School of Engineering

CFD Lab ME4112

Student Name Student ID Number:

Class 4th Energy Systems Engineering

Assignment Number & Title: Assignment 1/ Blood Flow and Plaque Lab

Submission Date: 10/10/2023

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 1. Introduction

Cardiovascular diseases, including atherosclerosis, remain a leading global health concern.

Atherosclerosis, characterized by arterial plaque buildup, contributes to life-threatening
conditions like coronary artery disease, peripheral artery disease, vascular diseases, and strokes.
This study employs Computational Fluid Dynamics (CFD) modelling to enhance understanding of
cardiovascular disease diagnosis and treatment. This lab delves into the hemodynamic effects of
atherosclerosis in blood vessels, offering vital insights for enhanced medical approaches.
The main objective of this study is to provide a complete understanding of the complex interplay
between hemodynamic forces and vessel walls in the process of plaque development. For this
purpose, Ansys Design Modeler and Meshing tools are used to develop a realistic 3D model of a
vessel segment including stenosis, accurately reproducing the clinical setting. Using Ansys Fluent
to model the blood flow in the vessel that considers plaque. This includes choosing a suitable fluid
model and defining boundary conditions.
It studies their influences on blood flow by investigating principal hemodynamic parameters such
as velocity profiles, pressure distributions, wall shear stress and turbulence levels. It converges
the simulations and validates the results against known physiological conditions to verify the
accuracy of the CFD model.
The implications of this research question reach well beyond the academy. In the real world,
tangible consequences can be seen from what is found in this study. Understanding the intricate
relationship between atherosclerotic plaque and blood flow dynamics has the potential to
revolutionize clinical practice in several ways. The results may improve hemodynamic
consequences of plaque formation that can help facilitate the development of more accurate
diagnostics for early identification and evaluation of atherosclerosis. Armed with a better
knowledge of how plaque affects blood flow, clinicians can develop more focused treatment
approaches—lessening the demand for invasive interventions and increasing patient outcomes.
The data from this kind of study may help foster the implementation of preventive strategies to slow
down atheroprogression, decreasing its cardiovascular-related consequences.

2. Analysis method and underlying theory

In the pursuit of understanding the hemodynamic effects of atherosclerosis within blood vessels
and its implications for cardiovascular health, the computational methods employed, and the
associated underlying theory are outlined. The plans encompass the following aspects:

2.1.Governing Equations:
The foundation of computational fluid dynamics (CFD) modelling is found in the fundamental
equations that govern fluid flow. Specifically, the conservation of mass, momentum, and energy
within a fluid domain is described by the Navier-Stokes equations. These equations, adapted to the
specific nature of the study, serve as the mathematical framework for the simulation of blood flow
within the vessel and the consideration of the presence of plaque.

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 𝜕𝑝 𝜕2𝑢 𝜕2𝑢 𝜕2𝑢 𝑑𝑢 𝜕𝑢 𝜕𝑢 𝜕𝑢
𝜌𝑔𝑥 − 𝜕𝑥 + 𝜇 (𝜕𝑥 2 + 𝜕𝑦 2 + 𝜕𝑧 2 ) = 𝜌 𝑑𝑡 + 𝜌(𝑢 𝜕𝑥 + 𝑣 𝜕𝑦 + 𝑤 𝜕𝑧 ) for X momentum
𝜕𝑝 𝜕2𝑣 𝜕2𝑣 𝜕2𝑣 𝑑𝑣 𝜕𝑣 𝜕𝑣 𝜕𝑣
𝜌𝑔𝑦 − 𝜕𝑦 + 𝜇 (𝜕𝑥 2 + 𝜕𝑦 2 + 𝜕𝑧 2 ) = 𝜌 𝑑𝑡 + 𝜌(𝑢 𝜕𝑥 + 𝑣 𝜕𝑦 + 𝑤 𝜕𝑧 ) for Y momentum
𝜕𝑝 𝜕2 𝑤 𝜕2𝑤 𝜕2𝑤 𝑑𝑤 𝜕𝑤 𝜕𝑤 𝜕𝑤
𝜌𝑔𝑧 − 𝜕𝑧 + 𝜇 ( 𝜕𝑥 2 + 𝜕𝑦 2 + )=𝜌 + 𝜌(𝑢 𝜕𝑥 + 𝑣 𝜕𝑦 + 𝑤 𝜕𝑧 ) for Z momentum
𝜕𝑧 2 𝑑𝑡
𝜕𝜌 𝜕(𝜌𝑢) 𝜕(𝜌𝑣) 𝜕(𝜌𝑤)
+ + + )=0 for continuity
𝜕𝑡 𝜕𝑥 𝜕𝑦 𝜕𝑧
𝜕(𝜌𝑐𝑇) 𝜕(𝜌𝑐𝑢𝑇) 𝜕(𝜌𝑐𝑣𝑇) 𝜕(𝜌𝑐𝑤𝑇) 𝜕 𝜕𝑇 𝜕 𝜕𝑇 𝜕 𝜕𝑇
+( + + ) = [𝜕𝑥 (𝑘 𝜕𝑥 ) + 𝜕𝑦 (𝑘 𝜕𝑦) + 𝜕𝑧 (𝑘 𝜕𝑧 )] + Φ + 𝑠𝑇 for energy
𝜕𝑡 𝜕𝑥 𝜕𝑦 𝜕𝑧

