Excerpt from the Proceedings of the COMSOL Users Conference 2006 Birmingham
Simulation of Blood Flow through the Mitral Valve of the Heart: A
Fluid Structure Interaction Model.
Daniel M. Espino*1, Michael A. Watkins1, Duncan E.T. Shepherd1, David W.L. Hukins1 and
Keith G. Buchan2
1
Department of Mechanical and Manufacturing Engineering, University of Birmingham,
Birmingham, UK, 2Aberdeen Royal Infirmary, Aberdeen, UK
*Corresponding author: Department of Mechanical and Manufacturing Engineering, University of
Birmingham, Birmingham, UK, d.m.espino@bham.ac.uk
Abstract: Mitral valve failure causes death if it
is not corrected surgically. Such surgical repair
can be improved by understanding mitral
biomechanics. A two-dimensional FSI model of
the mitral valve was generated, using an ALE
mesh. A simple approximation of the heart
geometry was used, the valve dimensions were
based on measurements made. The viscosity of
blood and the elastic properties of the valve
leaflets were obtained from the literature. Valve
closure was simulated using contact equations.
The simulation predicted a large vortex behind
the anterior leaflet during inflow of blood into
the left ventricle, in agreement with MRI scans
available in the literature. Leaflet deformations
agreed with results from experiments in the
literature and with our previous experimental
results. In conclusion, a two-dimensional model
of the mitral valve has been developed, and will
be further developed to investigate heart valve
failure and subsequent surgical repair.
Keywords: Mitral valve, Fluid-Structure
Interaction, Biomechanics.
1. Introduction
Failure of the mitral valve of the heart can be
fatal if it is not corrected surgically (Espino et
al., 2005, 2006a). Improvement in the
understanding of the biomechanics of the mitral
valve would aid current knowledge of mitral
valve function, its failure and possible surgical
correction. Therefore, a Fluid-Structure
Interaction (FSI) model of the mitral valve has
been generated.
The mitral valve is present in the left side of
the heart, and functions normally to allow blood
to flow into the left ventricle of the heart when it
is filling. This valve then closes when blood is
pumped out from the heart towards the body. In
doing so, it prevents the regurgitation of fluid.
Several Finite Element (FE) models of the
mitral valve have been developed; however,
there are fewer that account for the effect of fluid
flow through the valve (Einstein et al., 2005a,b;
Van Loon et al., 2006; Watton et al., 2006). Of
the developed FSI models of the mitral valve, all
have simulated the flow of blood through the
valve in a conduit and ignored the effect of the
left ventricle of the heart on blood flow.
Furthermore, one model simulated a
polyurethane replacement mitral valve (Watton
et al., 2006), and another a single leaflet in a tube
(Van Loon et al., 2006). Only one FSI model of
an actual mitral valve, with two leaflets has been
developed (Einstein et al., 2005a,b).
The FSI model of the mitral valve we are
developing includes the walls of the left ventricle
of the heart, both anterior and posterior leaflets
of the valve, and the outflow tract of the aorta.
2. Methods
2.1 Model overview
A two-dimensional FSI model of the mitral
valve within the heart was generated using
Comsol Multiphysics (Version 3.2). Lagrange
multipliers have been used to apply the forces
exerted on the deforming structure due to the
flow of fluid, as has been done for other heart
valve FSI simulations (De Hart et al., 2003).
Velocity constraints were applied to the fluid on
the fluid-structure boundary, to ensure fluid at
that location moved at the same velocity as the
moving structure, as in other simulations (De
Hart et al., 2003). Structural deformation and
fluid dynamics are determined simultaneously.
An Arbitrary Lagrange Euler (ALE) mesh was
used, to allow FSI simulations to be performed.
 Excerpt from the Proceedings of the COMSOL Users Conference 2006 Birmingham
2.2 Geometry
Two geometries of the left ventricle of the
heart have been generated. Initially a simple
approximation of the heart was made, as being
elliptical in shape (i.e. half an ellipse), the major
and minor axis were 70 mm and 24 mm
respectively (based on measurements on heart
specimens, figure 1). The dimensions of the
valve leaflets were based on measurements made
(approximately 20 mm length and 0.7 mm thick;
figure 1b).
a) b)
Figure 1. Model of the left ventricle geometry used.
a) Elliptical model of the left ventricle; b) dissected
specimen of the mitral valve, with part of the heart
muscle dissected, showing the mitral valve.
A geometrically more accurate model has
also been generated that matches a study in
which measurements of pressure, flow and flow
patterns were used to quantitatively validate the
prediction of the model, for inflow during valve
opening (diastole; Reul et al., 1980).
The simplified elliptical model has been used
to simulate systolic ventricular pressures applied
to generate blood flow within the heart chamber,
causing valve closure, and blood flow through
the aortic outlet.
2.3 Parameters
The viscosity of blood and the elastic
properties of the valve leaflets were obtained
from the literature (Table 1).
Table 1. Values of parameters used to describe blood
and heart valves during simulations.
Parameter Value
Blood density (kg/m3) 1.06 × 103
Blood viscosity (Pa.s) 2.70 × 10-3
Leaflet density (kg/m3) 1.06 × 103
Anterior leaflet Young’s
modulus (MPa) 2.0 × 106
Posterior leaflet Young’s
modulus (MPa) 1.0 × 106
Leaflet Poisson’s ratio 0.49
2.4 Boundary conditions
Inflow boundary conditions were applied to
simulate valve opening during diastole and valve
closure during systole. During diastole an inflow
velocity was applied at the atrium and a pressure
condition was applied at the apex of the heart, to
apply the relevant ventricular pressures. During
systole, ventricular pressure was applied from
the apex of the heart, and outflow boundary
conditions were applied at the aortic outlet.
During systole only the stage of outflow of blood
was simulated.
2.5 Contact simulation
Valve closure was simulated using contact
equations between the boundaries of the two
mitral valve leaflets that come into contact.
Integration coupling variables were used to allow
information regarding the position of the
contacting boundaries available to each other all
along the boundary of the leaflets.
The two contacting boundaries were
separated into small segments, with nodes at the
end of each small segment. The distance between
nodes of one boundary on one leaflet and the
whole boundary on the other leaflet was
determined, and applied to equation 1.
 Pe − gk / P g > 0
F = 1
 P − gk g ≤ 0
In equation 1, P is the applied fluid pressure,
k is the stiffness of the contact, and g the
distance between the two contacting points. F is
the resulting contact force at each node.
 Excerpt from the Proceedings of the COMSOL Users Conference 2006 Birmingham

