Study of Cardiovascular System

Using Time Variance Elastance Model

Course No: ME 400

Submitted By-
Tasfin Ahmed
Student ID: 1510082
Mushfiq Ahmad Siddiqui
Student ID: 1510141

Submitted To-
Department of Mechanical Engineering
in partial fulfillment of the requirements for the degree of Bachelor of Science in Mechanical
Engineering.

Supervised by-
Dr. Sheikh Mohammad Shavik
Assistant Professor
Department of Mechanical Engineering

Bangladesh University of Engineering and Technology (BUET) Dhaka-

1000, Bangladesh
October 2021
CERTIFICATION

This is to certify that the work presented in the thesis is an outcome of the investigation
carried out by the authors under the supervision of Dr. Sheikh Mohammad Shavik,
Department of Mechanical Engineering, Dhaka. It is declared that this thesis has been
submitted only for the award of graduation.

Authors

Tasfin Ahmed Mushfiq Ahmad Siddiqui

Signature of the Supervisor

Dr. Sheikh Mohammad Shavik

Assistant Professor
Department of Mechanical Engineering
Bangladesh University of Engineering and Technology (BUET)
ACKNOWLEDGEMENT

We would like to express our deepest gratitude to our supervisor Dr. Sheikh Mohammad Shavik for
his guidance on this project showing us the path of conducting successful research and above all for
always being there as our mentor. He shared his wisdom with us in analyzing subject matters and at the
same time valued our thinking approach to synthesize those topics. His suggestions drove us towards
better ways of thinking, his reviews enriched us in solving problems, and his support gave us strength at
the time of our disappointment. We shall forever cherish the memories of working with him. We deeply
thank our friends and families for always believing in us even at the moment when we were losing our
confidence.
ABSTRACT

Cardiovascular system, including both pulmonary and systemic, is a closed loop system that is solely
responsible for the circulatory motion of blood and nutrients around the body. Being one of the most
important and sensitive system of human body, many studies have been performed about it, although
most of the studies only focused on the left ventricular motion and related vascular system. The right
ventricular myocardium along with pulmonary vascular system are severely understudied. In this study,
we have taken an approach to construct the modeling of the combined cardiovascular system using
MATLAB. We used time varying elastance model to compute and graphically explain the mechanical
properties of both left and right myocardium. The model parameters can be tuned to simulate healthy
and diseased heart.
NOMENCLATURE

The following are the list of variables used in

this thesis:

CAO: Compliance of Aorta (ml Pa-1)

LV: Left Ventricle
e(t): time-varying activation function
RV: Right Ventricle (mmHgml−1)
RA: Right Atrium
E(t): time-varying elastance function
LA: Left Atrium (mmHgml−1)

Ao: Aorta EES: end-systolic elastance (mmHgml−1)

PA: Pulmonary Artery Ea: Arterial Elastance

MV: Mitral Valve EDPVR: end-diastolic pressure–volume

relationship
TV: Tricuspid Valve
ESPVR: end-systolic pressure–volume
AV: Aortic Semilunar Valve relationship

PV: Pulmonary Valve

VLV: Volume of Left Ventricle (ml)

VRV: Volume of Right Ventricle (ml)

VRA: Volume of Right Atrium (ml)

VLA: Volume of Left Atrium (ml)

PLV: Pressure of Left Ventricle (mmHg)

PRV: Pressure of Right Ventricle (mmHg)

PRA: Pressure of Right Atrium (mmHg)

PLA: Pressure of Left Atrium (mmHg)

RMV: Mitral Valve Resistance (Pa ms ml-1)

RTV: Tricuspid Valve Resistance (Pa ms ml-1)

RAV: Aortic Valve Resistance (Pa ms ml-1)

RPV: Pulmonary Valve Resistance (Pa ms ml-1)

CVEN: Venous Compliance (ml Pa-1)

CARTE: Arterial Compliance (ml Pa-1)

CPA: Pulmonary Artery Compliance (ml Pa-1)

TABLE OF CONTENTS

Page

1. Introduction
1.1. Cardiovascular System…………………………………………………………………….... 1
1.2. Pressure Volume Loop…………………………………………………………………….... 3
1.3. Time Varying Elastance Model……………………………………………………………... 4

