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1 Department of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, Palo Alto, California 94301; 2 Department of Mechanical Engineering, Linköping University, S-581 83 Linköping, Sweden; Departments of 3 Cardiothoracic Surgery, 4 Cardiovascular Medicine, and 5 Anesthesia, Stanford University School of Medicine, Stanford 94305; and 6 Cardiac Surgery and Cardiology Sections, Department of Veterans Affairs Medical Center, Palo Alto, California 94304
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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To study the three-dimensional size, shape, and motion of the mitral leaflets and annulus, we surgically attached radiopaque markers to sites on the mitral annulus and leaflets in seven sheep. After 8 days of recovery, the animals were sedated, and three-dimensional marker positions were measured by computer analysis of biplane videofluorograms (60/s). We found that the oval mitral annulus became most elliptical in middiastole. Both leaflets began to descend into the left ventricle (LV) during the rapid fall of LV pressure (LVP), before leaflet edge separation. The anterior leaflet exhibited a compound curvature in systole and maintained this shape during opening. The central cusp of the posterior leaflet was curved slightly concave to the LV during opening. Markers at the border of the "rough zone" were separated by 10 mm during systole. We conclude that coaptation occurs very near the leaflet edges, that the annulus and leaflets move toward their open positions during the rapid fall of LVP, and that leaflet edge separation, the last event in the opening sequence, occurs near the time of minimum LVP.
leaflets; annulus; radiopaque markers; coaptation; sheep
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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THE MITRAL VALVE takes <100 ms during each cardiac cycle to transform from a tightly closed configuration capable of withstanding high left ventricular (LV) systolic pressure to a widely open configuration permitting almost explosive early LV diastolic filling. Long a subject of interest, the function of the mitral valve and its relationship to the chordae tendinae were recognized by Erasistratus a century after its anatomic description by Hippocrates (ca. 400 BC). Eighteen centuries later, Vesalius (32) provided its modern name, likening it to an episcopal miter.
Interest in the mitral valve intensified in the 20th century with the development of new technology and new techniques for medical and surgical treatment of valvular disease (34). Beginning 40 years ago, single-plane and biplane radiographic techniques were used to study the dynamics of radiopaque markers affixed to the valve annulus and leaflets (19, 22, 27-30) and contrast material adherent to the posterior leaflet (25). Subsequent echocardiographic studies made major contributions to our understanding of mitral valvular function (6, 12-14, 18, 19). Recent developments in magnetic resonance imaging promise to increase this fund of knowledge markedly (34).
Despite such extensive attention, however, no data are available concerning the instantaneous three-dimensional dynamics of specific, fixed sites in the mitral valvular annulus and leaflets throughout the cardiac cycle. Here, we provide such data describing the dynamics of mitral valve opening derived from biplane radiographic techniques developed in our laboratories (9). The ovine heart was chosen for study because of its anatomic similarity to the human heart (33) and its highly consistent, reproducible anatomy, function, and patterns of dysfunction (15).
We describe our findings that, before leaflet separation, the central portion of the anterior leaflet of the closed mitral valve assumed a compound shape, the posterior leaflet was slightly concave to the LV, and the mitral annulus was oval and nearly planar. Mitral valve opening began with an annular shape change at the time when LV pressure (LVP) had just begun to fall from systolic levels. The opening process continued with leaflet and annulus shape changes during the rapid fall of LVP, the leaflet edges still apposed, and the valve still sealed. Finally, both leaflet edges moved rapidly into the LV cavity, creating a widely open mitral orifice.