Using sonomicrometry array localization, or SAL, which is an ultrasonic technique, we placed eight transducers around the annulus and additional transducers on the tips and bases of both papillary muscles. Over the first 8 weeks after infarction we also found that the annular area increased from about 6 cm2 to about 10 cm2.

We also found that annular stretching does include the fibrous trigone. Interestingly the muscular annulus closest to the anterior commissure stretches the most. Surprisingly the annulus closest to the infarct only stretches about 20% as compared with the much greater stretch of the muscular and fibrous annuli closest to the anterior commissure.

The distance between the tip of the anterior papillary muscle to both commissures increases dramatically. The greatest increase (about 1 cm) is between the anterior commissure and the tip of the posterior papillary muscle. However there is no change in the distance between the tip of the posterior papillary muscle and the posterior commissure. These findings highlight the ventricular component of this disease and of this model. The data also confirm the need for a saddle-shape annulus, which reduces leaflet stress as shown using finite element analysis by the same group headed by Ivan Salgo. Thus we agree that repair requires an annular ring that is complete and not C-shaped and that does not exclude the fibrous trigone.

DR TIBAYAN: Thank you, Dr Edmunds, for those comments. I'd like to take this time to thank you and your laboratory for your incredible generosity and expertise. Your lab, now headed by Dr Gorman, basically taught us how to do his model. And we would still be working on it if not for the very open sharing of your experience. So thank you very much.

DR EUGENE A. GROSSI (New York, NY): I have two questions. The first question is, you didn't tell us anything about the asymmetry in these changes in terms of these dimensions. You have dimensional data. Would it occur more anteroposterolateral, or was it equally distributed throughout, these changes in both the intertrigonal distance and the muscular distance?

And the second question is, I'd rather like to challenge your statement about the interpretation of the data. Yes, you show a 15% change in the intertrigonal distance and a 19% change in the intramuscular distance. But if you look at the absolute distances, you have a fourfold increase in the muscular changes as compared to the trigonal changes. If, indeed, we would argue that you could accomplish that clinically with a strong semi-rigid device which supports posteriorly from trigone to trigone.

DR TIBAYAN: As far as the symmetry of the remodeling of the annulus, looking at the individual eight segments, the segments between the two trigones certainly remodeled less than those of the muscular annulus. No formal individual comparison of the remaining six segments was really done, but perhaps that subject may be something we can look at in the future.

As far as the relative size of the dilation in the muscular and intertrigonal portions, although it was only a 4-mm increase in the intertrigonal distance, again, this occurred over only 7 weeks and perhaps over a greater amount of time this would be an area in which more considerable dilation may occur.

DR DAVID D. YUH (Baltimore, MD): The most surprising thing about your study to me is the variance in the fibrous perimeter of the mitral annulus. Do you have any plans or any expectation that there might be some histologic changes in that fibrous perimeter that might account in the case of ischemic MR for that elongation? Or can this be extrapolated to other forms of MR in terms of myxomatous disease and so forth?

DR TIBAYAN: This has been looked at somewhat in the human scenario. There is a recent paper by Hueb and colleagues that looked at idiopathic-dilated cardiomyopathy as well as ischemic-dilated cardiomyopathy, pathological specimens in which they found significant dilation in the fibrous annulus as well as the muscular annulus. So I think it may in fact be something that can happen generally over a large amount of time, perhaps in a wide variety of etiologies of heart failure.