2. Research Methodology…………………………………………………………………………. 6

3. Mathematical Formulation and Physical Modeling………………………………………….. 7

4. Computational Method & Results

4.1. Figure Generated from the Code……………………………………………………………. 11

5. Conclusion
5.1. Limitations……………………………………………………………………………….…. 15
5.2. Recommendations & Future Aspect

6. Bibliography ……………………………………………………………………………………. 16
 Page |1

CHAPTER 1

I NTRODUCTION

1.1 Cardiovascular System

The heart is a muscular pump connected to the systemic and pulmonary vascular systems. Working together,
the principal job of the heart and vasculature is to maintain an adequate supply of nutrients in the form of
oxygenated blood and metabolic substrates to all of the tissues of the body under a wide range of conditions. It
is a closed loop which has two main fluid pumps and a network of vascular tubes. It can be divided into the
pulmonary vascular system which contains the right ventricle, the pulmonary arteries, the pulmonary capillaries
and pulmonary veins and the systemic vascular system which contains the left ventricle, the systemic arteries,
the systemic capillaries and the systemic veins.

Figure 1.1: Block diagram of cardiovascular system

 Page |2

1.1.1 Pulmonary Vascular System

Pulmonary Vascular System includes the right side of the heart. Here the circulation that happens is called
pulmonary circulation. In pulmonary circulation, there is vast network of a vast network of arteries, veins,
and lymphatics that function to exchange blood and other tissue fluids between the heart, the lungs, and
back. Pulmonary circulation has some unique functions, such as ventilation and gas exchange. The
circulation moves blood between the heart and the lungs. Transportation of deoxygenated blood to the
lungs to absorb oxygen and release of carbon dioxide. The oxygenated blood then flows back to the heart.
In the pulmonary loop, deoxygenated blood exits the right ventricle of the heart and passes through the
pulmonary trunk. The pulmonary trunk splits into the right and left pulmonary arteries. These arteries
transport the deoxygenated blood to arterioles and capillary beds in the lungs. There, carbon dioxide is
released, and oxygen is absorbed. Oxygenated blood then passes from the capillary beds through venules
into the pulmonary veins. The pulmonary veins transport it to the left atrium of the heart. The pulmonary
arteries are the only arteries that carry deoxygenated blood, and the pulmonary veins are the only veins that
carry oxygenated blood.

Fig 1.2: Pulmonary Circulation

 Page |3

1.1.2 Systemic Vascular System

Systemic vascular system includes the left side of the heart. Here systemic circulation happens. In systemic
circulation, blood moves between the heart and the rest of the body. It sends oxygenated blood out to cells
and returns deoxygenated blood to the heart. In the systemic loop, oxygenated blood is pumped from the
left ventricle of the heart through the aorta, the largest artery in the body. The blood moves from the aorta
through the systemic arteries, then to arterioles and capillary beds that supply body tissues. Here, oxygen
and nutrients are released and carbon dioxide and other waste substances are absorbed. Deoxygenated
blood then moves from the capillary beds through venules into the systemic veins. The systemic veins feed
into the inferior and superior venae cava, the largest veins in the body. The venae cavae flow deoxygenated
blood to the right atrium of the heart.

Figure 1.3: Systemic Circulation Flow Chart

 Page |4

1.2 Pressure Volume Loop

To determine a considerable amount of cardiac performance P-V loops are used. Scientists have historically
relied on systemic blood pressure, blood flow, and ventricular pressure to report changes in heart performance.
These are all important parameters, but only form part of the picture of heart performance.
Pressure-Volume (PV) loops provide a range of hemodynamic parameters which are not readily measurable by
other methods, including changes in contractility, elastance, power, energetics and efficiency. What is even
more powerful about PV loops is that they provide quantitative measurements of parameters, not just qualitative
results.

Figure 1.4: Pressure Volume loop

1.2.1 End-Diastolic Pressure (EDP)

Pressure in the ventricle at the end of diastole.

1.2.2 End-Diastolic Volume (EDV)

Volume in the ventricle at the end of diastole

1.2.3 End-Diastolic Pressure Volume relationship (EDPVR)

The EDPVR describes the passive filling curve for the ventricle and thus the passive properties of the
myocardium. The slope of the EDPVR at any point along this curve is the reciprocal of ventricular
compliance (or ventricular stiffness).