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Surgical preparation. Seven healthy adult male sheep (63 ± 9 kg) were premedicated with ketamine (27 mg/kg im) and atropine sulfate (0.05 mg/kg iv) and anesthetized with thiopental sodium (6.8 mg/kg iv), intubated, and placed on artificial ventilation (Servo Anesthesia Ventilator, Siemens-Elema, Solna, Sweden). An orogastric tube was placed on intermittent suction. General anesthesia was maintained with inhalational isoflurane (1-2.2%) and supplemental oxygen. Single doses of cefazolin sodium (1 g iv) and gentamicin sulfate (80 mg iv) were given preoperatively, and antibiotic therapy was continued throughout the postoperative period (1 g of cefazolin sodium iv every 4 h and 80 mg of gentamicin sulfate iv every 8 h). By use of sterile technique, an incision was made in the left neck, exposing the jugular vein and carotid artery for catheterization. A micromanometer-tipped pressure transducer (model MPC-500, Millar Instruments, Houston, TX) was zeroed in a water bath and inserted into the left carotid artery to monitor systemic arterial pressure. A left thoracotomy was performed through the fifth intercostal space, the heart was suspended in a pericardial cradle, and miniature tantalum radiopaque helices (0.8 mm ID, 1.3 mm OD, 1.5-3.0 mm long, some having different small extensions or "tails" to facilitate subsequent radiographic identification) were inserted into the LV wall and septum. Each marker was placed on the obturator of a modified spinal needle (20 gauge), inserted through a stab wound in the epicardial surface, and deposited into the myocardium by withdrawal of the obturator from the sheath. Eight markers (Fig. 1, 2, 3, 5, 6, 9, 10, 12, and 13) were placed into the LV subepicardium along four equally spaced longitudinal meridians around the LV, in the anterior (from the origin of the left anterior descending coronary artery to the apex), lateral (obtuse margin), posterior (inferior wall along the posterior descending coronary artery), and septal walls. Epicardial echocardiographic guidance was used to place septal markers at the desired sites. Each meridian contained LV markers at two levels, in equatorial and apical planes. Four additional markers were sutured to the left atrial (LA) epicardium (Fig. 1, 4, 8, 11, and 14). A marker was placed at the LV apex (Fig. 1, 1).
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Experimental protocol.
After 8 days of recovery (range 6-10), each animal was
taken to the animal cardiac catheterization laboratory for hemodynamic and videofluorographic data acquisition. The animals were premedicated with ketamine (27 mg/kg iv), intubated, and mechanically ventilated (Veterinary Anesthesia Ventilator 2000, Hallowell EMC, Pittsfield, MA)
with 100% oxygen. Sedation was maintained with ketamine (1-4 mg · kg
1 · h1
iv infusion) and supplemental diazepam (5 mg iv), administered as
needed. UL-FS 49 (Boehringer-Ingelheim, Ridgefield, CT) was administered (8 mg iv, single dose) to lower heart rate. Such heart rate reduction [group mean heart rate was 118 ± 8 (SD)
beats/min] facilitated subsequent cinefluoroscopic
visualization and tracking of marker motion. Hemodynamic and biplane
videofluoroscopic data were obtained with hearts in normal sinus rhythm
and with ventilation briefly arrested at end expiration.
Data acquisition. All imaging studies were conducted with the animal in the right lateral decubitus position with utilization of an Optimus 2000 biplane Lateral ARC 2/Poly DIAGNOST C2 system (Philips Medical Systems, North America Company, Pleasanton, CA) with the image intensifiers in the 9-in. cinefluoroscopic mode. The 45° right anterior oblique and 45° left anterior oblique biplane fluoroscopic images were recorded simultaneously on two Sony U-Matic 5800 3/4-in. videocassette recorders. The analog LVP signal was recorded in digital format on each individual video image using a vertical time-base encoder (Grey Engineering, Los Angeles, CA). At the completion of the study, images of 1-cm grids and biplane images of a three-dimensional helical phantom of known dimensions were recorded. The two-dimensional coordinates of each marker in each projection were digitized frame-by-frame, employing semiautomated image-processing and digitization software developed in our laboratory (17) and run on a microcomputer system (RS/20, Hewlett-Packard, Palo Alto, CA, equipped with MVP/AT/NP image-processing boards, Matrox, Dorval, PQ, Canada). Data from the two views were merged using software previously described (4) to yield the three-dimensional coordinates of the centroid of each marker every 16.7 ms.
During video data acquisition, two channels of analog data (LVP and surface lead electrocardiogram) were also acquired and digitized simultaneously at 240 Hz using a microcomputer (486-33, JDR Microdevices, San Jose, CA) with a high-speed data acquisition card (DT 3831-G, Data Translation, Marlboro, MA) controlled by data acquisition software (Labtech Control 3.2.0, Laboratory Technology, Wilmington, MA). These analog signals were also simultaneously recorded on a multichannel color display recorder (model 580CDR/16, Vidco, Beaverton, OR) at a paper speed of 25 mm/s. To circumvent technical limitations in the videotape LVP channel, the 240-Hz pressure signal from the computer was time aligned with the pressure signal from the videotape by a program that minimized the difference between these two signals. The 240-Hz pressure was then used as the pressure value for each frame.Data analysis.
