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J Thorac Cardiovasc Surg 1997;113:292-301
© 1997 Mosby, Inc.
SURGERY FOR ACQUIRED HEART DISEASE |
Supported by grants HL-29589 and HL-48837 from the National Heart, Lung, and Blood Institute and the Veterans Administration Medical Research Service. Drs. Komeda and Glasson are Carl and Leah McConnell Cardiovascular Surgical Research Fellows. Dr. Glasson is also supported by The Thoracic Surgery Foundation Research Fellowship Award.
Received for publication May 6, 1996 revisions requested July 16, 1996; revisions received Oct. 4, 1996 accepted for publication Oct. 9, 1996. Address for reprints: D. Craig Miller, MD, Department of Cardiovascular and Thoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247.
Abstract
Objectives. Mitral valve homografts, despite theoretical advantages, are not widely used, in part because of lack of basic information about the three-dimensional geometry of the mitral apparatus. Methods: Radiopaque markers were used in the study of eight closed-chest dogs under four conditions: (1) baseline, (2) caval occlusion, (3) tachycardia (atrial pacing), and (4) nitroprusside infusion. Using a cylindrical coordinate system, defined with the origin at the midpoint between the anterior and posterior commissures, and the left ventricular long axis (z-axis), defined by the origin and the left ventricular apex, DTIP-MA (the z-coordinate [millimeters] of the papillary muscle tip), was measured at 10 time points throughout the entire cardiac cycle. DBASE-MA (the z-coordinate of the papillary muscle base) and LPM (the length of the papillary muscle [millimeters]) were also measured. Results: DTIP-MA varied slightly with time (p < 0.001 by analysis of variance), but the magnitude of change was negligible (<0.9 mm) (e.g., DTIP-MA of the anterior papillary muscle was 20.7 ± 2.7/20.8 ± 2.8 [end-diastolic/end-systolic, mean ± 1 standard deviation]; DTIP-MA of the posterior papillary muscle was 25.8 ± 4.8/25.5 ± 4.5). DTIP-MA was minimally influenced by the above perturbations. DBASE-MA and LPM of each papillary muscle, however, changed throughout the cardiac cycle (p < 0.001 by analysis of variance) by about 4 mm, and both parameters were dependent on loading conditions. Conclusions. Papillary muscle length changed to keep the DTIP-MA distance constant such that the papillary muscle and left ventricular wall functioned together as a unit ("J-shaped complex"). These results provide a physiologic rationale for measuring DTIP-MA, define its potential surgical usefulness, and imply that using the entire length of the donor's papillary muscle (i.e., maintaining the entire J-shaped complex) is important in operations in which homograft or stentless xenograft mitral valves are used.
Use of a mitral valve homograft in the clinical setting was first reported by Senning and Largiadér
1 three decades ago and was supported by encouraging results from laboratory studies. 2-4 Because of its anatomic features, the mitral homograft may function like a normal mitral valve in preserving valvular-ventricular interaction, 5-7 sphincteric motion of the anulus, 8-11 and the saddle shape 12 of the anulus more completely than other types of valve substitutes. Mitral homograft or stentless xenograft valves have not been widely used in patients, however, because of discouraging clinical results. 13-18 Problems encountered with mitral homografts include limited durability of the leaflets, chordae tendineae, or papillary muscles (PMs) (including the suture lines 15,16) and difficulty with surgical implantation. Such technical challenges (including proper sizing 19 and orientation) may be due in part to lack of basic information about the functional three-dimensional geometry of the mitral valve anulus and subvalvular apparatus. Recently, with improved tissue preservation techniques (e.g., cryopreserved aortic homograft 20) and increased experience in reparative mitral surgery, 21 mitral homografts and stentless mitral xenograft valves are again attracting attention. 22-25 In this article we report an interesting, well-regulated spatial relationship between the PM and the mitral anulus, which is termed the J-shaped complex. The long descending limb of the J-shaped complex is the left ventricular (LV) wall extending from the anulus to the PM base, and the short ascending limb is defined as the PM. This quantitative approach may be of clinical utility for homograft sizing and orientation, as well as for planning extensive mitral reparative operations.
