Article Outline - JACC: Cardiovascular Imaging

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FIGURE LEGENDS
Figure 1. Flow Chart for Virtual Mitral Valve Modeling and Computational
Simulation of MV Function
Three-dimensional (3D) geometric information of the mitral valve (MV) and its
apparatus at peak systole and at end diastole is obtained from 3D transesophageal
echocardiography (TEE) data. First, the annulus and leaflets at peak systole are
traced and reconstructed in eighteen cut-plane images in a cylindrical coordinate
system from 3D TEE volume data followed by 3D surface modeling. The locations of
papillary muscle tips are determined and chordae tendineae are modeled to complete
virtual MV modeling. Electrocardiogram (ECG)-gated annular motion between peak
systole and end diastole obtained from 3D TEE data and physiologic transvalvular
pressure gradient are incorporated for computational simulation. Computational
simulation of MV function across the cardiac cycle is performed using finite element
analysis techniques to calculate deformation and stress distribution in the MV structure
as well as leaflet coaptation. (A) Flow chart for the MV evaluation protocol using
patient-specific MV geometric information from 3D TEE and computational simulation.
(B) Representative images of 3D TEE data, virtual MV modeling process, and
computational simulation in the MV evaluation protocol described in (A).
Figure 2. Images of a Normal MV
(A) Volumetric MV images from 3D TEE data demonstrating normal leaflet coaptation
(atrial view). Images are displayed from end diastole (left) to peak systole (right). See
Online Video 1. (B) Corresponding images of the virtual MV model from computational
simulation demonstrating dynamic motion of the saddle-shaped annular morphology
and stress distribution over the leaflets. Note that large leaflet stress is observed only
near the posteromedial commissural area at peak systole. See Online Video 2. A =
anterior; Al = anterolateral; P = posterior; Pm = posteromedial.
Figure 3. Images of a Pathologic MV With Posterior Chordal Rupture
(A) Volumetric MV images from 3D TEE data demonstrating posterior leaflet prolapse
(atrial view). We found that both the P2 and P3 scallops in the flail leaflet were
involved with chordal rupture. Images are displayed from end diastole (left) to peak
systole (right). More detailed diagnosis and characterization of this pathologic MV are
described in Figure 7. See Online Video 3. (B) Corresponding images of the virtual MV
model with ruptured chordae from computational simulation clearly demonstrating flail
posterior leaflet prolapse in the same region as the 3D TEE images in (A). Note that
large stress values are widely spread over not only the flail posterior leaflet but also
the anterior leaflet at peak systole. See Online Video 4. Abbreviations as in Figure 2.
Figure 4. Case 1 – A Normal MV With Complete Coaptation; A-D (Peak Systole),
E-H (End Diastole)
(A) Volumetric MV image from 3D TEE data demonstrating normal leaflet coaptation at
peak systole (ventricular view). (B) 2D Doppler TEE image at 60 demonstrating a
cross-sectional commissural (Al-Pm) view at peak systole; red arrow line in (A). Little
regurgitation is observed. (C) Stress distribution across the leaflets at peak systole
computed from simulation of MV function (atrial view). The virtual MV model
demonstrated relatively symmetric stress distribution across the leaflets and large
stress values only in a small region in the anterior leaflet. (D) Distribution of contact
pressure between the leaflets demonstrating complete coaptation at peak systole
(posterior view). Note that contact pressure for fully closed coaptation was taken as
2.0 kPa (red) for this study. (E) Volumetric MV image from 3D TEE data clearly
demonstrating two fully open leaflets at end diastole (ventricular view). (F) 2D TEE
image at 0 at end diastole; red arrow line in (E). (G) Stress distribution across the
leaflets at end diastole (atrial view). Note that the stress threshold for red color in the
legend was set as 0.4 MPa for this study. (H) Morphology of the virtual MV at end
diastole, which corresponds to the 2D TEE image data in (F). Abbreviations as in
Figure 2.
Figure 5. Case 2 – A Degenerative MV With Mild Regurgitation and Small Annular
Dilation; A-D (Peak Systole), E-H (End Diastole)
(A) Volumetric MV image from 3D TEE data demonstrating defective coaptation
(yellow circle) leading to mild regurgitation at peak systole (ventricular view). (B) 2D
Doppler TEE image at 60 demonstrating the mild regurgitant jet near the
posteromedial commissure region at peak systole; red arrow line in (A). (C) Stress
distribution across the leaflets at peak systole computed from simulation of MV
function (atrial view). Asymmetrically distributed large stress values were observed
across both the anterior and posterior leaflets. (D) Contact pressure distribution
demonstrating faulty contact between two leaflets near the posteromedial commissure
region (yellow circle) at peak systole, which corresponds to defective coaptation
shown in (A). (E) Volumetric MV image from 3D TEE data demonstrating two fully
open leaflets at end diastole (ventricular view). (F) 2D TEE image at 0 at end diastole;
red arrow line in (E). (G) Stress distribution across the leaflets at end diastole (atrial
view). (H) Morphology of the virtual MV at end diastole, which corresponds to the 2D
TEE image data in (F). Abbreviations as in Figure 2.