At each sample time, marker centroid coordinates were rotated and
translated from their original laboratory reference frame to a moving
internal Cartesian reference system (Fig.
2) having its origin at the midpoint of the
line joining markers 22 and 18, its negative
y-axis passing through apical
marker 1, and markers 22 and 18 in the
z = 0 plane, with the positive
z-axis direction being toward the
anterior commissure. The angle 
was calculated as
arctan(
y/z)
(Fig. 2), and the angle 
was between the
x-axis and the line connecting
markers 18 and
22.
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![<IT>D</IT><SUB><IT>i j</IT></SUB> = [(<IT>x<SUB>i</SUB></IT> − <IT>x</IT><SUB><IT>j</IT></SUB>)<SUP>2</SUP> = (<IT> y</IT><SUB><IT>i</IT></SUB> − <IT>y</IT><SUB><IT>j</IT></SUB>)<SUP>2</SUP> + (<IT>z</IT><SUB><IT>i</IT></SUB> − <IT>z</IT><SUB><IT>j</IT></SUB>)<SUP>2</SUP>]<SUP>1/2</SUP>.](/content/vol274/issue2/fulltext/H552/img001.gif)
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34 is illustrated in Fig.
3). A similar approach was used to obtain
the angles between an annular reference vector defined from
marker 18 to
22 and vectors from annular
marker 18 to posterior leaflet
markers 35 and
36 (e.g.,
35 is illustrated in Fig. 3).
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0.1(LVPmax LVPmin) and
LVPlow = LVPmin + 0.1(LVPmax LVPmin) were computed. The time
sample immediately preceding
LVPlow was assigned the value
t = 0 (Fig. 4), and the time sample
immediately following LVPhigh was
taken as the onset of LV rapid pressure decay. The period of rapid
pressure decay was defined between the times of LVPhigh and
LVPlow (Fig. 4).
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Statistics. Values are means ± SE. Minimum and maximum values were determined from unsmoothed data. The significance of differences between values of a given variable at different times or between times of events during the interval of interest was assessed using Student's t-test for dependent (paired) observations, comparing the mean difference with zero. A two-tailed P < 0.05 was taken as significant.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Figure 5 displays mean LVP for each sample
over the interval studied. The maximum value of mean LVP was 135.1 ± 2.1 mmHg at t = 117 ms,
and the minimum value of mean LVP was 2.5 ± 2.0 mmHg at
t = +50 ms. Mean LVP fell from maximum
to 123.3 ± 1.5 mmHg (P < 0.001) or by 9% of its total excursion at
t = 67 ms and to 22.0 ± 1.9 mmHg (P < 0.001) or by 86% of its
total excursion at t = 0 ms in
accordance with the definition of t = 0 described in METHODS.
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Mitral annular geometry.
Figure 5 also shows the mean values of the mitral annular
septal-lateral dimension, i.e., the distance between
markers 18 and
22 (D18-22,
Fig. 1). The late systolic minimum of 2.53 ± 0.03 cm occurred at
t = 67 ms, when LVP had fallen
~10%. At t = 0 this dimension had
increased to 2.59 ± 0.04 cm (P < 0.001) or 33% of its total increase during the period analyzed.
D18-22 reached a maximum value of 2.71 ± 0.03 cm at
t = +83 ms, just after the time of
minimum LVP. It then fell rapidly, reaching a local minimum of 2.53 ± 0.02 cm, identical to the late systolic minimum
(P = NS).
33 ms, 33 ms later
(P = 0.02) than the
D18-22
minimum. It increased to 3.43 ± 0.07 cm (P = 0.03) at
t = 0, then to a maximum of 3.68 ± 0.05 cm
(P < 0.001) at
t = 83 ms, 17 ms after the maximum of
the septal-lateral dimension. It then decreased slowly over the
remainder of the interval studied.