Materials and methods
Surgical preparation.
Eight healthy adult mongrel dogs (30 ± 5 kg, mean ± standard deviation) were premedicated with acepromazine (0.01 to 0.05 mg/kg intramuscularly) and atropine sulfate (0.05 mg/kg intravenously). Details of this preparation have been described elsewhere. 11 The dogs were anesthetized with sodium thiopental (20 mg/kg intravenously), intubated, and supported with a ventilator. General anesthesia was maintained with inhalational isoflurane at 1% to 2.2%. The left side of the chest was opened in the fifth intercostal space, pneumatic occluders were applied to the inferior and superior venae cavae, and the heart was exposed and suspended in a pericardial cradle. Miniature tantalum radiopaque helices (inner diameter 0.8 mm, outer diameter 1.3 mm, length 1.5 to 3.0 mm) were inserted into the LV wall and interventricular septum at selected sites (Fig. 1, A). Eight markers were placed into the LV subepicardial layer along four equally spaced longitudinal meridians around the circumference of the ventricle (in the anterior, lateral, posterior, and septal walls). Each meridian contained markers at two levels (the basal-equatorial and apical-equatorial planes). A ninth marker was placed at the LV apex. The septal markers were inserted with the aid of two-dimensional epicardial echocardiographic guidance to place the markers at the desired sites on the right ventricular surface of the interventricular septum. The animal was heparinized (300 IU/kg intravenously), and cardiopulmonary bypass (CPB) was instituted; a 14F or 16F arterial cannula was inserted into the right femoral artery, and a two-stage venous cannula was inserted into the right atrium and inferior vena cava. CPB was instituted with a roller pump and bubble oxygenator. The ascending aorta was crossclamped, and the heart was arrested with 500 ml of cold crystalloid cardioplegic solution delivered in an antegrade fashion. Topical cold saline solution was used subsequently to keep the LV myocardial temperature less than 16° C. The left atrium was opened, exposing the mitral apparatus. As illustrated in Fig. 1, A, one miniature gold marker was sewn to the largest tip of each PM and one tantalum marker to the base of each PM. Four miniature tantalum markers were then sutured to the mitral anulus, one near each commissure and one each on the midanterior and midposterior anulus. An implantable Königsberg pressure transducer (P 4.5X, Königsberg Instruments, Inc., Pasadena, Calif.) was placed in the LV lumen via the apex for subsequent monitoring of LV chamber pressure. The aortic crossclamp was released, the left atriotomy closed, the heart defibrillated if needed, and the dog weaned from CPB. Heparin was reversed with protamine sulfate, and the pericardium was loosely reapproximated. Chest tubes were placed, and the incision was closed. The animals recovered in the intensive care unit of the Stanford University Department of Laboratory Animal Medicine. Oxymorphone hydrochloride (Numorphan, 0.05 to 0.2 mg/kg intravenously, DuPont Merck Pharma, Manatic, Puerto Rico) was used to minimize discomfort.
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26 was also administered (4 to 6 mg intravenously in a single dose) to lower the heart rate further, if needed. Data were obtained in normal sinus rhythm in all but one dog, which was atrially paced at 120 min-1 because of rate-dependent atrioventricular dissociation. Baseline hemodynamics and biplane videofluoroscopic data recordings were obtained during steady-state conditions and during preload reduction by vena caval occlusion. Subsequently, data were taken during tachycardia by atrial pacing. Finally, data were acquired during afterload reduction induced by intravenous infusion of sodium nitroprusside. 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 the Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by the National Institutes of Health (DHEW [NIH] publication No. 85-23, revised 1985). The study was approved by the Stanford University Medical Center Laboratory Research Animal Review Committee and conducted according to Stanford University policy.