    References
 Top
 Footnotes
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 

  1. Yiu S.F., Enriquez-Sarano M., Tribouilloy C., Seward J.B., Tajik A.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.[Abstract/Free Full Text]
  2. Otsuji Y., Handschumacher M.D., Liel-Cohen N., et al. 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.[Abstract/Free Full Text]
  3. Tahta S.A., Oury J.H., Maxwell J.M., Hiro S.P., Duran C.M. Outcome after mitral valve repair for functional ischemic mitral regurgitation. J Heart Valve Dis 2002;11:11-18.[Medline]
  4. Grigioni F., Enriquez-Sarano M., Zehr K.J., Bailey K.R., Tajik A.J. Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment. Circulation 2001;103:1759-1764.[Abstract/Free Full Text]
  5. Llaneras M.R., Nance M.L., Streicher J.T., et al. Pathogenesis of ischemic mitral insufficiency. J Thorac Cardiovasc Surg 1993;105:439-442.[Abstract]
  6. Moon M.R., DeAnda A., Jr, Daughters G.T., Ingels N.B., Miller D.C. Effects of chordal disruption on regional left ventricular torsional deformation. Circulation 1996;94(Suppl):II143-II151.
  7. Carpentier A., Deloche A., Dauptain J., et al. A new reconstructive operation for correction of mitral and tricuspid insufficiency. J Thorac Cardiovasc Surg 1971;61:1-13.[Medline]
  8. Cosgrove D.M., III, Arcidi J.M., Rodriguez L., Stewart W.J., Powell K., Thomas J.D. Initial experience with the Cosgrove-Edwards annuloplasty system. Ann Thorac Surg 1995;60:499-503.[Abstract/Free Full Text]
  9. Burr L.H., Krayenbuhl C., Sutton M.S. The mitral plication suture: a new technique of mitral valve repair. J Thorac Cardiovasc Surg 1977;73:589-595.[Abstract]
  10. Pellegrini A., Quaini E., Colombo T., Lanfranchi M., Russo C., Vitali E. Posterior annuloplasty in the surgical treatment of mitral insufficiency. J Heart Valve Dis 1993;2:633-638.[Medline]
  11. Choo S.J., Olomon J., Bowles C., et al. An in vitro study of the correlation between aortic valve diameter and mitral intertrigonal distance: a simple method to select the correct mitral annuloplasty ring size. J Heart Valve Dis 1998;7:593-597.[Medline]
  12. Hueb A.C., Jatene F.B., Moreira L.F., Pomerantzeff P.M., Kallas E., de Oliveira S.A. Ventricular remodeling and mitral valve modifications in dilated cardiomyopathy: new insights from anatomic study. J Thorac Cardiovasc Surg 2002;124:1216-1224.[Abstract/Free Full Text]
  13. Bolling S.F., Deeb G.M., Bach D.S. Mitral valve reconstruction in elderly, ischemic patients. Chest 1996;109:35-40.[Abstract/Free Full Text]
  14. Timek T.A., Dagum P., Lai D.T., et al. Pathogenesis of mitral regurgitation in tachycardia-induced cardiomyopathy. Circulation 2001;104(Suppl):I47-I53.
  15. Llaneras M.R., Nance M.L., Streicher J.T., et al. Large animal model of ischemic mitral regurgitation. Ann Thorac Surg 1994;57:432-439.[Abstract]
  16. Gorman J.H., III, Jackson B.M., Gorman R.C., Kelley S.T., Gikakis N., Edmunds L.H., Jr Papillary muscle discoordination rather than increased annular area facilitates mitral regurgitation after acute posterior myocardial infarction. Circulation 1997;96(Suppl):II7.
  17. Green G.R., Dagum P., Glasson J.R., et al. Mitral annular dilatation and papillary muscle dislocation without mitral regurgitation in sheep. Circulation 1999;100(Suppl):II95-II102.
  18. Otsuji Y., Kumanohoso T., Yoshifuku S., et al. Isolated annular dilation does not usually cause important functional mitral regurgitation: comparison between patients with lone atrial fibrillation and those with idiopathic or ischemic cardiomyopathy. J Am Coll Cardiol 2002;39:1651-1656.[Abstract/Free Full Text]
  19. Messas E., Guerrero J.L., Handschumacher M.D., et al. Chordal cutting: a new therapeutic approach for ischemic mitral regurgitation. Circulation 2001;104:1958-1963.[Abstract/Free Full Text]
  20. Lai D.T., Tibayan F.A., Myrmel T., et al. Mechanistic insights into posterior mitral leaflet inter-scallop malcoaptation during acute ischemic mitral regurgitation. Circulation 2002;106(Suppl):I40-I45.
  21. Myrmel T., Lai D.T., Lo S., et al. Ischemia-induced malcoaptation of scallops within the posterior mitral leaflet. J Heart Valve Dis 2002;11:823-829.[Medline]
  22. Kunzelman K.S., Reimink M.S., Cochran R.P. Annular dilatation increases stress in the mitral valve and delays coaptation: a finite element computer model. Cardiovasc Surg 1997;5:427-434.[Medline]
  23. Glasson J.R., Komeda M., Daughters G.T., et al. Early systolic mitral leaflet "loitering" during acute ischemic mitral regurgitation. J Thorac Cardiovasc Surg 1998;116:193-205.[Abstract/Free Full Text]
  24. Lai D.T., Timek T.A., Dagum P., et al. The effects of ring annuloplasty on mitral leaflet geometry during acute left ventricular ischemia. J Thorac Cardiovasc Surg 2000;120:966-975.[Abstract/Free Full Text]
  25. Timek T.A., Lai D.T., Tibayan F.A., et al. Septal-lateral annular cinching (SLAC) reduces mitral annular size without perturbing normal annular dynamics. J Heart Valve Dis 2002;11:2-9.[Medline]
  26. Flachskampf F.A., Chandra S., Gaddipatti A., et al. Analysis of shape and motion of the mitral annulus in subjects with and without cardiomyopathy by echocardiographic 3-dimensional reconstruction. J Am Soc Echocardiogr 2000;13:277-287.[Medline]
  27. Gorman R.C., McCaughan J.S., Ratcliffe M.B., et al. Pathogenesis of acute ischemic mitral regurgitation in three dimensions. J Thorac Cardiovasc Surg 1995;109:684-693.[Abstract/Free Full Text]
  28. Salgo I.S., Gorman J.H., III, Gorman R.C., et al. Effect of annular shape on leaflet curvature in reducing mitral leaflet stress. Circulation 2002;106:711-717.[Abstract/Free Full Text]
  29. Gorman J.H., III, Gorman R.C., Jackson B.M., et al. Distortions of the mitral valve in acute ischemic mitral regurgitation. Ann Thorac Surg 1997;64:1026-1031.[Abstract/Free Full Text]
  30. Timek T., Glasson J.R., Dagum P., et al. Ring annuloplasty prevents delayed leaflet coaptation and mitral regurgitation during acute left ventricular ischemia. J Thorac Cardiovasc Surg 2000;119:774.[Abstract/Free Full Text]
  31. Glasson J.R., Komeda M., Daughters G.T., et al. Three-dimensional dynamics of the canine mitral annulus during ischemic mitral regurgitation. Ann Thorac Surg 1996;62:1059-1067.[Abstract/Free Full Text]
  32. McCarthy P.M. Does the intertrigonal distance dilate? Never say never. J Thorac Cardiovasc Surg 2002;124:1078-1079.[Free Full Text]
  33. Rabkin E., Aikawa M., Stone J.R., et al. Activated interstitial myofibroblasts express catabolic enzymes and mediate matrix remodeling in myxomatous heart valves. Circulation 2001;104:2525-2532.[Abstract/Free Full Text]
  34. Mukherjee R., Brinsa T.A., Dowdy K.B., et al. Myocardial infarct expansion and matrix metalloproteinase inhibition. Circulation 2003;107:618-625.[Abstract/Free Full Text]



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