Figure 6 displays the instantaneous ratio
of D18-22 to
D16-20 over
the interval studied. This ratio is an estimate of the shape of the
oval annulus (a ratio closer to 1.0 suggesting a more circular annulus,
a ratio closer to 0.0 a more oval annulus, although
D18-22 and
D16-20 are
not necessarily in the same plane). Annular shape was relatively
unchanged during the latter half of ejection, with a minimum ratio of
0.73 ± 0.01 (i.e., the septal-lateral dimension was about
three-fourths of the intercommissure dimension) at
t = 100 ms. The ratio rose steadily (more circular annulus) during rapid pressure decay, reaching
a broad maximum of 0.75 ± 0.01 near
t = 0 (P < 0.001 compared with minimum).
It then decreased steadily (more elliptical annulus) from the time of
minimum pressure onward to an early diastolic minimum of 0.69 ± 0.01 at t = +150 ms
(P < 0.001 compared with maximum).
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and (Fig. 2), respectively. In late systole, was 19.6 ± 6.4°
and was 14.3 ± 2.9°. In early diastole, decreased 3.3 ± 1.6° (P = 0.03) to its
minimum at t = +100 ms and then
increased. Later, fell, decreasing 3.6 ± 1.1°
(P < 0.001) by
t = +150 ms.
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Mitral leaflet geometry. Figure 10 plots the coordinates of markers defining the midline of the anterior leaflet (22 and 31-34) and posterior leaflet (18, 35, and 36, Fig. 1) during opening, from t = 0 to t = +83 ms. Figure 10A plots the projection of the marker centroids in the x-y plane, and Fig. 10B plots the projection in the x-z plane. The consistency of position of each marker at each time suggests that 1) the variability of leaflet size and anatomy between animals was small, 2) the placement of markers was highly reproducible, 3) the beat-to-beat physiological variability was small, 4) the submillimeter spatial resolution in locating marker centroids (4) was adequate to resolve leaflet position, and 5) the 60-Hz sampling rate was adequate to capture the essential dynamics of the rapidly moving leaflets.
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0.4 ± 0.6 mm anteriorly (P = 0.05).
Figure 11 shows the sum of the chord
lengths for the posterior leaflet
(D18-36 + D36-35)
and for the anterior leaflet (D22-31 + D31-32 + D32-33 + D33-34)
vs. time. These lengths were virtually unchanged during late systole, rapid pressure decay, and until t = +33 ms. This implies that the leaflets are very stiff in the radial
direction during this period, inasmuch as LVP varied by >130 mmHg
during this time. Each component of the chord length sum was invariant
over this time; thus this constant sum was not the result of some
chords lengthening and others shortening by a compensating amount.
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35 (Fig. 3) and
36 between the septal-lateral axis,
D18-22, and
the vectors from marker 18 to
markers 35 and
36, respectively, vs. time. The angle
35 was essentially constant
(range 54.8 ± 1.9 to 56.0 ± 1.8°) during late systole and
rapid pressure decay, with a minimum of 54.8 ± 1.9° at
t = 100 ms. It was 55.4 ± 1.9° at t = 0 (P = NS) and increased rapidly from
55.5 ± 1.5° at t = +33 ms to a
maximum of 91.5 ± 2.7° at t = +83 ms (P < 0.001). It fell steadily
to 74.2 ± 3.4° at t = +167 ms
(P < 0.001 from maximum). Similarly, the angle 36 was essentially
constant (with the same value as 35: range 54.3 ± 4.4 to
57.1 ± 4.3°) during late systole and rapid pressure decay and
began to increase rapidly at t = 0 to a maximum of 99.2 ± 2.7° at t = +83 ms (P < 0.001 relative to late
systole) just after the time of minimum LVP. Thereafter, it fell
steadily to 84.0 ± 5.4° at t = +167 ms (P < 0.001 relative to
maximum).