Data acquisition.
All imaging studies were conducted with the animal in the right lateral decubitus position with the use of a Philips Optimus 2000 biplane Lateral ARC 2/Poly DIAGNOST C2 system (Philips Medical Systems International B.V., Best, The Netherlands) with the image intensifiers in the 7-inch cine mode. The 45-degree right and left anterior oblique biplane images were recorded simultaneously at a rate of 60 frames/sec on Sony U-Matic 5800 
-inch videocassette recorders (Sony Electronics, Inc., Montvale, N.J.). The analog LV pressure signal was digitized and recorded on each individual video image by means of a custom intelligent video controller (Control Video Corp., Campbell, Calif.); the upstroke of the R wave of the electrocardiogram was detected electronically and also digitally encoded on the videotape as an end-diastolic timing marker. At the completion of the study, images of grids containing 1 cm squares and biplane images of a three-dimensional helical phantom of known dimensions were recorded to determine radiographic distortion and magnification factors. The two-dimensional coordinates of each marker in each projection (x,y and y,z) were digitized frame by frame with the use of a semi-automated, computerized myocardial marker detection system (Hewlett-Packard RS/20 [Palo Alto, Calif.], equipped with Matrox MVP/AT/NP image processing boards [Dorval, Quebec, Canada]) and custom image-processing and digitization software developed in our laboratory. 27 The data from the two views were corrected for X-ray magnification and distortion and were merged with the use of custom software to yield the three-dimensional coordinates of each marker every 16.7 msec, as previously described. 28,29
During data acquisition, two channels of analog data (LV pressure and surface-lead electrocardiogram) were acquired and digitized simultaneously at 240 Hz with the use of a 486-based microcomputer (486-33, JDR Microdevices Inc., San Jose, Calif.) with a high-speed data acquisition card (DT 3831-G, Data Translation Inc., Marbolo, Mass.) controlled by commercially available software (Labtech Control 3.2.0, Laboratory Technology Corp., Wilmington, Mass.). These analog signals were simultaneously recorded on a multichannel recorder at a paper speed of 25 mm/sec. The 240 Hz pressure data were temporally aligned with the 60 Hz marker-derived geometry data by frequency-corrected convolution of the 240 Hz and 60 Hz signals.
Data analysis.
Hemodynamics.
To minimize the effects of intrathoracic pressure variation, only end-expiratory beats were selected for analysis. The time derivative of the LV pressure signal was computed to determine peak positive LV dP/dt (dP/dtmax) and peak negative LV dP/dt (-dP/dt). For each cardiac cycle, the time of end-diastole was defined as the videofluoroscopic frame containing the R-wave marker of the electrocardiogram, and end-systole was defined as the videofluoroscopic frame immediately before the frame that contained the point of maximum negative LV dP/dt. LV ejection fraction was calculated as ([EDV - ESV]/EDV) · 100%, where EDV and ESV are end-diastolic and end-systolic LV volumes. The method used to compute LV volume has been described previously. 11
Distance between the PM tip and mitral anulus.
The distances between the PM tip/base and the mitral anulus were measured as the z-coordinate by means of the cylindrical coordinate system 11 shown in Fig. 1, B. The origin was placed at the midpoint between the anterior and posterior commissures of the mitral anulus, and the LV long axis (z-axis) was directed toward the LV apex; the three-dimensional location of each marker is expressed as the distance to the anulus (z, millimeters), radial position from the z-axis (r, millimeters), and angle (
, degrees; 
= 0 degrees precisely between both commissures on the midposterior anulus, = +90 degrees at the anterior commissure and = -90 degrees at the posterior commissure). We also measured the length of each PM as the distance between markers at the PM tip and base.
Statistical analysis.