1.2.4 End-Systolic Pressure (ESP)

Pressure in the ventricle at the end of systole

1.2.5 End-Systolic Volume (ESV)

Volume in the ventricle at the end of systole

1.2.6 ESPVR (End-Systolic Pressure Volume Relationship)

The ESPVR describes the maximal pressure that can be developed by the ventricle at any given cardiac
chamber volume. This implies that the PV loop cannot cross over the line defining ESPVR for any given
contractile state.
 Page |5

1.3 Time Varying Elastance Model

The time-varying elastance theory of Suga et al. is widely used to simulate left ventricular function in
mathematical models and in contemporary in vitro models. It states that the relation between pressure and
volume variation in the LV is described by an elastance curve according to the following formulation:

P(t)= E(t)[V(t) – V0] (1)

Where, P(t) is the time-varying pressure (mm Hg), V(t) is the time-varying volume (ml), E(t) is the time-varying
elastance (mmHg/ml), and V0 is the volume at which the LV can no longer generate pressure (ml).

The curve is independent of ventricular preload and afterload within a physiological range, and its maximum
(Ees, end-systolic elastance) has been used widely as a marker of the contractility of the LV. Because it is
independent of the cardiac load, each individual case has its own elastance curve that only changes when the
basic contractile function of the heart changes.
 Page |6

CHAPTER2

RESEARCH METHODOLOGY

Characterizing circulatory dysfunction and choosing a suitable treatment is often difficult and
time consuming, and can result in a deterioration in patient condition, or unsuitable therapy choices.
A stable minimal model of the human cardiovascular system (CVS) is developed with the ultimate
specific aim of assisting medical staff for rapid, on site modelling to assist in diagnosis and
treatment. Models found in the literature simulate specific areas of the CVS with limited direct
usefulness to medical staff. The goal of this thesis was to study the modeling of combined
cardiovascular system using the time variance elastance model. We started the thesis work by
studying the system mechanics of left ventricular myocardium which is the most popular research
interest of Cardiovascular System. We then advanced to the understudied right ventricular
myocardium. We construct a combined model of left and right ventricular system with the help of
existing studies. Some simulation study has been done on MATLAB, to understand the system
behavior. A simulink model has been developed in MATLAB, for P-V closed loop system and the
system is analyzed for different circulatory values.

The difference in elasticity and fibre pressure of the various valves and ventricles of the cardio-
vascular system lead to unstable responses of the simulation, which was later fixed by adjusting the
model and code for new variable. This model was also used to evaluate vascular insufficiency
(Regurgitation).
 Page |7

CHAPTER 3

MATHEMATICAL FORMULATION & PHYSICAL MODELING

Ventricular mechanics can be expressed by end diastolic (PED) and end-systolic (PES) pressure–volume (P–V)
curves. Formulas for LV end-systolic and end-diastolic P–V relationships are

PLVES(VRV) = a(FCON)ELVES(VLV - VD,LV) (3.1)

PLVED(VLV) = P0,LV(exp(λLV(VLV - V0,LV)) - 1) (3.2)

For the RV, they are:

PRVES(VRV) = a(FCON)ERVES(VRV - VD,RV) (3.3)

PRVED(VRV) = P0,RV(exp(λRV(VRV - V0,RV)) - 1) (3.4)

Where, VD and V0 are the abscissa intercepts of the ESPVR and the EDPVR, respectively. P0 and λ are constants
used to fit the end-diastolic P–V relationship, as described below.

ELVES and ERVES are the maximum end-systolic elastances of the left and right ventricles under control
conditions (a(FCON) = 1), and are the slopes of Eqs. (1) and (3). Their values are constant and were obtained
from published data (Segers et al., 2001; Slama et al., 2000). The effect of myocardial contractility on end-
systolic behavior is denoted by a(FCON). It is determined by sympathetic neural activity (FCON). When
baroreflex control is absent, it is assumed to be 1, which corresponds to nominal values for left and right
ventricular end-systolic elastance.
A time-varying ventricular activation function e(t) provides a smooth transition between the EDPVR and ESPVR
relationships and is defined as a weighted sum of Gaussian time curves:

(1−𝐶𝑖)2
e(t) = ∑𝑁
𝑖=1 𝐴𝑖 exp(− ) (3.5)
2𝐵𝑖2

Here, e(t) represents the time course of instantaneous ventricular elastance. It establishes instantaneous
ventricular
pressure, as follows:

PLV(t) = e(t)PLVES(VLV) + [1 - e(t)]PLVED(VLV) (3.6)

PRV(t) = e(t)PRVES(VRV) + [1 - e(t)]PRVED(VRV) (3.7)

 Page |8

Figure 3.2B is used to plot the normalized activation function used in this study.