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31-34
(Fig. 3) between the septal-lateral axis,
D18-22, and
the vectors from marker 22 to markers 31-34, respectively. The
angle 31 decreased steadily throughout late systole and rapid pressure decay, to a minimum of 60.8 ± 2.0° at t = 17 ms. It
was 61.7 ± 2.1° at t = 0 (P = NS) and increased to a maximum of
72.1 ± 1.8° at t = +83 ms
(P < 0.001 relative to
t = 0). Thereafter it fell slowly to
69.3 ± 1.6° at t = +167 ms
(P < 0.01 relative to maximum). The
angle 32 fell during late
systole and rapid pressure decay to a minimum of 43.5 ± 1.7° at
t = 33 ms and began to increase
rapidly (more rapidly than
31) at
t = 0 to a maximum of 72.3 ± 1.9° at t = +83 ms
(P < 0.001 relative to late
systole). Thereafter, it fell (again, more rapidly than
31) to 58.0 ± 1.5° at
t = +167 ms
(P < 0.001 relative to maximum). The
angle 33 decreased during late systole and early in rapid pressure decay to a minimum of 36.6 ± 1.4° at t = 33 ms and began
to increase rapidly (more rapidly than
31 and
32) at
t = 0, reaching a maximum of 77.0 ± 2.8° at t = +100 ms
(P < 0.001 relative to late systolic
minimum). Thereafter, it fell (more rapidly than
31 and
32) to 53.1 ± 2.1° at
t = +167 ms
(P < 0.001 with respect to maximum).
Finally, the angle 34 to the
marker on the anterior leaflet edge decreased during late systole and
early rapid pressure decay to a minimum of 32.9 ± 1.7° at
t = +17 ms, essentially the same time
(P = NS) as the minimum of
35 on the posterior leaflet.
The angle 34 increased (more
rapidly than 31,
32, and
33), reaching a maximum of
77.0 ± 3.0° at t = +100 ms
(P < 0.001 relative to minimum). Thereafter, it fell (more rapidly than
31,
32, and
33) to 49.1 ± 2.0° at
t = +167 ms. Similar to the posterior
mitral leaflet, all portions of the anterior leaflet reached their
maximum angular displacements at a time just after the nadir of the
broad LVP minimum.
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Mitral annulus geometry. We found that the ovine mitral annulus is roughly elliptical, with its longest dimension from commissure to commissure, similar to that of other animals (29-31) and of humans (18, 20, 21, 24). The annular shape in the hearts we studied, however, was virtually constant during the latter half of systole rather than becoming more elliptical, as previously reported (18, 29, 31). We do not know the basis for this difference, but we believe that it could reflect, alone or in combination, 1) a difference in hemodynamic conditions between studies, 2) a difference due to the species studied, and 3) a difference in measurement technique between our computation of annular axis dimensions from the three-dimensional coordinates of fixed annular sites and previous measurements from two-dimensional coordinates.
During systole, constant annular shape was maintained by virtue of a small but equivalent shortening of both annular axes (Fig. 5). Whereas mitral annular size has been reported to decrease during systole (7, 18, 29, 31), Tsakiris et al. (29) observed that increases and decreases in annular size could be recorded during systole in the same heart depending on the hemodynamic conditions. Annular size may also depend strongly on LA and LV size (26). It is generally agreed, however, that mitral annular size is always less in systole (resulting in a significant reduction in the area that the leaflets must bridge) than in diastole (3, 18, 30), as we also found. Studies of human (18) and animal (5, 30) hearts have reported a minimum annular "size" in midsystole, with annular size increasing during isovolumic relaxation. We found this to depend on the dimension studied. Although, as shown in Fig. 5, the septal-lateral dimension indeed increased throughout isovolumic relaxation (presumably favoring opening by beginning the separation of the anterior and posterior leaflets), the commissure-commissure dimension continued to decrease until LVP had fallen by nearly one-half, when this dimension began to increase rapidly. Although a gradual increase in annular size after mitral valve opening to a maximum in late diastole in human (18) and animal (5, 30) hearts has been reported, we again found that this depended on the dimension examined. The hearts we studied exhibited at least a local maximum in annular dimensions 50-70 ms after mitral valve opening, with the septal-lateral dimension falling rapidly thereafter, whereas commissure-commissure dimensions fell very little (Fig. 5; i.e., there was a more elliptical annular shape). Thus we found that the annulus became slightly smaller and slightly more circular from the moment LVP began to drop at end systole. It became most "circular" (albeit still oval) when the leaflet edges were just beginning to separate, then rapidly resumed its more oval shape, and its dimensions increased as the leaflets opened widely during early filling. Levine et al. (12, 14) suggested, on the basis of their three-dimensional echocardiographic reconstructions, that the mitral annulus in the normal human heart is saddle-shaped (a hyperbolic paraboloid) in systole. They found the high points of the saddle (i.e., furthest from the LV apex) at the aortic insertion and posterior LV wall and the low points (closest to the apex) medially and laterally, near the commissures. Our annular