All data are reported as mean ± 1 standard deviation. The z-coordinate and PM length were compared with respect to time (i.e., at 10 time points during the cardiac cycle) by means of multivariate analysis of variance, with dog identification entered as a dummy variable to control for between-animal variability differences. Post hoc testing was performed by means of Bonferroni's correction. The z-coordinate of the PM markers and the true three-dimensional PM length were compared between baseline and each intervention (such as caval occlusion, nitroprusside infusion, and pacing) by t tests for paired observations. Statistical significance was inferred if the corrected p value was less than 0.05. For all statistical analyses, SYSTAT (version 5.02, SPSS Inc., Chicago, Ill.) was used.
Results
Hemodynamics.
Average heart rates were 108 ± 11, 103 ± 9, 108 ± 14, and 131 ± 5 min-1 during baseline, caval occlusion, nitroprusside infusion, and atrial pacing (p < 0.001 vs baseline), respectively. LV end-diastolic volumes (uncorrected for LV wall mass, inasmuch as these were epicardial marker measurements, which included myocardial volume) were 143 ± 16, 104 ± 13, 133 ± 11, and 139 ± 14 ml, respectively (p < 0.001, caval occlusion vs baseline; p < 0.05, nitroprusside or atrial pacing vs baseline). LV ejection fractions (epicardial) were 21% ± 5%, 11% ± 4%, 21% ± 4%, and 19% ± 4%, respectively (p < 0.001, caval occlusion vs baseline; p = 0.01, atrial pacing vs baseline). Maximum LV systolic pressures were 132 ± 23, 92 ± 20, 118 ± 19, and 137 ± 22 mm Hg, respectively (p < 0.001, caval occlusion and nitroprusside vs baseline; p = < 0.041, atrial pacing vs baseline). dP/dtmax values were 1591 ± 182, 1161 ± 206, 1554 ± 206, and 1700 ± 206 mm Hg/sec, respectively (p < 0.001, caval occlusion vs baseline; p < 0.05 [p = 0.018] atrial pacing vs baseline).
Anterior PM.
In baseline conditions, there were statistically significant differences (p < 0.001 by analysis of variance) between the 10 time points for the z-coordinate of the PM tip and base, as well as for PM length. The magnitude of change in the anterior PM tip z-coordinate, however, was less than 0.9 mm; this was a small change compared with the z-coordinate of the anterior PM base or the PM length distance, which varied by about 4 mm (Fig. 2).
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0.3 mm); conversely, during caval occlusion, the anterior PM length was shorter than the baseline measurements, especially during systole (p < 0.005). The percent change in the z-coordinate of the anterior PM tip and base and change in anterior PM length are shown in Fig. 3. The percent reduction in anterior PM length was greater during systole (i.e., up to 12%) than the fractional change in the z-coordinate of either the anterior PM base or tip (i.e., maximum changes of 8% and 3.5%, respectively, p < 0.001 by analysis of variance).
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The percent change in the z-coordinate of the posterior PM tip and base and the posterior PM length are illustrated in Fig. 5. Percent reduction in posterior PM length was greater during systole (i.e., up to 10%) than the relative change in the z-coordinate of either the posterior PM base or the tip (i.e., up to 5% and 2.5%, respectively, p < 0.001 by analysis of variance).
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The change of the z-coordinate of both PM tips was negligible for practical surgical purposes (e.g., less than 1 mm), when the reproducibility of echocardiography and accuracy of surgical visualization are taken into account. The relatively load-insensitive nature of the PM tip–mitral anulus distance demonstrated in this study may provide a sound physiologic rationale supporting the method of sizing mitral homografts reported by Acar and associates, 24 who used the following parameters: (1) the height of the anterior mitral leaflet in diastole, (2) the anteroposterior diameter of the anulus in systole, and (3) the distance between the anulus and the PM tip.
