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Ann Thorac Surg 1996;62:1059-1067
© 1996 The Society of Thoracic Surgeons
Department of Cardiovascular and Thoracic Surgery and Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford; and Cardiac Surgery and Cardiology Sections, Department of Veterans Affairs Medical Center, and Department of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, California
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. We used radiopaque markers and simultaneous biplane videofluoroscopy to measure three-dimensional in vivo lengths of eight MA segments in 7 sedated dogs before and after induction of ischemic MR (produced by circumflex coronary artery balloon occlusion and verified by Doppler echocardiography). As viewed from the left atrium, the MA segment between markers 1 and 2 (S12) was defined as starting at the posteromedial commissure, and remaining segments were numbered sequentially clockwise around the MA (ie, the posterior MA encompassed S12, S23, S34, S45; the anterior MA included S56, S67, S78, S81). Marker images obtained 7 to 12 days after implantation were used to construct x, y, and z coordinates of each marker at end-diastole and end-systole.
Results. During regional (posterolateral walls) left ventricular ischemia, the end-systolic MA area increased (4.9 ± 0.8 cm2 [control] versus 5.9 ± 0.6 cm2; p = 0.005). End-systolic MA segment lengths were as follows (control, ischemia [mm, mean ± standard deviation]): S12 = 9 ± 2, 10 ± 3; S23 = 10 ± 2, 12 ± 3; S34 = 13 ± 1, 15 ± 1; S45 = 8 ± 2, 9 ± 2; S56 = 11 ± 2, 11 ± 2; S67 = 12 ± 2, 12 ± 2; S78 = 10 ± 3, 11 ± 2; and S81 = 11 ± 1, 12 ± 1. Values for S12, S23, S34, and S81 were significant (p 
0.05 for control versus ischemia by paired t test).
Conclusions. During ischemic mitral regurgitation, the MA enlarged at end-systole, but in an asymmetric manner; most posterior annular segments lengthened, whereas most anterior annular segment lengths did not change. These data suggest that alterations in regional MA mechanics may be important in the pathogenesis of ischemic mitral regurgitation. Further three-dimensional studies of MA dynamics and shape should be conducted so that new knowledge may result in improved mitral valve surgical techniques.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Ischemic mitral regurgitation (MR) is a common entity, with up to 19% of patients having some degree of MR when evaluated for coronary artery disease after myocardial infarction [1]. Some of these patients experience progressive, moderate or severe MR over the ensuing months or years, and many ultimately require operative intervention. At present, the preferred operative treatment of ischemic MR is mitral valve repair when feasible [2], frequently including ring annuloplasty [3, 4], even though the role of the mitral annulus (MA) in the pathogenesis of ischemic MR is incompletely understood. Previous reports have suggested that ischemic MR results, at least in part, from generalized end-systolic MA dilatation [5, 6], but segmental MA dynamics during myocardial ischemia have not been described. To date, studies of MA motion (using cinefluoroscopy of lead beads sutured to the MA [7] or echocardiography to image the MA [8, 9]) have been limited by the inability to define and track the motion of discrete sites on the mitral apparatus in three-dimensional (3-D) space.
In this experiment (using the same cohort of animals as in a previous study [10]), circumflex coronary artery balloon occlusion was used to induce acute ischemic MR to assess the effects of acute posterolateral left ventricular (LV) ischemia and resultant MR on MA dynamics. We used myocardial marker technology [11] to measure in vivo changes in 3-D regional MA size and shape occurring throughout the cardiac cycle. The dynamics of the MA during posterolateral LV ischemia and MR were compared with those during preischemic control conditions.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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). Each meridian contained markers at two levels, in the basal-equatorial and apical-equatorial planes. A ninth marker was placed at the LV apex. Epicardial echocardiographic guidance was used to place the septal markers at the desired sites on the right ventricular endocardial side of the septum. This marker arrangement permitted visualization of the LV silhouette in both the 45-degree right anterior oblique and the 45-degree left anterior oblique videofluoroscopic projections.
