(Circulation. 2002;106:I-40.)
© 2002 American Heart Association, Inc.
Surgery for Valvular Heart Disease |
From the Department of Cardiovascular and Thoracic Surgery (D.T.L., F.A.T., T.M., T.A.T., P.D., G.T.D., N.B.I., D.C.M.), and Division of Cardiovascular Medicine (D.L.), Stanford University School of Medicine, Stanford, Calif.; Department of Cardiac Surgery, University Hospital, TROMSØ, Norway (T.M.); and Laboratory of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, Calif. (G.T.D., N.B.I.).
Correspondence to D. Craig Miller, MD, Department of Cardiovascular and Thoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247. E-mail dcm{at}stanford.edu
| Abstract |
|---|
|
|
|---|
Methods Radiopaque markers were sutured to the mitral annulus, papillary muscle tips, and leaflet edges in 13 sheep. Immediately postoperatively, under open-chest conditions, 3-D marker coordinates were obtained using high-speed biplane videofluoroscopy before and during echocardiographically verified acute ischemic mitral regurgitation produced by occlusion of the left circumflex coronary artery.
Results During acute ischemic mitral regurgitation, at end systole, the anterolateral edge of the central scallop was displaced 0.8±0.9 mm laterally and 0.9±0.6 mm apically away from the anterolateral scallop; such displacement correlated with lateral displacement of the lateral annulus (R2=0.7, SEE=0.7 mm, P<0.001) and movement of the right lateral annulus away from the nonischemic anterior papillary tip (R2=0.6, SEE=0.8 mm, P=0.002), respectively. End-systolic displacement of the posteromedial edge of the central scallop was 1.4±0.9 mm anteriorly and 0.9±0.6 mm laterally away from the posteromedial scallop, corresponding to anterior displacement of the mid-lateral annulus (R2=0.5, SEE=1.0 mm, P<0.001).
Conclusions Malcoaptation of the scallops within the posterior leaflet during acute left ventricular ischemia is a novel observation. The primary geometric mechanism underlying scallop malcoaptation in acute ischemic mitral regurgitation was annular dilatation, which hindered leaflet coaptation by drawing the individual scallops apart. These findings support the use of annular reduction in the repair of ischemic mitral regurgitation and also suture closure of prominent subcommissures between posterior leaflet scallops.
Key Words: Ischemic mitral regurgitation mitral valve 3-D geometry leaflet dynamics posterior mitral leaflet mitral scallops ischemic heart disease coronary artery disease
| Introduction |
|---|
|
|
|---|
| Methods |
|---|
|
|
|---|
Surgical Preparation
Miniature radiopaque markers were surgically implanted in 13 adult castrated male sheep with a mean body weight of 72±9 kg. A dense leaflet marker array was designed to elucidate the 3-D scallop dynamics of the mitral valve. General technical details have been described before4 and are only briefly summarized here. After establishing cardiopulmonary bypass, the mitral annulus was delineated with 8 markers (Figure 1). Markers were also placed at the tips of the anterior and posterior papillary muscles, and sutured to the mitral leaflet edges as depicted in Figure 1. Leaflet marker nomenclature Xy was based on anatomical position with "X" specifying the leaflet (A=Anterior; P=Posterior) and "y" the marker location on the leaflet (acom=near the anterior commissure; pcom=near the posterior commissure; a=anterolateral scallop; ac=anterolateral portion of the central scallop; pc=posteromedial portion of the central scallop; p=posteromedial scallop).
|
Experimental Protocol
Immediately postoperatively with the chest open, each animal was placed in the right lateral decubitus position and mechanically ventilated with 100% oxygen and anesthetized. Simultaneous biplane videofluoroscopic and hemodynamic data were acquired before and during ischemia. Animals were studied in normal sinus rhythm with ventilation arrested at end-expiration for a few beats during data acquisition runs to minimize the effects of respiration. To create acute posterolateral LV ischemia, the left circumflex coronary artery was occluded proximal to the first obtuse marginal artery by cinching an encircling suture. Before and following 2 to 3 minutes of ischemia, data were acquired at 60 Hz in the 7-inch mode of image magnification and two-dimensional images from each of the 2 x-ray views were digitized and merged to yield 3-D coordinates every 16.7 ms using custom designed software.5,6 Mitral regurgitation was graded from transesophageal color Doppler echocardiography by an experienced echocardiographer as none to trace (grade 0), mild (grade 1), moderate (grade 2) or severe (grade 3).