The results of this study show that the length of the PM changed in just the right way to keep the z-coordinate of the PM tip nearly constant with respect to the mitral anulus. To clarify this concept, we propose the notion of a "J-shaped complex" comprising two components working together: a long descending limb (LV wall from the anulus to the PM base) and a short ascending limb (the PM per se). We assume that one of the reasons for the short ascending limb offsetting the motion of the long descending limb in the z direction was the different curvature between the two limbs. The ascending limb (i.e., PM) has nearly no curvature, but the descending limb (i.e., LV wall) has a curved shape; thus shortening of fibers in the descending limb will not result in proportional shortening in the z-direction. Another reason relates to relatively more systolic thickening of the LV free wall than the PM.
Acar and associates 24 described the difficulty associated with implanting a mitral homograft valve in patients who had previously undergone mitral valve replacement, especially when the subvalvular apparatus had been excised during the previous operation. Under these circumstances, the remaining atrophic PM essentially eliminates the ascending limb of the J-shaped complex, and the PM tip cannot maintain a constant distance from the anulus. Acar and colleagues 24 also discussed problems stemming from transfixing sutures between the chordae of the homograft through the LV wall. These problems, again, may be related to either absence or dysfunction of the ascending limb of the J-shaped complex, resulting in geometric alterations of the mitral valve that possibly could lead to the development of mitral regurgitation.
Thus, if a recipient's PM is excised 25 or if the homograft's PM is sewn to the recipient's PM in a side-by-side fashion (especially when the homograft is sewn near the base of the recipient's PM 14) or a transpapillary suture is used, 18 the PM-anulus distance may not remain constant and the homograft may be exposed to excessive systolic motion and stresses, possibly resulting in mitral regurgitation; under these conditions, the PM tip may actually move in a similar fashion to the PM base. Even when the homograft is sewn to the tip of the recipient's PM, scar formation around the sutures may have some influence on PM function. The degree of this impact, however, should be much less than that occurring when the homograft is sewn to the recipient's PM mid-body or base or when the recipient's PM is infarcted or partially excised. Therefore care should be taken to try to sew the homograft only to the PM tip. The results of this study suggest the importance of using the entire length (or as much as possible) of the recipient's PM whenever possible to maintain the J-shaped complex.
One limitation of this work is that we studied only normal canine hearts (which are distinctly different from hearts exposed to volume overload from mitral regurgitation 16); however, these observations indicate that future study of the motion and geometry of the components of the J-shaped complex in dilated ventricles both before and after LV remodeling 19 (i.e., before and after surgical correction of mitral regurgitation) should yield even more useful clinical information. If the myocardium is not irreversibly damaged by chronic mitral regurgitation and previous myocardial infarction has not damaged the PM, the J-shaped complex should remain functionally intact, thereby theoretically allowing the distance between the PM tip and the mitral anulus to remain constant both before and after correction of mitral regurgitation.
There are several other limitations to this study. First, we used a normal canine model with PM and chordae tendineae anatomy similar, but not identical to, human anatomy. For example, human PMs (especially the anterior PM) project into the LV chamber more than canine PMs. This projection, however, probably would not alter the constancy of the distance between the PM tip and the anulus because longer PMs shorten and lengthen more. Second, because of the temporal sampling rate limit of the biplane cine x-ray system (60 Hz), it was necessary to reduce the heart rate with esmolol and UL-FS49. The tachycardia studies were conducted at a heart rate of 140 min-1. It is unknown whether the results would be different at a higher or lower heart rate. Third, we placed the markers on the largest tip of each PM even though multiple PM heads exist; we have no knowledge of the three-dimensional dynamics of the other PM heads.
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Appendix: Discussion
Dr. Robert W. Frater (Bronx, N.Y.).
I cannot find fault with Dr. Komeda's measurements, but I find them counterintuitive. We know, from frequent echocardiographic observations, that the tip of the ventricle unquestionably moves away from the anulus in diastole, presumably taking the PM along, and yet we do not see normal chordal bending. If the anulus-PM distance was constant, the chordae would have to bend for this to happen. We have made a whole series of observations in long-axis echoes of the distance between the tip of the PM and the plane of the anulus, and we find that in fact the tip moves toward the anulus in systole and away in diastole and the difference in length is between 10% and 20%. This does not happen in patients with posterior LV wall damage and happens much less often in hearts that are severely myopathic.