marker 22 (Figs. 1 and 8) was placed under direct visualization at the point of aortic insertion of the anterior leaflet and marker 18 at the point of LV insertion of the middle scallop of the posterior leaflet. The medial and lateral annular regions would be identified near our commissure markers 20 and 16. Thus, if the annulus is saddle shaped, the 22-18 axis would be the length of the saddle and the 16-20 axis its width. Figure 9 shows that if the annulus in these hearts is considered to be saddle shaped, then 1) the saddle is nearly flat except for the region nearest the aorta, identified by marker 22, and 2) unlike the finding of Levine et al. (12, 14), the annulus was asymmetric about the commissure-commissure (16-20) axis. These findings are consistent with our earlier observations of the shape of the canine mitral annulus (7). It is of interest that although annular dimensions changed (Fig. 5), three-dimensional annular shape (Fig. 9) was virtually invariant over the interval studied. It is possible that the mitral annulus of the sheep and dog are indeed roughly planar and do not resemble the saddle shape of the human heart. Furthermore, annular geometry may have been altered by surgery. The very definition of the mitral annulus may also be at issue here, however. The annulus is not a clearly defined anatomic structure (33). In the present study we chose to define it as the locus of points of attachment of the mitral leaflets to the surrounding atrial and ventricular tissue, which we observed directly and to which radiopaque markers were sutured. It is not as clear what should be used to define the "annulus" in echocardiographic and magnetic resonance images, which generally rely on the observed leaflet "hinge point." For example, these imaging modalities might not be capable of observing the subtle details of the shape of the anterior mitral leaflet connection to the aorta. Furthermore, our three-dimensional reconstructions utilize the coordinates of specific sites fixed on cardiac structures and stereoimaged at 60 samples/s. Other imaging modalities reconstruct the annulus from sites that may be changing with time, which may be obtained from data averaged over many cardiac cycles, and have coarser temporal resolution. Further experimental studies are needed to resolve the origin of these differences. Previous studies have suggested that the mitral annular plane is oriented at nearly right angles to the LV long axis (30) and that this orientation changes very little throughout the cardiac cycle (8, 30). We found that the septal-lateral and commissure-commissure axes of the annular plane were tilted roughly 75° to the LV long axis and that their orientation changed <4° from systole to diastole (Fig. 7). Besides being of basic physiological interest, mitral annular tilt may be of considerable importance in the clinical assessment of transmitral flow by echocardiographic and magnetic resonance imaging techniques. We believe that the unloaded shape of the mitral annulus in these hearts may be closely approximated by the minimum septal-lateral-to-commissure-commissure ratio of ~0.70 at t = +150 ms in Fig. 6, although residual stresses remain. At this middiastolic portion of the cardiac cycle there are presumably few forces distorting the annulus; LVP is at low diastolic levels, muscle in the annular region is relaxed, the LA is relaxed, LV myocardial and papillary muscles are relaxed, and the leaflets are open. Thus the change to a more circular shape of the annulus during systole most likely results from forces associated with myocardial contraction, papillary/chordal traction, and LVP acting on the closed mitral leaflet surfaces. When these forces are removed during early opening, particularly after mitral leaflet edge separation, the annulus rapidly resumes its more relaxed oval configuration. Note that this maximally oval configuration is brought about by means of a reduction in the septal-lateral dimension after edge separation, with the commissure-commissure dimension remaining elongated throughout the middiastolic period (Fig. 5). This suggests that the septal-lateral annular dimension is already moving toward its closed value during early valve opening and the annulus continues to move toward its closed configuration during rapid early diastolic filling. Thus the unloaded annular configuration in diastole may be moving toward valve closure, even while the leaflets are opening widely. We believe this is a new finding. Tsakiris et al. (30) found that annular regions adjacent to the posterior leaflet moved toward and away from relatively immobile annulus regions adjacent to the anterior leaflet. Any such movement of the lateral marker (18) toward the septal marker (22) moves the base of the posterior leaflet closer to the base of the anterior leaflet, a characteristic of potential importance to valve opening and closing (2).Mitral leaflet geometry. Rushmer et al. (22) noted that in intact, normal animals the valve did not bulge into the atrium during ventricular systole, and they attributed this to papillary muscle contraction. We also found that at no time during late systole and early diastole were any of the anterior or posterior leaflet markers observed on the atrial side of the septal-lateral (i.e., 22-18) mitral annular axis.