Figure 3.1. The equivalent hydraulic circuit of the heart model. The pressure-operated heart valves are modeled by a hydraulic diode-resistance pair. All
chambers are subject to intra-thoracic pressure. RA: right atrium, RV: right ventricle, LV: left ventricle, and LA: left atrium

Figure 3.2. Ventricular mechanics. (A) ESPVR and EDPVR curves for the left ventricle. (B) Normalized activation function of the ventricles (Segers et al.,
2001). (C) Resultant left ventricular P–V loop from ESPVR, EDPVR, and activation function. Points a, b, c, and d in Panels B, C, and D represent points on the
P–V loop corresponding to time points of the activation function. (D) Right ventricular ESPVR, EDPVR, and resultant P–V loop
 Page |9

Figure 3.3: Closed Loop of Cardiovascular System

Valves were assumed to open and close depending on weather the axial pressure gradient across the valves was
positive or negative. The rate of change in V was calculated assuming conservation of mass,

𝑑𝑉
= 𝑞𝑖𝑛 − 𝑞𝑜𝑢𝑡;
𝑑𝑡

Closed-Loop Systemic Circulatory Model

Models of the aorta and LV were coupled via a closed-loop modeling framework describing the systemic
circulatory system. Other components of the circulatory system were modeled using electrical analogs. Mass of
blood was conserved by the following equations relating the rate of volume change in each storage compartment
of the circulatory system to the inflow and outflow rate
𝑑𝑉𝐿𝐴(𝑡)
𝑑𝑡
= qven (t) - qmv (t); (3.8)

𝑑𝑉𝐿𝑣(𝑡)
𝑑𝑡
= qmv (t) - qao (t); (3.9)

𝑑𝑉𝑎𝑟𝑡(𝑡)
= qao (t) - qper (t); (3.10)
𝑑𝑡

𝑑𝑉𝑣𝑒𝑛(𝑡)
𝑑𝑡
= qper(t) - qven(t); (3.11)

Where, VLA, VLV, Vart, and Vven are volumes of each compartment, and qven, qmv, qao, and qper are flow rates
at different segments. Flow rate at different segments of the circulatory model depends on their resistance to flow
(Rao, Rper, Rven, and Rmv) and the pressure difference between the connecting storage compartments (i.e.,
pressure gradient). The
flow rates are given by,
𝑃𝐿𝑉,𝑐𝑎𝑣(𝑡)−𝑃𝑎𝑟𝑡,𝑐𝑎𝑣(𝑡)
; 𝑊ℎ𝑒𝑛, 𝑃𝐿𝑉, 𝑐𝑎𝑣(𝑡) ≥ 𝑃𝑎𝑟𝑡, 𝑐𝑎𝑣(𝑡)
qao(t)= { 𝑅𝑎𝑜 ; (3.12)
0; 𝑊ℎ𝑒𝑛, 𝑃𝐿𝑉, 𝑐𝑎𝑣(𝑡) ≤ 𝑃𝑎𝑟𝑡, 𝑐𝑎𝑣(𝑡)

𝑃𝑎𝑟𝑡,𝑐𝑎𝑣(𝑡)−𝑃𝑣𝑒𝑛,𝑐𝑎𝑣(𝑡)
qper(t)= ; (3.13)
𝑅𝑝𝑒𝑟
 P a g e | 10

𝑃𝑣𝑒𝑛(𝑡)−𝑃𝐿𝐴(𝑡)
qven(t)= ; (3.14)
𝑅𝑣𝑒𝑛

𝑃𝐿𝐴(𝑡)−𝑃𝐿𝑉,𝑐𝑎𝑣(𝑡)
; 𝑊ℎ𝑒𝑛, 𝑃𝐿𝐴(𝑡) ≥ 𝐿𝑉, 𝑐𝑎𝑣(𝑡)
qmv(t)= { 𝑅𝑚𝑣 ; (3.15)
0; 𝑊ℎ𝑒𝑛, 𝑃𝐿𝐴(𝑡) ≤ 𝑃𝐿𝑉, 𝑐𝑎𝑣(𝑡)

Pressure in each storage compartment is a function of its volume. A simplified pressure volume relationship,