The ejection fractions at the time of study were from 11% to 21%. This suggests to me that this is not an observation in a normal dog but an observation in a dog with a myopathic heart. Could you comment on that?
Dr. Komeda.
We measured the distance between the PM tip and the mitral anulus, not between the leaflet tip and the mitral anulus. As you pointed out, if the distance between the PM tip and mitral anulus is constant, something should bend during diastole when the leaflets open; it may be a leaflet, or the junction between the leaflet and chordae, chordae, or their combination. We are currently investigating this question.
When using echocardiography to measure this kind of distance, we must be very careful about which cross-section we are imaging and which precise site we are talking about. We presented a paper pertaining to this issue at the 1995 meeting of the American Heart Association, which will be published in Circulation. For instance, if we measure the distance between one point on the posterior anulus near the anterolateral commissure and the posterior papillary tip, it shortens significantly during systole. Similarly, the distance between a posterior annular point near the posteromedial commissure and the anterior papillary tip shortens. That is what we call the "oblique direction," which may be a more physiologic orientation for chordal resuspension during mitral valve replacement. But, if we measure the distance between a posterior annular locus in the vicinity of the posteromedial commissure and the posterior papillary tip, it is constant throughout the cardiac cycle; this was also the case between an annular point near the anterolateral commissure and the anterior papillary tip. We confirmed this observation with both radiopaque marker cinefluoroscopy and two-dimensional epicardial echocardiography, where we knew the exact orientation of the echo cross-section. Therefore measuring the distance between an annular point and a PM tip by transesophageal or transthoracic echocardiography without precisely confirming which cross-section is being imaged can be misleading; this is one of the reasons we measured the distance between the PM tip and a point representing the mitral annular plane.
LV ejection fraction was calculated by means of data derived from the epicardial markers. Hence this method did not take into account LV wall thickness or systolic wall thickness, which is a manor component of chamber (angiographic or echocardiographic) ejection fraction. When we corrected the ejection fraction estimate for wall thickness, the ejection fraction was approximately 35% and would be considerably higher had LV wall thickening been taken into consideration. Therefore we believe that LV systolic function in this experiment was only slightly depressed.
Dr. Radu C. Deac(Targu-Mures, Romania).
The data presented in this study confirm the known shortening of the PM up to 20% but point out the relatively constant distance between the mitral anulus and the tip of the PM. The physiologic significance of this observation has to be elucidated in the future.
Do you have any data about this dimension in ischemic conditions? Using this measurement as the principal dimension of a stentless mitral pericardial valve, we obtained a competent mitral substitute in each of the 23 patients operated on since 1989 in our unit. However, with changed PM–mitral anulus distance in a diseased ventricle, which is smaller in mitral stenosis and variable in mitral regurgitation or mixed mitral valve disease, we had to attach the graft at a different length than this measured distance, even at a different length for each PM, to obtain a competent valve. With the current technique of allograft and xenograft replacement of the mitral valve, it will be interesting to see how a normal mitral valve will function in a given diseased ventricle.
Dr. Komeda.
The geometry of the PMs and mitral anulus in the context of myocardial ischemia and mitral homograft replacement is a key clinical issue.
We presented the geometry of the PMs, mitral leaflets, and mitral anulus with or without ischemic mitral regurgitation (induced by proximal circumflex coronary artery occlusion) at the 1995 meeting of the American Heart Association. During ischemic mitral regurgitation, the z-coordinate of the posterior PM tip did not change; however, and quite unexpectedly, the anterior PM tip (on the nonischemic side) became translocated toward the LV apex because of ventricular dilatation and a normally functioning anterior PM. In the radial direction (r values), both the anterior and posterior PM tips were dislocated, but the magnitude of change was much larger on the posterior PMs (or ischemic side). We agree that when a mitral homograft or stentless mitral valve is used for patients with ischemic mitral regurgitation, this perturbed geometry needs to be contemplated.