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The left atrial appendage was opened. Eight miniature tantalum radiopaque markers were sutured at equal distances around the circumference of the MA (see Fig 1
, Fig 2), one near each commissure (markers 1 and 5) and three along the perimeters of the anterior (markers 6 to 8) and posterior (markers 2 to 4) leaflets. An implantable Konigsberg micromanometer pressure transducer (P4.5-X6; Konigsberg Instruments, Inc, Pasadena, CA) was placed in the LV chamber through the apex for subsequent LV pressure measurements. The heart was rewarmed, the left atriotomy was closed, the aortic cross-clamp was released, and the animal was weaned from cardiopulmonary bypass. Heparin was reversed with protamine, and the pericardium was loosely reapproximated. To reduce immediate postoperative pain, we performed an intercostal block (20 mL 0.25% bupivacaine) at the fourth, fifth, and sixth intercostal spaces. Chest tubes were placed, transducer leads and occluder tubes were exteriorized, and the incision was closed. Oxymorphone hydrochloride (Numorphan, 0.05 to 0.2 mg/kg IV; DuPont Merck Pharma, Manatic, Puerto Rico) was given as needed to minimize incisional discomfort, and the animals recovered in the intensive care unit of the Stanford University Department of Laboratory Animal Medicine.
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An 8-F Powerbase coronary guiding catheter (Advanced Cardiovascular Systems, Inc, Temecula, CA) was advanced into the left main coronary artery over a 0.014-in hi-torque floppy guidewire (Advanced Cardiovascular Systems, Inc) through the 8F left femoral artery sheath. A conventional 3.5-mm nonperfusion balloon dilation catheter was then advanced through the guiding catheter into the proximal left circumflex coronary artery (in 6 dogs) or into a large posterior descending branch (1 dog). Balloon size was selected to be fully occlusive. The balloon was inflated to 6 atm, with complete occlusion of the selected artery in all cases. The balloon was kept inflated for 2 to 3 minutes, producing acute myocardial ischemia in the posterolateral LV walls and resulting in ischemic MR. Ischemic MR was verified and graded by a single observer as none, mild to moderate, or moderate to severe using transthoracic Doppler echocardiography.
Data were obtained with the hearts in normal sinus rhythm, except for one (dog 7), which was atrially paced at 120 beats/min secondary to atrioventricular dissociation. Hemodynamic and biplane videofluoroscopic data recordings were obtained during steady-state conditions and over a physiologic range of peak LV systolic pressures during vena caval occlusion immediately before and after coronary artery balloon occlusion. The dogs were allowed to stabilize for 3 to 5 minutes between data acquisitions. Any sequences containing premature ventricular contractions were discarded and subsequently repeated.
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 (NIH publication 85-23, revised 1985). This study was approved by the Stanford Medical Center Laboratory Research Animal Review Committee and was conducted according to Stanford University policy.
Data Acquisition
All imaging studies were conducted with the animal in the right lateral decubitus position using a Philips Optimus 2000 biplane Lateral ARC 2/Poly DIAGNOST C2 system (Philips Medical Systems, North America Co, Pleasanton, CA) with the image intensifiers in the 7-in fluoroscopic mode. The 45-degree right anterior oblique and 45-degree left anterior oblique biplane fluoroscopic images were recorded simultaneously on two Sony U-Matic 5800 3/4-in video cassette recorders (Sony Corp, Japan). The analog LV pressure signal was recorded in digital format on each individual video image using a customized intelligent video controller (Grey Engineering Corp, Los Angeles, CA); the electrocardiographic (ECG) R wave was detected electronically and encoded digitally on the videotape as an end-diastolic timing marker. At the completion of the study, images of 1-cm grids and biplane images of a 3-D helical phantom of known dimensions were recorded to determine radiographic distortion and magnification factors. The 2-D coordinates of each marker in each projection were digitized frame by frame using semiautomated customized image-processing and digitization software developed in our laboratory [13] and run on a microcomputer system (Hewlett-Packard RS/20, Palo Alto, CA; equipped with Matrox MVP/AT/NP image-processing boards, Dorval, Quebec, Canada). Data from the two views were corrected for x-ray magnification and distortion, and right anterior oblique and left anterior oblique marker coordinates were merged using custom software as described previously [14] to yield 3-D coordinates of each marker every 16.7 milliseconds.
During data acquisition, two channels of analog data (LV pressure and surface lead ECG) were acquired and digitized simultaneously at 240 Hz using a microcomputer (486-33; JDR Microdevices Inc, San Jose, CA) with a high-speed data-acquisition card (DT 3831-G; Data Translation Inc, Marlboro, MA) controlled by data-acquisition software (Labtech Control 3.2.0; Laboratory Technology Corp, Wilmington, MA). These analog signals also were simultaneously recorded on a multichannel recorder (580CDR/16; Vidco Inc, Beaverton, OR) at a paper speed of 25 mm/s. The 240-Hz pressure data were merged with the 60-Hz marker-derived geometry data, aligning the LV pressure signals (or ECG R waves) from the two sources by calculating and minimizing a convolution of the 240-Hz and 60-Hz signals to be matched.