2.2.Assumptions and Simplifications:

To enable a computationally manageable simulation while retaining the fundamental physical
attributes of the problem, several assumptions and simplifications have been applied. These
considerations pertain to fluid properties, boundary conditions, and the geometric characteristics
of the blood vessel.
Key assumptions and simplifications in the study include the blood vessel under investigation is
assumed to possess a length of 25 mm and a diameter of 4 mm. The dimensions serve as the basis
for the computational domain, Within the blood vessel, a spherical plaque is situated 5 mm
downstream from the inlet of the blood flow. The radius of this plaque is varied across multiple
scenarios, with values of 1 mm, 2 mm, and 3 mm, enabling the exploration of different plaque sizes
and their effects on hemodynamics. In line with common practice, it is assumed that the blood
exhibits fluid dynamic properties resembling those of water. This approximation is valid under
standard conditions of 25°C and 1 atm pressure.
The boundary conditions apply to simulate blood flow within the blood vessel, at the inlet surface,
and a velocity inlet boundary condition specifies, utilizing normal speed with a prescribed value
of Vin = 2 m/s, on the outlet surface, an "outflow". This choice allows for a physically realistic
representation of the flow conditions at the outlet, accounting for variations in flow rates and
pressure, for the walls, incorporating both the blood vessel and the plaque.
The simulation is executed for 10-3 iterations until the specified convergence criteria are met. This
entails multiple iterations and calculations until the solution stabilizes to an acceptable level.
These assumptions and simplifications, while aiding in the feasibility of the simulation, are
recognized as idealizations and approximations.

2.3.Choice of Computational Mesh:

The mesh is generated using the Ansys Meshing Tool to capture the intricacies of the blood vessel
and plaque geometry, a fine mesh resolution is employed in proximity to the surfaces of interest.
Additionally, inflation layers are introduced to ensure that boundary layer behaviour near the
vessel walls and plaque surface is accurately captured. The introduction of these inflation layers
is deemed essential for the precise representation of boundary layer and wall effects.
Through the application of these computational methods, grounded in the theoretical framework
of fluid dynamics, a detailed and dependable simulation of blood flow within blood vessels is
enabled, and the intricate interactions between plaque build-up and hemodynamic parameters are
explored.

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 3. Results, data analysis and discussion
3.1.1. The results of 1 mm Plaque Radius:

Figure 1: The blood vessel with 1 mm radius plaque.

For this 1mm plaque radius scenario, a fine mesh resolution was employed, especially near the
plaque and vessel surfaces as shown in Figure 2 below.

Figure 2: The surface of vessel and 1 mm plaque are meshing.

The number of iterations required to reach convergence was 66.

A plot of equation residuals was monitored, showcasing their decrease with iterations until
convergence. This plot provides insight into the convergence behaviour of the simulation and
ensures that the governing equations were adequately satisfied as shown in Figure 3.

Figure 3: The equation residuals (1 mm).

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A monitor plot of average velocity at the outlet was created. This plot allows to track changes in
average velocity as the simulation progresses, offering valuable insights into the flow behaviour
as shown in Figure 4.

Figure 4: The average velocity at the outlet (1 mm).

A contour plot of pressure on a plane along the centerline of the blood vessel was generated to
provide a spatial representation of pressure variations within the vessel, highlighting areas of
interest as shown in Figure 5.

Figure 5: The pressure on a plane (1 mm).

A contour plot of wall shear stress on the surface of the blood vessel and the plaque was produced.
This plot reveals regions of elevated shear stress, which can be indicative of potential risk areas
associated with plaque buildup as shown in Figure 6.

Figure 6: The wall shear stress on the surfaces (1 mm).