Dr. Carlos M. G. Duran (Missoula, Mont.).
The message is that the distance between the tip of the PM and the anulus does not change during the cardiac cycle under any circumstance. This became obvious to me when I saw the videos of Dr. Van Zwinker, who showed this phenomenon very clearly. The morphologic explanation is the presence of two basal chordae to the anterior leaflet, which we call "stay chordae" and which can be seen very clearly by echocardiography. If I may be allowed a semantic comment, I suggest that instead of calling the ventriculomitral functional unit the "J-shaped complex," rather use the "ventricular loop" as a more appropriate term for a closed and not open complex.
My question for the authors is this: How do you expect this information to help in mitral homograft transplantation? In the three cases we have performed, we have used this principle as the key distance to correctly determine where to suture the donor to the recipient PMs.
Dr. Komeda.
You are correct, Dr. Duran. Functionally the PMs and the LV wall make a closed loop. Morphologically, however, there is a gap in this loop between the PM tip and mitral anulus, at least during diastole, when certain chordae may be redundant or slack; this is why we call this a "J-shaped" complex. By the term "complex," we meant not only the PM-anulus continuity, but also the geometric changes modulated by all elements of the entire structure (i.e., PMs and mitral anulus). Concerning your question about applying these findings to clinical mitral homograft surgery, if we can use the entire length of the recipient PM (and assuming it is viable), a relatively stable condition should result. On the other hand, if one resects the tip of the recipient PM or sews the donor's PM to the base of the recipient PM (as done in many previous reports), early failure of the homograft or substantial mitral regurgitation may result, perhaps caused in part by excessive motion or tension, or both.
Acknowledgments
We gratefully acknowledge the help of Byron W. Brown, PhD, Professor of Biostatistics at Stanford University, and the expert technical assistance of Marek A. Niczyporuk, BS, Mary K. Zasio, BA, Erin M. Schultz, BS, Geraldine C. Derby, RN, BS, Terrence L. Tye, MS, and Carol Mead, BA, in the performance of this work and Ms. Phoebe E. Taboada for her assistance in the preparation of the manuscript.
Footnotes
From the Department of Cardiovascular and Thoracic Surgerya and the Division of Cardiovascular Medicine,b Stanford University School of Medicine, Stanford, Calif., the Palo Alto DVA Medical Center,c Palo Alto, Calif., and the Department of Cardiovascular Physiology and Biophysics,d Research Institute, Palo Alto Medical Foundation, Palo Alto, Calif. 
Read at the Seventy-sixth Annual Meeting of The American Association for Thoracic Surgery, San Diego, Calif., April 28–May 1, 1996.
References
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N. Liel-Cohen, J. L. Guerrero, Y. Otsuji, M. D. Handschumacher, L. G. Rudski, P. R. Hunziker, H. Tanabe, M. Scherrer-Crosbie, S. Sullivan, and R. A. Levine Design of a New Surgical Approach for Ventricular Remodeling to Relieve Ischemic Mitral Regurgitation : Insights From 3-Dimensional Echocardiography Circulation, June 13, 2000; 101(23): 2756 - 2763. [Abstract] [Full Text] [PDF]
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T. Sakai, Y. Okita, Y. Ueda, T. Tahata, H. Ogino, K. Matsuyama, and S. Miki DISTANCE BETWEEN MITRAL ANULUS AND PAPILLARY MUSCLES: ANATOMIC STUDY IN NORMAL HUMAN HEARTS J. Thorac. Cardiovasc. Surg., October 1, 1999; 118(4): 636 - 641. [Abstract] [Full Text] [PDF]
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