Biomedical Engineering Reference
In-Depth Information
in the atrium during diastasis. A vortex also starts developing at the tip of each leaf-
let, probably enhancing the partial closing seen in mid-diastole. The vortex devel-
oping behind the anterior leaflet is larger and more intense than the vortex behind
the posterior leaflet. During the deceleration of the first filling wave (
t
= 180 ms),
the velocity distribution across the mitral annulus is slightly skewed. The inflow at
the anterior side of the annulus has ceased, while it is continuous at the posterior
side. In the two subsequent plots (
t
= 240 ms and
t
= 300 ms), the transmitral flow
is almost zero.
At the end of diastasis,
t
= 330 ms, the atrium contracts and the pressure gradient
increases causing a second acceleration of flow into the ventricle (
t
= 360 ms and
t
= 420 ms). The valve opens and the vortices at the leaflet tips become less intense.
The vortices developed in the atrium during diastasis disappear through the mitral
valve opening, resulting in a prominent asymmetric transmitral flow with a high ve-
locity at the posterior side. At the very end of diastole, the atrio-ventricular pressure
gradient decreases again. The flow is hindered as the leaflets drift back, but due to
inertia the blood continues to flow through the mitral valve (
t
= 420 ms), predomi-
nantly near the posterior side (Fig.
8.71
).
8.8.3
Closure
This example by Dahl et al. (2010) showed the prescribed motion of the left ven-
tricle during filling. It is evident that variations in shape and volume occur during
diastole. The results also indicate that important features of the flow field may not
be predicted by the use of symmetric leaflets or in the absence of an adequate model
for the left atrium, particularly during diastasis and atrial contraction.
8.9
Summary
FSI is being used as a demonstration of practicality of achieving a higher physi-
ological realism in haemodynamics analysis in applications such as atherosclerosis
in carotid bifurcation, calcified plaque rupture, aortic aneurysm, as well as coro-
nary artery bypass graft. The contributions from analysing these applications can
be summarized below.
• The presence of severe stenosis produces smaller flow reversal at advanced stag-
es of the disease. This leads to diminishing low wall shear stress in the stenotic
region. The stenosis apex experiences compressive stress which can intensify as
it grows which explains why plaque can still grow at advanced stages when the
wall shear stress is higher. The relationship between pulse pressure, maximum
displacement, and maximum principal stress suggest that elevated heart rates can
lead to a higher risk of stroke due to longer exposure to high vessel wall displace-
ment and stresses.
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