Data Analysis
Data from three consecutive steady-state beats during both preischemic control and ischemic MR conditions were averaged and analyzed as control and ischemia data, respectively.
HEMODYNAMIC INDICES.
To minimize the effects of intrathoracic pressure variation, we used only end-expiratory beats for analysis. The time derivative of the LV pressure signal was used to determine peak positive LV dP/dt (dP/dtmax) and peak negative LV dP/dt (-dP/dtmax). For each cardiac cycle, the time of end-diastole (ED) was defined as the videofluoroscopic frame containing the ECG R wave, and end-systole (ES) was defined as the videofluoroscopic frame immediately before the frame that contained the point of maximum negative LV dP/dt.
LEFT VENTRICULAR VOLUME.
Instantaneous LV volume was calculated with a multiple elliptic cylinder/cone model [15]. The eight LV epicardial markers, eight MA markers, and one apical marker (see Fig 1) define three cross-sectional marker layers from base to apex (annular, basal-equatorial, and apical-equatorial). The LV volume was computed as the sum of the volumes of two elliptic cylinders (between the annular and basal-equatorial layers, and the basal-equatorial and apical-equatorial layers) and one elliptic cone (between the apical-equatorial layer and the apex). This computed volume included both the myocardial volume and the volume of the blood contained within the LV chamber. We have previously shown that changes in this computed volume accurately reflect changes in LV chamber volume [16]. These volume differences were sufficient for our present purposes; we did not attempt to estimate absolute LV chamber volume in this study.
SYSTOLIC LEFT VENTRICULAR FUNCTION.
Systolic performance was assessed as LV end-systolic elastance, measured from the end-systolic pressure-volume relation [17]. We determined LV end-systolic pressure (Pes) and volume (Ves) instantaneously during preload reduction using an iterative computer algorithm to define the end-systolic pressure-volume relation [18]. Least-squares linear regression was used to fit a line of the form: Pes = Ees (Ves - V0) to these end-systolic points, where Ees and V0 are the slope and volume axis intercept, respectively.
MITRAL ANNULAR DYNAMICS.
Segmental lengths between adjacent MA markers were computed from the 3-D MA marker coordinates at ED and ES. Percentage systolic shortening for each segment was calculated as ([Led - Les]/Led) • 100%, where Led and Les are end-diastolic and end-systolic segment lengths; negative values indicate systolic lengthening. The MA area and perimeter were also computed from the 3-D marker coordinates, without assuming circular or planar geometry. The MA perimeter was calculated as the sum of the eight contiguous segments (see Fig 2). The MA area was computed as the summation of six triangular areas derived from triplets of MA marker coordinates. Percentage changes for area and perimeter were calculated as ([Aed - Aes]/Aed) • 100% and ([Ced - Ces]/Ced) • 100%, where Aed and Aes are end-diastolic and end-systolic areas, and Ced and Ces are end-diastolic and end-systolic perimeters.
MITRAL ANNULAR SHAPE.
A cylindric coordinate system was defined with the origin at the midpoint of the chord joining the commissural markers (markers 1 and 5), and with the negative z-axis directed through the LV apical marker. The z-axis coordinate of each MA marker was calculated at ED and ES. Using this system, positive z coordinates were toward the left atrium, and negative z coordinates were toward the LV apex.
STATISTICAL ANALYSIS.
All data are reported as mean ± 1 standard deviation. The MA area, perimeter, and segmental length measurements at ED and ES were compared using Student's t test for paired observations, for both preischemic control and ischemic MR conditions independently. The MA marker z coordinates during control and ischemic conditions were compared using Student's t test for paired observations. Evaluation of segmental length changes was also performed using two-way analysis of variance with segment number and presence of myocardial ischemia as independent variables, and with dog ID as a dummy variable to control for interanimal variability. When indicated by a significant F statistic (p 0.05), specific segmental differences were examined using the Bonferroni correction for multiple comparisons.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Hemodynamic Indices
Mitral regurgitation, assessed by echocardiography, was successfully induced in all 7 dogs; 5 dogs had mild to moderate MR and 2 dogs had moderate to severe MR. None of the dogs had evidence of MR before balloon occlusion of the circumflex coronary artery.