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A vector plot of fluid velocity on the plane along the centerline of the blood vessel was created to
illustrate the flow direction and magnitude within the vessel, offering insights into the impact of
the 1mm plaque on flow patterns as shown in Figure 7.

Figure 7: The fluid velocity on the plane (1 mm).

3.1.2. The results of 2mm Plaque Radius:

Figure 8: The blood vessel with 2 mm radius plaque.

For this 2mm plaque radius scenario, a fine mesh resolution was employed as shown in Figure 9
below.

Figure 9: The surface of vessel and 2 mm plaque are meshing.

The number of iterations required to reach convergence was 77.

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A plot of equation residuals was monitored, showcasing their decrease with iterations until
convergence as shown in Figure 10.

Figure 10: The equation residuals (2 mm).

A monitor plot of average velocity at the outlet was created as shown in Figure 11.

Figure 11: The average velocity at the outlet (2 mm).

A contour plot of pressure on a plane along the centerline of the blood vessel was generated as
shown in Figure 12.

Figure 12: The pressure on a plane (2 mm).

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A contour plot of wall shear stress on the surface of the blood vessel and the plaque was produced
as shown in Figure 13.

Figure 13: The wall shear stress on the surfaces (2 mm).

A vector plot of fluid velocity on the plane along the centerline of the blood vessel was created as
shown in Figure 14.

Figure 14: The fluid velocity on the plane (2 mm).

3.1.3. The Results of 3mm Plaque Radius:

Figure 15: The blood vessel with 3 mm radius plaque.

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For the scenario with a 3mm plaque radius, a fine mesh resolution was employed as illustrated in
Figure 16 below.

Figure 16: The surface of vessel and 3 mm plaque are meshing.

The convergence process required a total of 93 iterations to reach stability.

A plot of equation residuals was meticulously monitored throughout the simulation as shown in
Figure 17.

Figure 17: The equation residuals (3 mm).

A monitor plot of average velocity at the outlet was diligently tracked as shown in Figure 18.

Figure 18: The average velocity at the outlet (3 mm).

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As shown in Figure 19, a contour plot of pressure on a plane along the centerline of the blood
vessel was generated.

Figure 19: The pressure on a plane (3 mm).

A contour plot of wall shear stress on the surface of both the blood vessel and the plaque was
produced as illustrated in Figure 20.

Figure 20: The wall shear stress on the surfaces (3 mm).

In Figure 21, a vector plot of fluid velocity on a plane along the centerline of the blood vessel was
created.

Figure 21: The fluid velocity on the plane (3 mm).

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 3.2.Data Analysis:
The results of the computational fluid dynamics (CFD) simulation for three different plaque radius
scenarios: 1mm, 2mm, and 3mm, provided insights into the hemodynamic effects on blood flow
dynamics within the vessels. Key parameters, including equation residuals, average velocity,
pressure distribution, wall shear stress, and flow patterns, were examined.

3.2.1. Analysis of 1mm Plaque Radius Scenario:

The equation residuals plot showed a gradual decrease with iterations until convergence was
reached at 66 iterations. This convergence behaviour indicated the satisfactory fulfilment of the
governing equations, ensuring the reliability of the simulation results.
The monitor plot of average velocity at the outlet revealed that the average velocity stabilized at
1.99 m/s after approximately 25 iterations. This stability in velocity indicated an equilibrium state
of flow influenced by the 1mm plaque.
The pressure contour plot on a plane along the centerline of the blood vessel revealed localized
variations in pressure. Between the vessel inlet and the plaque, higher pressure was observed at
12.96 Pa. After the plaque, pressure significantly decreased to -936.1 Pa.
The wall shear stress contour plot identified regions of elevated shear stress. The highest shear
stress was observed on the plaque surface at 99.5 Pa, while lower shear stress (20-40 Pa) was
observed on the blood vessel surface.
The vector plot of fluid velocity on the plane along the centerline of the blood vessel depicted flow
direction and magnitude. Higher velocities (2.5 m/s) were observed between the plaque and the
vessel outlet.