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 [NIH] Publication 85 to 23, revised 1985). This study was approved by the Stanford Medical Center Laboratory Research Animal Review Committee and conducted according to Stanford University policy.
Data Analysis
Data from 2 consecutive steady-state beats during control and acute ischemic conditions were averaged and analyzed. End-systole was defined as the videofluoroscopic frame immediately preceding the peak negative rate of LV pressure change (-dP/dtmax), and end-diastole was defined as the videofluoroscopic frame containing the peak of the R-wave on the ECG. All dimensional data reported herein were measured at the time of end-systole.
| Internal Coordinate Reference System and Geometric Variables |
|---|
|
|
|---|
|
The origin of the reference system was translated to Pa to simplify interpretation of Pa Pac coaptation (ie, position of Pac relative to Pa). Similarly, the origin was translated to Pp to study Pp Ppc coaptation. Using these coordinate systems, displacements were defined as the change in end-systolic position of each marker during LV ischemia relative to its nonischemic position. The following measurements were computed from 3-D marker coordinates before and during ischemia at end-systole: Inter-scallop distances, inter-leaflet distances, distances between the papillary tips and the lateral annular markers, lateral annular segmental lengths, and septal-lateral and commissure-commissure annular dimensions. These distances are independent of the coordinate system chosen.
Statistical Analysis
All results are reported as mean ±1 SD. The geometric variables measured before and during ischemia at end-systole were compared using a two-tailed Students t test for paired observations. The 3-D geometry of the mitral leaflets is ultimately governed by the material properties of the leaflets and the 3-D geometry of the structures attached to the leaflets, that is, mitral annulus and papillary muscle tips. Thus, any change in the 3-D geometry of the mitral annulus and papillary muscle tips during acute LV ischemia will produce changes in leaflet geometry that could lead to ischemic MR. To determine the changes in annular and papillary muscle tip geometry most closely associated with specific changes in observed leaflet geometry, we used a multivariable statistical model with leaflet geometry change as the dependent variable and changes in annular and papillary muscle tip geometry the independent variables. A stepwise linear regression model (SPSS for Windows, Release 10.0.0, SPSS Inc., Chicago, IL) was used to identify predictors of leaflet geometry change, that is, change in 3-D scallop geometry. The aim of the multivariable analysis was to determine which component of the annular and papillary muscle tip geometry was most important with respect to a specific change in leaflet geometry. Such statistical analysis sheds light on the geometric mechanisms underlying changes in leaflet geometry and consequently ischemic MR.
| Results |
|---|
|
|
|---|
Mitral Valve Competence
Of the 13 animals, mild baseline MR was observed in 4, trace MR in 8 and no MR in 1 before ischemia. After 2 to 3 minutes of ischemia, the 4 animals with mild MR developed moderate (n=2) or severe (n=2) holosystolic MR, and the other 9 animals developed mild (n=3), moderate (n=3), or severe (n=3) MR. Overall, MR increased from an average grade of 0.3 at baseline to a grade of 2.2 (P<0.001) during acute LV ischemia. We could not determine precisely the specific location of the MR jet, but it was broadly central.
Hemodynamics
The acute ischemic injury was substantial, producing a 38% decrease in LV dP/dtmax (from 1,860±471 mm Hg/s to 1,149±227 mm Hg/s, P<0.001), a 37% drop in end-systolic LV pressure (from 92±17 mm Hg to 63±11 mm Hg, P<0.001), a 26% decrease in maximal LV pressure (from 112±9 mm Hg to 83±8 mm Hg, P<0.001), and a 37% increase in end-diastolic LV pressure (from 18±5 mm Hg to 24±5 mm Hg, P<0.001). There was no significant change in heart rate (94±10 bpm versus 91±14 bpm respectively).