𝑉𝑣𝑒𝑛(𝑡) − 𝑉𝑣𝑒𝑛,0
Pven(t) = 𝐶𝑣𝑒𝑛

Closed-Loop Pulmonary Circulatory Model

Models of the pulmonary and RV were coupled via a closed-loop modeling framework describing the pulmonary
circulatory system. Other components of the circulatory system were modeled using electrical analogs. Mass of
blood was conserved by the following equations relating the rate of volume change in each storage compartment
of the circulatory system to the inflow and outflow rate
𝑑𝑉𝑅𝐴(𝑡)
= qvc(t) - qtv(t); (3.16)
𝑑𝑡

𝑑𝑉𝑅𝑣(𝑡)
𝑑𝑡
= qtv(t) - qpv(t); (3.17)

𝑑𝑉𝑃𝐴(𝑡)
𝑑𝑡
= qpv(t) - qper(t); (3.18)

𝑑𝑉𝑣𝑐(𝑡)
𝑑𝑡
= qper(t) - qvc(t); (3.19)

Where, VRA, VRV, VPAt, and Vvc are volumes of each compartment, and qac, qtv, qpv, and qper are flow rates at
different segments. Flow rate at different segments of the circulatory model depends on their resistance to flow
(Rac, Rper, Rac, and Rtv) and the pressure difference between the connecting storage compartments (i.e., pressure
gradient). The
flow rates are given by,

𝑃𝑅𝑉,𝑐𝑎𝑣(𝑡)−𝑃𝑝𝑎,𝑐𝑎𝑣(𝑡)
; 𝑊ℎ𝑒𝑛, 𝑃𝑅𝑉, 𝑐𝑎𝑣(𝑡) ≥ 𝑃𝑝𝑎, 𝑐𝑎𝑣(𝑡)
qpv(t)= { 𝑅𝑝𝑣 ;
0; 𝑊ℎ𝑒𝑛, 𝑃𝑅𝑉, 𝑐𝑎𝑣(𝑡) ≤ 𝑃𝑝𝑎, 𝑐𝑎𝑣(𝑡)

𝑃𝑝𝑎,𝑐𝑎𝑣(𝑡)−𝑃𝑣𝑐,𝑐𝑎𝑣(𝑡)
qper(t)= ;
𝑅𝑝𝑒𝑟

𝑃𝑣𝑐(𝑡)−𝑃𝑅𝐴(𝑡)
qven(t)= ;
𝑅𝑣𝑐

𝑃𝑅𝐴(𝑡)−𝑃𝑅𝑉,𝑐𝑎𝑣(𝑡)
; 𝑊ℎ𝑒𝑛, 𝑃𝑅𝐴(𝑡) ≥ 𝑃𝑅𝑉, 𝑐𝑎𝑣(𝑡)
qtv(t)= { 𝑅𝑡𝑣
0; 𝑊ℎ𝑒𝑛, 𝑃𝑅𝐴(𝑡) ≤ 𝑃𝑅𝑉, 𝑐𝑎𝑣(𝑡)

Pressure in each storage compartment is a function of its volume. A simplified pressure volume relationship,

𝑉𝑎𝑐(𝑡) − 𝑉𝑎𝑐,0
Pac(t) = 𝐶𝑎𝑐
 P a g e | 11

CHAPTER 4

COMPUTATIONAL METHOD & RESULTS

The model was constructed through using time varying elastance theory. We applied the theory to both of our
Pulmonary circulation and Systematic circulation. Then after getting the mathematical equations necessary to get
the desired values, we used MATLAB for our computational software.

The goal of this study was to develop models for both systemic circulatory system and pulmonary circulatory
system. After generating the model we ran some analysis to get the graphs where it shows some data of the different
parts of the system.

4.1 Figure Generated from the Code

Figure 6.1: Pressure Volume Diagram of the Left Ventricle

 P a g e | 12

Figure 6.2: Pressure in LV, aorta, and LA during cardiac cycle

Figure 6.3: Pressure Volume diagram of left artrium

 P a g e | 13

Figure 6.4: Pressure Volume Diagram of the right Ventricle

Figure 6.5: Pressure in RV, Pulmonary artery, and RA during cardiac cycle
 P a g e | 14

Figure 6.6: Pressure Volume diagram of right atrium

From the code we generated some pressure volume diagrams and Pressure in parts of the system during cardiac
cycle. Normally P-V diagrams of the systemic cardiovascular system is common to see as most of the studies
occurred about the systemic circulation. Thus it is rare to find the model and data of pulmonary circulation. So we
had to estimate the data of the pulmonary systems to make the diagrams.
 P a g e | 15

CHAPTER 5

CONCLUSION

The goal of this study was to develop models for both systemic circulatory system and pulmonary
circulatory system. After generating the model, we ran some analysis to get the graphs where it shows the
pressure and volume of the circulation system parts. By analyzing those graphs, we can get some idea about
the model of our heart. The model parameters can be further tweaked to simulate heart in different
conditions.