3.2.2. Analysis of 1mm Plaque Radius Scenario:

In the case of the 2mm plaque radius scenario, the equation residuals plot demonstrated a gradual
decrease with iterations, ultimately converging at 77 iterations. This convergence behaviour
underscores the fulfilment of the governing equations, affirming the reliability of the simulation
results.
The monitoring plot of average velocity at the outlet yielded crucial insights into flow behaviour.
It revealed that average velocity stabilized at precisely 2 m/s after approximately 35 iterations.
This stabilized velocity indicates an equilibrium state of flow influenced by the 2mm plaque.
Examination of the pressure contour plot on a plane along the blood vessel's centerline unveiled
localized pressure variations. Between the vessel inlet and the plaque, higher pressures were
observed, ranging from 277.6 to 458 Pa. However, beyond the plaque, pressure significantly
dropped to -322 Pa.
Investigation of the wall shear stress contour plot identified regions of elevated shear stress. The
highest shear stress was pinpointed on the plaque surface, precisely at 132.5 Pa, while the blood
vessel surface exhibited lower shear stress values, ranging between 0.8 and 27.15 Pa.
Delving into the vector plot of fluid velocity on the plane along the blood vessel's centerline
showcased flow direction and magnitude. Specifically, higher velocities (2.858 m/s) were observed
between the plaque and the vessel outlet.

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 3.2.3. Analysis of 3mm Plaque Radius Scenario:
The equation residuals plot displayed a gradual decrease with iterations, ultimately converging at
93 iterations.
Monitoring the average velocity at the outlet provided valuable insights into flow behaviour. It
revealed that the average velocity increased to 2.6 m/s as the simulation progressed to 40
iterations, then decreased to 2.2 m/s at 60 iterations before stabilizing. This stabilized velocity
indicates an equilibrium state of flow influenced by the 3mm plaque.
Examination of the pressure contour plot on a plane along the blood vessel's centerline unveiled
localized pressure variations. Between the vessel inlet and the plaque, higher pressures were
observed, reaching 1.507 kPa. However, beyond the plaque, pressure significantly dropped to -20
kPa.
Investigation of the wall shear stress contour plot identified regions of elevated shear stress. The
highest shear stress was pinpointed on the plaque surface, measuring 574.9 Pa, while the blood
vessel surface exhibited lower shear stress values, at 0.737 Pa.
Delving into the vector plot of fluid velocity on the plane along the blood vessel's centerline
showcased flow direction and magnitude. Specifically, higher velocities (2.175 m/s) were observed
between the plaque and the vessel outlet.

3.2.4. Comparative Analysis (Hemodynamic Effects of Different Plaque Radius Scenarios):

Across all three scenarios above, the equation residuals exhibited a similar pattern of gradual
decrease with iterations until convergence was reached. This behaviour underscores the reliable
satisfaction of governing equations in each case, confirming the validity of simulations.
Notably, the stability of average velocity at the outlet differed among the scenarios. In the 1mm
scenario, the velocity stabilized at approximately 1.99 m/s, while in the 2mm scenario, it reached
2 m/s, and in the 3mm scenario, it initially increased to 2.6 m/s, then decreased to 2.2 m/s, and
ultimately stabilized.
These variations in velocity behaviour suggest that plaque size impacts the equilibrium state of
flow within the vessels. While smaller plaques appear to lead to a lower average velocity, larger
plaques can initially disrupt flow patterns, causing fluctuations before reaching equilibrium.
Across the scenarios, it was observed variations in pressure distribution. In all cases, higher
pressure was noted between the vessel inlet and the plaque, but the pressure decreased significantly
after passing the plaque. Interestingly, the 3mm scenario exhibited the highest pressure drop after
the plaque, potentially indicating greater resistance to flow. On the other hand, increasing the
radius of the plaque caused an increase in the pressure between the vessel inlet and the plaque and
a decrease in the pressure between the plaque and the vessel outlet. This observation warrants
further investigation into the clinical implications of pressure changes associated with varying
plaque sizes.
Wall shear stress patterns were similar in that they identified regions of elevated shear stress on
plaque surfaces and lower shear stress on vessel surfaces. However, the magnitude of shear stress
differed between scenarios. The 3mm scenario displayed the highest shear stress on the plaque
surface, potentially indicating a more turbulent flow regime near larger plaques. This emphasizes
the importance of understanding shear stress variations in relation to plaque size.

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Vector plots of fluid velocity on the centerline of the blood vessel revealed variations in flow
dynamics. The 1mm scenario showed lower velocity between the plaque and vessel outlet, while
the 2mm and 3mm scenarios exhibited higher velocities.
These differences highlight the complex interplay between plaque size and flow dynamics,
indicating that smaller plaques may cause flow disturbances, whereas larger plaques can lead to
higher velocities near the plaque.