These contact forces were calculated at each

node for both leaflet boundaries that came into
contact. The force acting along the whole
boundary was then determined by interpolation
between the two nodes at the end of each
boundary (equation 2). It was assumed that the
force in between two nodes would be
continuous.

Fb = (r1/r2 × (F2 –F2)) + F1 2

In equation 2, F1 is the contact force at node-

1 and F2 the contact force at node-2 (where node-
1 and node-2 define the start and end points of a
boundary, respectively). Fb defines the contact
force at any point on the boundary. While. r1/r2
defines the ratio of the distance from node-1 to a
given point (r1), to the whole length of the
boundary (r2).
3. Results
The flow of blood caused the valve leaflets to
deform, in turn altering the flow of blood. The
simulation predicted a large vortex behind the
anterior leaflet during inflow of blood into the
left ventricle (figure 2), in agreement with MRI
scans available in the literature (Bronzino, 2000).
Figure 3. Predicted flow through a model of the left
ventricle with a geometry that corresponds directly to
a heart from which measurements of flow and
subsequent flow patterns were made.
Leaflet deformations, during opening and
closure, agreed with results from experiments in
the literature (figure 4). During systole, outflow
of blood occurred through the aortic outlet (as
reported in the medical literature), and mitral
valve leaflet closure agreed with our previous
experimental results (Espino et al., 2006b).