Figure 6. Case 3 – A Degenerative MV With Severe Regurgitation and Large
Annular Dilation; A-D (Peak Systole), E-H (End Diastole)
(A) Volumetric MV image from 3D TEE data clearly demonstrating defective
coaptation in the P1 and P2 scallops (yellow circle) leading to mitral regurgitation at
peak systole (atrial view). (B) 3D Doppler TEE image demonstrating regurgitation near
the anterolateral commissure region at peak systole, which corresponds to the region
of defective coaptation in the 3D TEE images (yellow circle) in (A). (C) Stress
distribution across the leaflets at peak systole computed from simulation of MV
function (atrial view). The computational simulation demonstrated defective coaptation
in the anterolateral commissure region (yellow circle). Large stress values are widely
spread across both leaflets. (D) Distribution of contact pressure between the leaflets
from computational simulation demonstrates that the anterolateral commissure region
has no contact between two leaflets (yellow circle) at peak systole (posterior view),
which corresponds to defective coaptation and the area of regurgitation shown in (A),
(B), and (C). Note the extent of leaflet contact and overall coaptation height are much
smaller than for the normal MV displayed in Figure 4 (D). (E) Volumetric MV image
from 3D TEE data demonstrating two fully open leaflets at end diastole (atrial view). (F)
3D Doppler TEE image at end diastole. (G) Stress distribution across the leaflets at
end diastole computed from simulation of MV function (atrial view). (H) Morphology of
the virtual MV at end diastole, which corresponds to the 3D Doppler TEE images in (F).
Abbreviations as in Figure 2.
Figure 7. Case 4 – A Degenerative MV With Severe Regurgitation due to
Ruptured Chordae; A-D (Peak Systole), E-H (End Diastole)
(A) Volumetric MV image from 3D TEE data clearly demonstrating flail posterior leaflet
prolapse in the P2 and P3 scallops leading to severe regurgitation at peak systole
(atrial view). We found that at least two primary chordae tendineae were ruptured and
involved in the flail posterior leaflet prolapse. (B) 2D Doppler TEE image at 105
demonstrating the eccentric regurgitant jet parallel to the anterior leaflet surface due to
prolapse of the P2 and P3 scallops at peak systole; red arrow line in (A). (C)
Computational simulation was performed without modeling the chordae tendineae in
the P2 and P3 scallops. Morphology of the virtual MV at peak systole (atrial view) well
demonstrated excessive bulging of the posterior leaflet in the P2 and P3 scallops
corresponding to the flail posterior leaflet shown in (A). Large stress values were found
near the boundaries of the ruptured chordae in both the anterior and posterior leaflets.
This indicates that excessive force was induced in the remaining intact chordae
around the ruptured ones and large stress concentration was caused across the
leaflets near the remaining chordae. This eccentric large stress concentration can
further damage leaflet tissue structure leading to tissue failure. The maximum stress
value was four times larger than that of the normal MV in Figure 4 (C). (D) Contact
pressure distribution from computational simulation demonstrating the prolapsed
posterior leaflet with no contact between two leaflets in the P2 and P3 scallops (yellow
circle) at peak systole (posterior view), which corresponds to the flail leaflet and severe
regurgitation shown in (A), (B), and (C). (E) Volumetric MV images from the 3D TEE
data demonstrating two fully open leaflets at end diastole (atrial view). (F) 2D TEE
image at 132 (long axis view) at end diastole; red arrow line in (E). (G) Stress
distribution across the leaflets at end diastole computed from simulation of MV function
(atrial view). Note that the chordae tendineae in the P2 and P3 scallops were not
modeled to create chordal rupture in the computational simulation. (H) Morphology of
the virtual MV at end diastole, which corresponds to the 2D TEE images in (F). Ao =
aorta; other abbreviations as in Figure 2.
Figure 8. Assessment of Annular Reaction Force and Chordal Stress
Distribution; Normal MV (Case 1) Versus MV With Ruptured Chordae (Case 4)
Reaction force distribution exerted along the mitral annulus and chordal stress
distribution at peak systole were determined to evaluate the relationships between size
and morphology of the annulus, annular reaction force distribution, chordal stress
distribution, and MV pathology. (A) Annular force distribution of the normal MV
demonstrating relatively symmetric reaction forces along the annulus, particularly with
low reaction forces in the posterior annular region (atrial view). (B) Chordal stress
distribution for the normal MV demonstrating small stress distribution overall in the
chordae tendineae (posterior view). (C) Annular force distribution of the pathologic MV
with ruptured chordae demonstrating asymmetric reaction force distribution along the
annulus with several regions of large reaction force concentration (atrial view). Note
that the regions of large reaction forces correspond to the regions with excessive
stress concentrations for both the anterior and posterior leaflets shown in Figure 7 (C).
This indicates that large stress concentrations over the leaflets and large reaction
force concentrations in the annulus closely interact by sharing and reducing
excessively exerted force concentrations to prevent tissue damage. (D) Chordal stress
distribution of the pathologic MV with ruptured chordae demonstrating increased stress
values in the remaining intact chordae around the ruptured ones in the P2 and P3
scallops (posterior view). This extends the presumption above indicating that intact
chordae tendineae play important roles to reduce excessive force concentrations over
the MV apparatus.
Figure 9. Contact Pressure Distribution Between the Leaflets; Normal MV (Case
1) Versus MV With Ruptured Chordae (Case 4)
(A) Images of distribution of contact pressure between the leaflets in the normal MV
from computational simulation of MV function across the cardiac cycle (posterior view).
Images are displayed from end diastole (left) to peak systole (right). When the two
leaflets began contacting, contact pressure increased around the leaflet edge region
over time and completed fully closed coaptation at peak systole. See Online Video 5.
(B) Images of distribution of contact pressure between the leaflets in the pathologic
MV with ruptured chordae across the cardiac cycle (posterior view). The extent of
leaflet contact was much smaller than for the normal MV displayed in (A). Contact
pressure occurred around the leaflet edge region when the leaflets began coaptation
except where chordae were not modeled (P2 and P3 scallops). Note that prolapse of
the posterior leaflet occurred as soon as the leaflets began coaptation indicating this
pathologic MV creates the regurgitant jet constantly while the MV is closed. See
Online Video 6.
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