5.1 Limitations

Some of the data that we needed for the variables of the model was hard to find and some further studies are
needed in order to find the precise data that the model requires. Some assumptions were

5.2 Recommendations and Future Aspect

Some data were hard to get hold of as the work done on the pulmonary system is very low. There weren’t
enough data so had to assume a lot of the data that we worked on. In the future this model can be more
precise if we could get hold of a real-life model and get the data from there so the results we get can get as
close to the actual results.
 P a g e | 16

BIBLIOGRAPHY

[1] Dr. Henry Gray and Dr. Henry Vandyk;

Gray’s Anatomy, 41st Edition.

[2] Sir Stanley Davidson

Davidson’s Principal and Practice of Medicine, 23rd Edition.

[3] Norman S. Nise.

Control Systems Engineering.
Wiley, 6th edition binder ready version edition, 12 2010.

[4] Sheikh Mohammad Shavik, Zhenxiang Jiang, Seungik Baek, and Lik Chuan Lee.
High spatial resolution multi-organ finite element modeling of ventricular-arterial coupling.
Department of Mechanical Engineering, Michigan State University, East Lansing, MI, United States,
2018.

[5] Daniel Burkhoff, MD, PhD

Mechanical Properties of the Heart and its interaction with Vascular System.
Columbia University, 2002.

[6] Sotirios Kakaletsis , William D. Meador , Mrudang Mathur , Gabriella P. Sugerman , Tomasz
Jazwiec , Marcin Malinowski , Emma Lejeune , Tomasz A. Timek , Manuel K. Rausch
Right Ventricular Myocardial Mechanics: Multi-Modal deformation, microstructure, modeling, and
comparison to the last ventricle.

[7] Bram W Smith, J. Geoffrey Chase, Roger I. Nokes, Geoffrey M. Shaw, Graeme Wake
Minimal haemodynamic system model including ventricular interaction and valve dynamics.

[8] Shahnaz Javani, Ali N Azadani

Regional Mechanical Properties and Microstructure of Ovine Heart Chambers.
Faculty of the Daniel Felix Ritchie School of Engineering and Computer Science,
University of Denver, 2016.

[9] Roy R Ha, Junhui Qian, David L Ware, Joseph B Zwischenberger, Akhil Bidani, John W Clark
An Integrative Cardiovascular Model of the Standing and Reclining Sheep.

[10] Kenneth A Brown, MD and Roy V Ditchey, MD.

Human Right Ventricular End-Systolic Pressure-Volume Relation Defined by Maximal
Elastance.

[11] Wenqiang Liu, Zhijie Wang.

Current Understanding of the Biomechanics of Ventricular Tissues in Heart Failure
 P a g e | 17
[12] Selim Bozkurt.
Mathematical modeling of cardiac function to evaluate clinical cases in adults and children.
Institute of Cardiovascular Science, University College, London.

[13] Stijn Vandenberghe, Patrick Segers, Paul Steendijk, Bart Meyns, Robert A E Dion, James F
Antaki, Pascal Verdonck.
Modeling Ventricular Function during Cardiac Assist: Does Time-Varying Elastance Work?

[14] Brian Oomen, Mustafa Karamanoglu, Sandor J Kovacs.

Modeling Time Varying Elastance: The Meaning of “Load Impedence”.

[15] Keith R Walley.

Left Ventricular function: time-varying elastance and left ventricular aortic coupling.

[16] Hao Gao, Liuyang Feng, Nan Qi, Colin Berry, Boyce E Griffith, Xiaoyu Luo.
A coupled mitral valve-left ventricle model with fluid -structure interaction.

[17] Segers P, Steendijk P, Stergiopulos N, Westerhof N.

Predicting systolic and diastolic aortic blood pressure and stroke volume in the intact sheep

[18] Nishida T, Meyns B, Zietkiewicz M, Perek B, Xia Z, Goebel C, Ruel H, Flameng W.

The effect of sudden failure of a rotary blood pump on left ventricular performance in normal
and failing hearts.

[19] Leeuwenburg BPJ, Steendijk P, Helbing WA, Baan J.

Indexes of diastolic RV function: Load dependence and changes after chronic RV pressure
overload in lambs.