Anterior leaflet. During the latter half of systole, in all hearts and all beats analyzed, the curvature of the central portion of the anterior leaflet, the shape of which is approximated by the sequence of line segments joining markers 22 and 31-34, was found to be compound (Fig. 15). Although concave curvature of this leaflet has been reported from echocardiographic studies in canine (19) and human (12, 14) hearts, Levine et al. (13) emphasized the importance of the appropriate long-axis echocardiographic view to evaluate this aspect of leaflet shape and its relationship to the mitral annulus. Echo long-axis views have shown anterior leaflet curvature convex to the LV in human hearts, as we found in the annular region of the anterior leaflet in these ovine hearts (Fig. 5 in Ref. 13 and Figs. 3 and 6 in Ref. 12). Leaflet curvature convex to the LV implies an interplay between myocardial/papillary/chordal forces and annular tension on the leaflet, because without such external forces the anterior leaflet would be expected to assume a concave shape to the LV in response to the forces on the leaflet associated with the high systolic LVP. In these sheep hearts, as in the human heart (Figs. 2-7 in Ref. 1 and Fig. 6 in Ref. 10), numerous chordae attach to the ventricular surface ("rough zone") of the anterior leaflet, away from the leading edge, although no chordae are attached to the midportion of the leaflet along which markers 31-34 were attached. We presume that, during systole, these chordae (including the 2 strut chordae) pull the central portion of the anterior leaflet into a convex shape from their adjacent leaflet attachment sites nearer the commissures. Sufficient chordal attachments exist to account for a wide variety of complex (and compound) anterior leaflet curvatures in systole, depending strongly on the forces applied to the leaflets by the chordae throughout systole.
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Posterior leaflet. Unlike the anterior leaflet, the mean shape of the central scallop of the posterior leaflet, as defined by markers 18, 35, and 36, exhibited slight curvature concave to the LV during late systole or rapid pressure decay in the x-y plane (Fig. 15), although some variations, either convex or concave to the LV, were noted in individual hearts. Previous studies also reported both convex (12) and concave (25) posterior leaflet curvature with respect to the LV in closed valves. If LVP alone were acting on the surface of the posterior leaflet that was tethered at its edges, one would expect the leaflet to appear concave to the LV in the x-y plane during systole and rapid pressure decay. Thus, to the extent that any convex curvature to the LV is observed, both myocardial/papillary/chordal forces and annular tension would also have to be acting on the posterior leaflet to maintain such a profile. Although the posterior leaflet is considerably smaller than the anterior leaflet, there are ample chordal attachments to its margins and its LV surface to provide such forces (10). Chordal attachment angles differ between anterior and posterior leaflets, however, and the posterior leaflet also has many direct chordal attachments to the nearby LV endocardium, as well as to the papillary muscles; thus the nature of the force balance between chordal tension and LVP of the posterior leaflet is likely to be quite different from that of the anterior leaflet.
During ejection, the posterior leaflet markers moved slightly closer to the mitral annulus (i.e.,35
and 36 decreased; Fig. 12).
Again, as with the anterior leaflet, we speculate that this most likely
resulted from a progressive reduction in chordal tension during
ejection (23), which changed the leaflet force balance, resulting in
the hydrodynamic force due to LVP pushing the leaflet toward the
annulus. This force balance appeared to reverse at an ever-increasing
rate during the last half of rapid pressure decay, when posterior
leaflet curvature began to change, as evidenced by the increase in
36 after
t = 33 ms in Fig. 12, with no
equivalent change in 35.
We found that, during opening, on average, the central portion of the
posterior leaflet appeared (in the x-y
plane) to continue to curve slightly concave to the LV before edge
separation and vary this curvature somewhat throughout opening (Fig.
15). The posterior leaflet marker 36 began to move away from the annulus (demonstrating a slightly
flattening leaflet) when LVP had fallen by approximately one-half (Fig.