3.3.Discussion:

The simulations demonstrated that all three scenarios exhibited a consistent pattern of equation
residuals gradually decreasing with iterations until convergence was achieved. This uniform
behaviour indicated the robust satisfaction of the governing equations, validating the reliability of
the CFD simulations. This foundational aspect ensured that the model accurately captured the
fluid dynamics within vessels.
One of the most notable findings of the study was the impact of plaque size on the average velocity
at the outlet of the blood vessel. Smaller plaques (1mm) led to a lower average velocity, indicating
that they created a less obstructed flow path, reducing the rate of blood flow. In contrast, larger
plaques (2mm and 3mm) initially disrupted flow patterns, causing fluctuations in velocity before
reaching a stable equilibrium.
These observations align with the clinical understanding that plaque size was a critical factor in
assessing the severity of blood vessels. The simulations highlight the need for individualized
approaches to patient management based on plaque characteristics.
The analysis of pressure distribution revealed variations in pressure gradients within the vessel.
In all scenarios, higher pressure was consistently observed between the vessel inlet and the plaque,
likely due to flow constriction caused by the plaque. However, the pressure significantly decreased
after passing the plaque. Of particular interest was the 3mm plaque scenario, which exhibited the
most pronounced pressure drop after the plaque. This finding may have significant clinical
implications, as it suggests that larger plaques could lead to increased resistance to blood flow,
potentially resulting in elevated blood pressure and heightened cardiovascular risks.
The simulations also assessed wall shear stress patterns. While all scenarios identified regions of
elevated shear stress on plaque surfaces and lower shear stress on vessel surfaces, the magnitude
of shear stress differed significantly. The 3mm plaque scenario displayed the highest shear stress
on the plaque surface, indicative of a more turbulent flow regime. Understanding these shear stress
variations was vital, as elevated shear stress on plaque surfaces may be associated with a higher
risk of plaque rupture and subsequent cardiovascular events. This finding underscores the
importance of considering plaque size when evaluating shear stress-related risks.
Vector plots of fluid velocity illustrated variations in flow dynamics. The 1mm plaque scenario
exhibited lower velocities between the plaque and vessel outlet, while the 2mm and 3mm scenarios
demonstrated higher velocities near the plaque. These differences emphasize the complex interplay
between plaque size and flow dynamics, where smaller plaques may cause flow disturbances, while
larger plaques can lead to higher velocities in their vicinity.

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 4. Conclusions:

This study ventured into the intricate world of blood vessels, utilizing computational fluid dynamics
(CFD) simulations to explore how plaque size influences hemodynamics within blood vessels. The
investigation encompassed three scenarios with plaque radii of 1mm, 2mm, and 3mm.
First and foremost, the reliability of CFD model was confirmed through consistent convergence
patterns in all scenarios. This foundational assurance underpins the accuracy and validity of the
findings. The CFD simulations were demonstrated to serve as invaluable tools in unravelling the
complexities of blood flow within vessels.
The impact of plaque size on average velocity. Smaller plaques emerged as flow restrictors,
resulting in lower average velocities. In contrast, larger plaques initially disrupted flow patterns,
causing transient fluctuations before reaching stability. These observations underscore the
dynamic nature of blood flow in the presence of plaques and emphasize the need for individualized
treatment strategies that account for plaque size.
Pressure distribution emerged as another critical variable of interest. In all scenarios, we observed
higher pressures upstream of the plaque, followed by a significant pressure drop downstream.
Notably, larger plaques exhibited more pronounced pressure decreases post-plaque, suggesting
greater resistance to flow.
The analysis of wall shear stress patterns revealed consistent findings, with elevated shear stress
on plaque surfaces and lower shear stress on vessel surfaces across scenarios. However, the
magnitude of shear stress varied with plaque size, highlighting the potential for more turbulent
flow near larger plaques.
Lastly, vector plots of fluid velocity along the centerline of the blood vessel illuminated variations
in flow dynamics. Smaller plaques induced flow disturbances, while larger plaques led to higher
velocities near the plaque. These findings emphasize the intricate interplay between plaque size
and flow dynamics, suggesting that smaller plaques may cause localized disruptions, while larger
plaques can induce more complex flow patterns.

5. References:

Anderson, J.D. (1995) Computational Fluid Dynamics: The basics with applications. 1st edn. New
York etc., NY: McGraw-Hill.

NASA (no date) Navier-stokes equations, NASA. Available at: https://www.grc.nasa.gov/www/k-

12/airplane/nseqs.html (Accessed: 02 October 2023).

Versteeg, H.K. and Malalasekera, W. (2007) An introduction to computational fluid dynamics: The
Finite Volume Method. 2nd edn. Harlow, Essex CM20 2JE: Pearson Education Limited.

White, F.M. (2016) Fluid mechanics. 8th edn. New York, NY: McGraw-Hill education.

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