Figure 4. Simulated closure of the mitral valve of the

heart.

Results of simulating the closure of the mitral

Figure 2. Large vortex behind anterior leaflet valve leaflets using the contact equations, are
generated during diastole.
shown in figure 5. Little overlap occurred
between the two leaflets, which had different
Measurements were taken from specific
material properties (table 1).
points (figure 3), for quantitative comparison
with published experimental results (Reul et al.,
1980). Reasonable agreement was obtained.
 Excerpt from the Proceedings of the COMSOL Users Conference 2006 Birmingham
a)
b)
c)
Figure 5. Simulated mitral valve leaflet closure. a)
Leaflets before application of pressure; b) leaflet
closure position after application of pressure; c) close
up of leaflet section in contact.
4. Discussion
A two dimensional FSI model of the mitral
valve within the heart has been generated, and
transient simulations have been performed.
Simulations performed include the inflow of
blood into the left ventricle of the heart, and
outflow of blood through the aorta. The latter
simulation has required the use of contact
equations to simulate the closure.
One of the models simulated was developed
to match the geometry of a heart investigated in a
study where flow patterns and measurements of
flow and pressure were made. This has allowed
direct quantification of some results. A more
generalized model has been used more
extensively, but validation is more qualitative,
e.g. comparison to our previous experimental
results (Espino et al., 2005, 2006a,b), and
general literature (Bronzino et al., 2000; Reul et
al., 1980). Overall, our predicted results show
good agreement with observations available in
the literature.
This model will be used in future, to
determine stresses experienced by mitral valves
undergoing in vitro testing in our Laboratory to
understand the stresses the valve experienced.
Furthermore, it is to be developed into a three-
dimensional model.
5. Conclusions
A two-dimensional model of the mitral valve of
the heart has been developed. The results from
simulations agree with observations in the
medical literature. The model will be used to
investigate heart valve failure and subsequent
surgical repair.
6. References
Bronzino, Biomedical Engineering Handbook.
CRC Press LLC, Boca Raton (2000).
De Hart et al., A three-dimensional
computational analysis of fluid–structure
interaction in the aortic valve, Journal of
Biomechanics, 36, 103-112 (2003).
Espino et al., The role of chordae tendineae in
mitral valve competence, Journal of Heart Valve
Disease, 14, 603-609 (2005).
Espino et al., Mitral valve repair: an in vitro
comparison of the effect of surgical repair on the
pressure required to cause mitral valve
regurgitation, Journal of Heart Valve Disease,
15, 375-381 (2006a).
Espino et al., Determination of the pressure
required to cause mitral valve failure, Medical
Engineering and Physics, 28, 36-41 (2006b).
Einstein et al., The relationship of normal and
abnormal microstructural proliferation to the
mitral valve closure sound, Journal of
Biomechanical Engineering, 127, 134-147
(2005a).
Einstein et al., Non-linear fluid-coupled
computational model of the mitral valve, Journal
of Heart Valve Disease, 14, 376-385 (2005b).
Reul et al., Fluid mechanics of the natural mitral
valve , Journal of Biomechanics, 14, 361-372
(1980).
Van Loon et al., A fluid-structure interaction
method with solid-rigid contact for heart valve
 Excerpt from the Proceedings of the COMSOL Users Conference 2006 Birmingham

dynamics, Journal of Computational Physics,

217, 806-823 (2006).
Watton et al., Dynamic modelling of prosthetic
chorded mitral valves using the immersed
boundary method, Journal of Biomechanics, In
Press (2006).

7. Acknowledgements

The authors thank: The British Heart

Foundation for a Junior Fellowship awarded to
DME (FS/05/033), and the Nuffield Foundation
for an Undergraduate Research Bursary awarded
to MAW.