12). The posterior leaflet edge marker
35 moved toward its open position 67 ms later. These
findings are in agreement with those of Sovak et al. (25), who
concluded that the opening movement of the posterior leaflet did not
start at the free margin, but rather at the center of the cusp.
During mitral opening, the markers on the posterior leaflet, unlike
those on the anterior leaflet, showed no increase in
z-coordinate, but instead moved
parallel to the septal-lateral (i.e.,
22-18) axis (Fig.
10B). Thus, unlike the anterior
leaflet, the net excursion of the central portion of the posterior
leaflet into the LV during opening was simply away from the
interventricular septum. As with the anterior leaflet, the posterior
leaflet swung widely into the LV, becoming nearly perpendicular to the
septal-lateral axis at maximum excursion (Fig.
10A). Also, unlike the anterior
leaflet, the posterior leaflet edge marker described an arc with
decreasing radius about its basal hinge
(18) marker during earliest opening (because of the increasing curvature of the leaflet), then maintained this arc throughout subsequent opening (Fig.
10A).
Leaflet coaptation. There is an anatomic demarcation line on each leaflet that can be visually observed at surgery (33, 34). On the marginal side of this line, there is a so-called "coaptation zone," where the leaflet is thin and smooth surfaced on the atrial side. On the annular side of this line, the leaflet is thicker and rougher in texture. Coaptation is thought to occur by apposition of the coaptation zones of both leaflets. Marker 33 was placed at the demarcation line on the anterior leaflet and marker 36 at the demarcation line on the posterior leaflet. It became clear that actual coaptation was not at these points, inasmuch as they are separated by >10 mm during systole and rapid pressure decay (Fig. 10A). Marker 34 was placed on the LV side of the anterior leaflet margin and marker 35 on the LV side of the posterior leaflet margin (Fig. 3). These markers are separated by only 5 mm during systole and rapid pressure decay (Fig. 14). With consideration of the size of the markers (we measured the position of their center points) and the thickness of the leaflet tissue, this suggests that the actual coaptation region in these hearts was essentially at the very edge of each leaflet (Fig. 15). Coaptation at this location requires rather precise positioning of each leaflet with respect to the other, positioning that is likely the result of the leaflets being tightly coupled anatomically at the commissures and aligned by the chordae from each papillary muscle. That the edge-edge distance D34-35 (Fig. 14) is remarkably constant throughout late systole (changing LV volume) and rapid pressure decay (changing LV pressure) suggests that the geometry of the coaptation region over this interval, which is likely to be the apposition of two leaflet surfaces concave to the LV, as shown in Fig. 15, is rather insensitive to LV size and pressure.
Leaflet edge separation did not occur until LVP was nearly at its minimum value (Fig. 14). In contrast, all other annular and leaflet structures began moving toward their open configuration during rapid pressure decay. Previous workers have reported rapid leaflet opening at (19) or before (28) diastolic pressure crossover and that mitral flow may begin before leaflet separation (11). Thus leaflet edge separation is the last event in a cascade of changes occurring throughout the mitral valvular and subvalvular apparatus during the rapid fall of LVP.| |
ACKNOWLEDGEMENTS |
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The authors gratefully acknowledge B. W. Brown for help with the statistical analysis.
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FOOTNOTES |
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This work was supported by National Heart, Lung, and Blood Institute Grants HL-48837 and HL-29589 and by the Department of Veterans Affairs Medical Research Service. J. R. Glasson and M. Komeda are Carl and Leah McConnell Cardiovascular Surgical Research Fellows. M. O. Karlsson was supported by the Swedish Ministry of Education, the Pharmacia Research Foundation, and the Ingeströmska Research Foundation.
1 Maximum anterior leaflet velocity during opening, computed from three-dimensional marker coordinates, was 0.49 ± 0.03 m/s, equivalent to maximum opening velocities we and others (25) measured with M-mode echocardiography, suggesting that inertial loading of the leaflets by the markers is minimal.
Address for reprint requests: N. B. Ingels, Jr., Dept. of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, 860 Bryant St., Palo Alto, CA 94301.
Received 9 January 1997; accepted in final form 20 October 1997.
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Top
Abstract
Introduction
Methods
Results
Discussion
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