Inter-Scallop Malcoaptation
As shown in Figure 3, the scallops of the posterior mitral leaflet moved apart at end systole during LV ischemia: Pa Pac and Pp Ppc distances increased by 1.1±1.1 mm (P=0.004) and 1.4±1.1 mm (P<0.001), respectively. As shown in Figure 4A, Pac was displaced 0.8±0.9 mm laterally (P=0.005) and 0.9±0.6 mm apically (P<0.001) away from Pa, producing inter-scallop septal-lateral separation and restriction. Ppc was displaced 0.9±0.6 mm laterally (P<0.001) and 1.4±0.9 mm anteriorly (P<0.001) away from Pp, producing inter-scallop separation in the septal-lateral and anterior-posterior (inter-commissural) direction (Figure 4B).
|
|
Inter-Leaflet Malcoaptation
The anterior and posterior leaflets also moved apart during acute LV ischemia: Aacom Pac, Apcom Ppc, and Apcom Pp distances increased by 0.9±0.9 mm (P=0.002), 2.5±1.4 mm (P<0.001) and 1.4±1.1 mm (P<0.001), respectively (Figure 3). The Aacom Pa inter-leaflet distance, however, did not change.
Mitral Annulus
During acute LV ischemia, the septal-lateral (from marker 1 to marker 5, Figure 1) and commissure-commissure (from marker 3 to marker 7, Figure 1) annular dimensions increased by 5.0±3.3 mm (30.2±9.4 to 35.2±13.5 mm, P<0.001) and 2.6±1.7 mm (39.2±8.8 to 41.6±9.0 mm, P<0.001), respectively. Figure 3 depicts the significant changes with LV ischemia in lateral annular dimensions at end-systole which increased by 1.1±1.2 mm (11.1±1.5 mm to 12.4±2.0 mm, P=0.007) between the anterior commissure (marker 3) and left lateral annulus (marker 4), 2.0±1.3 mm (13.1±3.2 mm to 15.1±0.4 mm, P<0.001) between the left lateral (marker 4) and mid-lateral annulus (marker 5), 1.8±1.0 mm (18.7±6.5 mm to 20.4±5.8 mm, P<0.001) between the mid-lateral (marker 5) and right lateral annulus (marker 6) and 3.8±2.3 mm (15.5±4.6 mm to 19.1±7.6 mm, P<0.001) between the right lateral annulus (marker 6) and posterior commissure (marker 7). Statistically significant displacements of the lateral annulus relative to Pa are depicted graphically in Figure 4A, and those relative to Pp are shown in Figure 4B. The septal annular distance between the fibrous trigones (markers 2 to 1 to 8) did not change significantly during acute LV ischemia (25.6±7.5 versus 25.9±8.0, P=0.13).
Papillary Muscle Tips
Statistically significant end-systolic displacements of the anterior papillary muscle tip relative to Pa and the posterior papillary tip relative to Pp during LV ischemia are depicted in Figures 4A and 4B, respectively.
Annular-Papillary Distances
During LV ischemia, the distances between the tip of the nonischemic anterior papillary muscle and each of the lateral annular marker sites increased (Table 1), particularly that to the right lateral annulus. The distance between the ischemic posterior papillary tip and both the right lateral and mid-lateral annulus did not change during ischemia, while the distance between the posterior papillary tip and the left lateral annulus increased during ischemia (Table 1).
|
Predictors of Inter-Scallop Malcoaptation From Stepwise Linear Regression
During acute ischemic MR, Pac was displaced 0.8 mm laterally, drawn by the 2.2 mm lateral displacement of the mid-lateral annulus (R2=0.7, SEE=0.7 mm, P<0.001) (Refer to Figures 4A and 4B). A 3.7 mm movement of the anterior papillary muscle tip away from the right lateral annulus predicted Pac restriction of 0.9 mm (R2=0.6, SEE=0.8 mm, P=0.002). Ppc was displaced 1.4 mm anteriorly and 0.9 mm away from Pp, drawn by the 3.1 mm anterior displacement of the mid-lateral annulus (R2=0.5, SEE=1.0, P<0.001).