The mean heart rate for all dogs did not differ significantly between preischemic control (105 ± 18 beats/min) and ischemic MR conditions (106 ± 16 beats/min). With ischemia, the ejection fraction fell from 0.22 ± 0.04 during control conditions to 0.15 ± 0.03 (p < 0.005); LV end-diastolic pressure increased from 21 ± 6 to 32 ± 6 mm Hg (p = 0.005); LV stroke work decreased from 3,640 ± 464 to 1,970 ± 465 mm Hg • mL (p < 0.001); LV dP/dtmax decreased from 1,610 ± 307 to 1,234 ± 344 mm Hg/s (p < 0.001); and Ees decreased from 2.3 ± 0.4 to 1.4 ± 0.3 mm Hg/mL (p = 0.001).
Mitral Annular Dynamics
Figure 3 shows the typical changes in MA area and perimeter from one heart throughout the cardiac cycle, during both the preischemic control and ischemic MR conditions. The MA orifice size was larger during ischemic MR than during control conditions throughout the entire cardiac cycle. For the 7 dogs, the mean ischemic MA area was 15% ± 14% larger at ED but 21% ± 13% larger at ES, and the mean MA perimeter was 7% ± 6% larger at ED and 9% ± 6% larger at ES, as compared with control values (Fig 4). Figure 3 also shows that systolic MA orifice reduction still occurred during ischemic MR. For the group, from ED to ES, the MA area decreased 14% ± 9% (5.7 ± 0.8 to 4.9 ± 0.8 cm2; p < 0.005) during the control condition and 10% ± 3% (6.5 ± 0.6 to 5.9 ± 0.6 cm2; p < 0.001) during ischemic MR (p = not significant, control versus ischemia); the MA perimeter decreased 6% ± 4% (8.9 ± 0.6 to 8.3 ± 0.6 cm; p < 0.01) during the control condition and 4% ± 1% (9.5 ± 0.4 to 9.1 ± 0.4 cm; p < 0.001) during ischemic MR (p = not significant, control versus ischemia).
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summarizes the ED segment lengths, and Table 2 the ES segment lengths, during control and ischemic MR conditions for all dogs. As can be seen from Table 1, all eight MA segments at ED were somewhat longer than control lengths during ischemic MR, although only the elongation in MA segments S34, S45, S67, and S81 reached statistical significance (p 0.05, control versus ischemia). However, the changes from control measurements in MA segment lengths at ES during ischemic MR occurred in a more distinct pattern. Table 2 reveals that ES MA enlargement during ischemic MR was not symmetric; the posterior annular segments lengthened significantly (S12, S23, and S34), whereas the length of all anterior MA segments (except for one segment [S81] contiguous with the posterior MA) did not change. This asymmetric ES MA enlargement during ischemic MR is shown graphically in Figure 5.
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demonstrates the group mean percentage systolic shortening of each segment during control and ischemic MR conditions. The greatest shortening from ED to ES occurred in the region of the midposterior MA (S34), during both control (18% ± 5%, p 0.001 versus zero) and ischemic MR (11% ± 4%, p 0.001 versus zero) conditions. This systolic shortening of S34 was significantly less during ischemic MR (p < 0.01 versus control). As can be seen in Figure 6, S67, which overlaps the region of aortic-mitral continuity, lengthened from ED to ES during control conditions (-7% ± 7%, p 0.01 versus zero), as reported recently from this laboratory [10]; moreover, this S67 lengthening during LV ejection continued even in the presence of posterolateral LV ischemia and MR (p = not significant, control versus ischemia).
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show the MA marker positions along the z-axis at ED and ES during control and ischemic MR conditions, respectively; the anterior MA sites had positive z coordinates and the posterior MA sites had negative z coordinates, indicating a "tilted saddle" shape [10, 19, 20]. This shape was generally maintained during ischemic MR, but certain significant differences occurred. At ED (see Fig 7), the posterior MA (markers 1, 2, and 3) had significantly greater negative z values during ischemic MR than during control conditions, but the height of the anterior MA, or "saddlehorn" (markers 6 and 7), did not change significantly. At ES (see Fig 8), however, the anterior MA "saddlehorn" had significantly smaller positive z values during ischemic MR compared with control conditions (p 0.01 for markers 6 and 7, control versus ischemia), indicating a reduction in height of the MA in the area of aortic-mitral continuity. This lowered height at ES of the anterior MA "saddlehorn" region during ischemic MR is shown in Figure 9.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Hemodynamic Indices
All data were obtained from healthy adult dogs in normal sinus rhythm (except for dog 7, which was atrially paced throughout data collection, as noted previously) during autonomic blockade with esmolol and atropine sulfate. The proximal circumflex coronary artery was occluded to induce ischemic MR in 6 dogs; dog 7 had a large posterior descending coronary artery branch that was occluded successfully to induce ischemic MR. The hemodynamic indices for dog 7 were not statistically different from those of the other study animals; therefore, the data presented include all 7 study animals. Substantial LV ischemia was produced in all dogs, as verified by ECG ST-segment elevations, an increase in LV end-diastolic pressure, and decreases in ejection fraction, LV stroke work, LV dP/dtmax, and Ees.
Mitral Annular Dynamics
The area and perimeter of the MA orifice increased during acute ischemia and attendant MR as compared with control measurements. This enlargement was present at both time points in the cardiac cycle (see Fig 3), but enlargement at ES was greater than that at ED for both indices. In addition, the enlargement was not symmetric; at ES, the posterior MA segments were longer during ischemia, whereas most of the anterior MA segments did not change length (see Table 2, Fig 5). This finding of nonhomogeneous annular enlargement is consistent with recent observations in sheep [21]. Such asymmetric enlargement may be explained by the MA anatomic architecture. The posterior part of the MA is interposed between the myocardium of the left atrium and ventricle, being supported only by muscle [22], whereas the anterior MA contains the area of aortic-mitral continuity and bridges the left and right fibrous trigones. Therefore, one intuitively would think that the anterior MA is less likely to dilate [23].
Our current finding that the MA area and perimeter during acute ischemic MR were relatively larger at ES than at ED implies that systolic contraction of the MA or the contiguous LV myocardium was impaired during regional ischemia, as suggested by previous investigators [24]. Even though Figure 3 shows that MA shrinkage continued to occur from ED to ES during ischemic MR, regional analysis revealed that systolic shortening was significantly less in the midposterior MA region (see Fig 6, S34). Such a reduction in posterior MA segmental systolic shortening, alone or in combination with MA dilatation, may be an instrumental factor in the genesis of MR secondary to posterolateral LV ischemia [25, 26].
Anterior MA segmental systolic length changes were generally preserved during ischemic MR. As we reported previously [10], the part of the MA overlapping the area of aortic-mitral continuity (S67) actually lengthened from ED to ES; the current study demonstrated that this anterior MA segmental systolic lengthening is still present during ischemic MR (see Fig 6). Thus, although posterior MA shortening during LV ejection was reduced during ischemic MR, lengthening of the anterior MA during LV ejection persisted. The mechanism responsible for this systolic lengthening of S67 is unknown; we have postulated that this may be due to traction forces exerted by contraction of the surrounding basal LV fibers [10]. Further investigations using anterior LV ischemia may define more precisely the mechanism of this anterior MA systolic lengthening.
Mitral Annular Shape
We have previously described the MA shape in normal canine hearts as resembling a "tilted saddle," with the "saddlehorn" of the MA located near the area of aortic-mitral continuity (markers 6 and 7) [10]; this shape was also seen in the current study (see Figs 7–9). Although anterior MA systolic lengthening was preserved during ischemic MR, acute posterolateral LV ischemia resulted in a significant reduction in the height of the anterior MA "saddlehorn" near the aortic valve at ES (see Figs 8, 9), as assessed by the MA marker z positions. This upward displacement (relative to the LV) of the anterior MA toward the left atrium during systole may provide a path that minimizes resistance to outflow during LV ejection. Thus, acute posterolateral LV regional ischemia, in addition to limiting the extent of posterior MA systolic shortening, modified the overall MA shape. If resistance to LV outflow were increased by this change in anterior MA shape, it could potentially augment the severity of MR. Fluid dynamic studies of LV-chamber blood flow patterns, both with and without regional LV ischemia and MR, are needed to define more clearly the implications of MA shape changes.
Surgical Implications
These data reveal that the ES MA enlargement associated with acute posterolateral LV ischemia and MR is due primarily to posterior MA lengthening, with the majority of the anterior MA segments maintaining their functional integrity. Hence, patients with inferior LV ischemia and resultant MR might benefit most from a posterior annuloplasty, thereby not interfering with anterior MA motion. Although anterior MA shape was perturbed by acute regional LV ischemia in this study, fixation of the anterior MA would eliminate systolic lengthening in the region of aortic-mitral continuity. In fact, van Rijk-Zwikker and associates [27] reported that a stiff anterior MA (after rigid ring insertion) was pushed beneath the aortic valve during systole, resulting in mild subvalvular obstruction to LV outflow. Furthermore, a flexible ring, rather than a rigid one, may help maintain continuous physiologic MA mobility throughout the cardiac cycle [28]. David and colleagues [29] reported that LV systolic pump performance (as assessed by LV pressure-volume as well as stroke volume–end-diastolic volume relations) early after mitral valve reconstruction for chronic MR was enhanced in patients with flexible rather than rigid annuloplasty rings, although this may have been a transient phenomenon because no major difference was seen after 1 year [29]. This hemodynamic benefit may, in part, have to do with maintaining the flexibility of the entire MA, especially portions of the anterior MA. Before contemplating modification of our current clinical techniques, however, further 3-D investigations of fixation of specific parts of the MA, both with and without ischemic MR (generated by posterior as well as anterior regional LV ischemia), are needed to elucidate the importance of MA shape and mobility.
Limitations
This experiment was designed to study solely the alterations in regional MA dynamics that occur during acute posterolateral LV ischemia with resultant MR. Our observations revealed that posterior MA elongation and impaired systolic shortening, as well as altered anterior MA shape, may contribute to the MR resulting from posterolateral LV ischemia. This study did not address other factors (such as papillary muscle dysfunction or LV shape changes [21, 25, 30]) that may also play a role in the development of ischemic MR. Furthermore, the degree of MR was not quantified in this study; Doppler echocardiography was used to grade MR subjectively as none, mild to moderate, or moderate to severe. Ongoing experiments in our laboratory using aortic flow probes in conjunction with markers to calculate the mitral regurgitant fraction have been designed to investigate further the pathogenesis of ischemic MR.
The use of myocardial markers for 3-D assessment of cardiac dynamics allows accurate and reproducible determination of marker position, with a mean overall error of 0.1 ± 0.6 mm every 16.7 milliseconds [14]. The length of a segment of the MA between two adjacent markers was estimated by a chord, however, rather than the actual arc length of the segment. The error in estimating arc length by using chord length (for a sector angle of 45 degrees, the ideal in this case) is -2.5%, and this value is virtually constant between ED and ES. Thus, we estimate that the percentage changes in segmental lengths reported here are within 0.2% of what the actual arc lengths would be.
The animals in this study had normal hearts but were autonomically blocked to control heart rate and to avoid the influence of reflex responses. Because of the autonomic blockade, the hearts studied had depressed LV systolic function, and it is possible that they also had subnormal systolic MA motion. However, each animal served as its own control, and the dose of esmolol remained constant throughout the study. Furthermore, the calculated LV ejection fractions (0.22 ± 0.04 and 0.15 ± 0.03) are based on epicardial marker motion and therefore do not take into account LV wall thickening, which represents a major proportion of LV chamber volume reduction during ejection. Nevertheless, it is probable that the relative changes between control and ischemic conditions might be more pronounced in unblocked animals.
This experiment was conducted in dogs, which have been reported to have a greater muscular component to the cardiac endoskeleton than humans [7]. The findings of the current study, therefore, may not be totally applicable to patients, particularly those with dilated hearts and markedly limited LV systolic function, eg, in the setting of chronic MR. In addition, because regional ischemia was associated with decreased LV performance (as indicated by significant reductions in LV ejection fraction, stroke work, dP/dtmax, and Ees during ischemia), it is possible that the MR observed in this study was also due in part to changes in LV function and geometry, which may have contributed to incomplete mitral leaflet coaptation. Further 3-D studies of mitral leaflet motion, LV geometry, and MA dynamics in other animal models, both with and without ischemic MR, are clearly needed to confirm the present findings, as well as to define more clearly other mechanisms contributing to the pathogenesis of ischemic MR. We are currently using an ovine model to address some of these issues.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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We gratefully acknowledge Mary K. Zasio, BA, Carol W. Mead, BA, Erin M. Schultz, BS, and Geraldine C. Derby, RN, for their technical expertise in surgical preparation, data acquisition, and data reduction; Terrence L. Tye, MS, for his help with intraoperative epicardial echocardiography; and Phoebe E. Taboada, BA, for her help in preparing the manuscript and figures.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Address reprint requests to Dr Miller, Department of Cardiovascular and Thoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247.
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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 J. R. Glasson, M. Komeda, G. T. Daughters, A. F. Bolger, M. O. Karlsson, L. E. Foppiano, M. Hayase, S. N. Oesterle, N. B. Ingels Jr., and D. C. Miller Early systolic mitral leaflet "loitering" during acute ischemic mitral regurgitation J. Thorac. Cardiovasc. Surg., August 1, 1998; 116(2): 193 - 205. [Abstract] [Full Text] [PDF]
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