| Discussion |
|---|
|
|
|---|
Three-dimensional analysis demonstrated that:
By correlating 3-D perturbations of mitral annular and papillary muscle tip geometry in a multivariable linear regression model, this study showed that annular-papillary displacement was responsible for scallop restriction (inter-scallop separation perpendicular to the annular plane). To illustrate the mechanism, one can imagine a length of rope running from the anterior papillary tip to Pac and then bending toward the right lateral annulus (marker #6). As the right lateral annulus is displaced away from the nonischemic anterior papillary tip, the rope is straightened, and Pac is drawn down into the LV cavity toward the LV apex. In contrast, displacement of left lateral annulus away from the posterior papillary tip did, however, not produce Ppc restriction because of movement of the ischemic posterior papillary muscle tip toward the annular plane, which tended to prolapse Ppc.8
The multivariable model also demonstrated that the scallops were drawn apart in directions parallel to the annular plane by dilatation of the mitral annulus. Thus, septal-lateral annular dilatation drew Pac laterally away from Pa (Figure 4A). An increase in lateral annular dimensions also correlated with anterior and lateral displacement of Ppc away from Pp (Figure 4B). To explain the unexpected lateral displacement of Ppc, one can imagine a length of rope running from the mid-lateral annulus (marker #5) to Ppc and bending toward the right lateral annulus (marker #6). As the mid-lateral annulus moves anteriorly away from the right lateral annulus, the bend in the rope straightens which displaces Ppc laterally and also anteriorly away from Pp.
Separation of scallops parallel to the annular plane occurred in all 3 scallops, whereas scallop separation perpendicular to the annular plane was seen in only 2 of 3 scallops (Pac and Pa). Thus, we surmised that mitral annular dilatation (responsible for scallop separation parallel to the annular plane) was relatively more important than annular-papillary displacement (responsible for scallop separation perpendicular to the annular plane) in the pathogenesis of scallop malcoaptation during acute LV ischemia.
| Clinical Inferences |
|---|
|
|
|---|
|
| Limitations |
|---|
|
|
|---|
| Conclusions |
|---|
|
|
|---|
| Acknowledgments |
|---|
| References |
|---|
|
|
|---|
2. Ranganathan N, Lam JH, Wigle ED, et al. Morphology of the human mitral valve. II. The value leaflets. Circulation. 1970; 41: 459467.
3. Myrmel T, Lai DT, Liang DH, et al. Acute ischemic mitral regurgitation can be caused by malcoaptation of the scallops within the posterior leaflet. Circulation. 2000; 102 (suppl II): II-475.
4. Glasson JR, Komeda M, Daughters GT, et al. Most ovine mitral annular three-dimensional size reduction occurs before ventricular systole and is abolished with ventricular pacing. Circulation. 1997; 96 (suppl II): II-115122.
5. Niczyporuk MA, Miller DC. Automatic tracking and digitization of multiple radiopaque myocardial markers. Comput Biomed Res. 1991; 24: 129142.[CrossRef][Medline] [Order article via Infotrieve]
6. Daughters GT, Sanders WJ, Miller DC, et al. A comparison of two analytical systems for 3-D reconstruction from biplane videoradiograms. IEEE Comput Cardiol. 1989; 15: 7982.
7. Grigioni F, Enriquez-Sarano M, Zehr KJ, et al. Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment. Circulation. 2001; 103: 17591764.
8. Gorman JH III, Jackson BM, Gorman RC, et al. Papillary muscle discoordination rather than increased annular area facilitates mitral regurgitation after acute posterior myocardial infarction. Circulation. 1997; 96 (suppl II): II-124127.
9. Bolling SF, Pagani FD, Deeb GM, et al. Intermediate-term outcome of mitral reconstruction in cardiomyopathy. J Thorac Cardiovasc Surg. 1998; 115: 381386.
10. Yiu SF, Enriquez-Sarano M, Tribouilloy C, et al. Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction: a quantitative clinical study. Circulation. 2000; 102: 14001406.
11. Liel-Cohen N, Guerrero JL, Otsuji Y, et al. Design of a new surgical approach for ventricular remodeling to relieve ischemic mitral regurgitation: insights from 3-dimensional echocardiography. Circulation. 2000; 101: 27562763.
12. Kono T, Sabbah HN, Rosman H, et al. Left ventricular shape is the primary determinant of functional mitral regurgitation in heart failure. J Am Coll Cardiol. 1992; 20: 15941598.[Abstract]
13. Lai DT, Timek TA, Dagum P, et al. The effects of ring annuloplasty on mitral leaflet geometry during acute left ventricular ischemia. J Thorac Cardiovasc Surg. 2000; 120: 966975.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2002 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |