Physics of Fluids ARTICLE pubs.aip.

org/aip/pof

Pulsatile flow dynamics in an artery with multiple

pathologies: A fluid–structure interaction study
Cite as: Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599
Submitted: 5 February 2025 . Accepted: 11 April 2025 .
Published Online: 17 July 2025

Priyanshu Soni,1 Abhra Bhattacharyya,1 Abdullah Y. Usmani,2 Sanjay Kumar Rai,1

and B. V. Rathish Kumar3,a)

AFFILIATIONS
1
School of Biomedical Engineering, Indian Institute of Technology BHU, Varanasi 221005, Uttar Pradesh, India
2
Department of Mechanical Engineering, Zakir Husain College of Engineering and Technology, AMU, Aligarh 202002,
Uttar Pradesh, India
3
Department of Mathematics and Statistics, Indian Institute of Technology Kanpur, Kanpur 208016, Uttar Pradesh, India

a)
Author to whom correspondence should be addressed: [email protected]

ABSTRACT
Cardiovascular diseases are a major cause of premature mortality, often due to arterial stenosis and aneurysms. This study investigates the
interplay between hemodynamics and biomechanics in arteries with coexisting stenosis and aneurysms using one-way fluid–structure interac-
tion (FSI) modeling. Three-dimensional artery models with stenosis severities of 50%, 70%, and 90% (cases 1–3) and an eccentric model (case
4) are created, each featuring a 50% downstream aneurysm to examine its interaction with upstream stenosis. The viscoelastic arterial wall,
modeled with a 2.5 mm thickness using a generalized Maxwell model, is subjected to physiological pulsatile velocity and pressure profiles to
simulate realistic blood flow conditions. FSI analysis captures key hemodynamic indicators along with biomechanical responses, including
arterial wall deformation and von Mises stress. Results reveal severe stenosis (>70%) induces intense, persistent vortical structures and pro-
motes pronounced three-dimensional flow disturbances, significantly increasing thrombus risk, aneurysm progression, and localized wall
stress, especially in 90% stenosis (case 3). Vortical dynamics become more complex with stenosis severity, as eccentric stenosis introducing
asymmetry, leading to wall-adjacent vortex migration and prolonged flow disturbances. Eccentric stenosis (case 4) redistributes shear stress,
reducing localized stress concentrations but maintaining complex flow patterns, causing the highest wall deformation of 1.9 mm and peak
von Mises stress of 8.8 kPa. Severe stenosis requires urgent medical attention due to increased rupture risk, while eccentricity moderates local-
ized stress yet sustains vascular risks. This study highlights the role of FSI in connecting flow dynamics with arterial biomechanics, aiding in
vascular risk assessment and targeted surgical interventions.
Published under an exclusive license by AIP Publishing. https://doi.org/10.1063/5.0263599

I. INTRODUCTION the coexistence of stenosis and aneurysms in small vessels like coro-
According to the World Heart Federation (2023) report, cardio- nary and renal arteries and large vessels like the aorta. A stenosed
vascular diseases (CVDs) are the leading cause of illness, disability, and artery manifesting an aneurysm downstream accelerates aneurysm
death globally.1 CVDs encompass conditions affecting blood flow and growth, increases rupture risk, and promotes vascular inflammation.
heart function with abnormal vasoconstriction and vasodilation play- This interplay generates vortices upstream of the aneurysm, heighten-
ing critical roles in their progression. Atherosclerosis, caused by plaque ing the WSS downstream, thinning the endothelial layer, and increas-
deposition from low-density lipoproteins and cholesterol on arterial ing the risk of thrombus formation and fatal bleeding. A detailed in
walls, leads to artery hardening2 and stenosis, restricting blood flow to silico investigation is essential to understand these dynamics and
vital organs.3 In large vessels (diameter > 5 mm), flow separation due enable early rupture prediction.
to adverse pressure gradients downstream of stenosis results in vortex Recent studies14–20 have highlighted the effects of stenosis and
formation.4,5 Vortices elevate the wall shear stress (WSS) on the arte- aneurysms on the cardiovascular system, demonstrating that computa-
rial wall. A heightened WSS with a positive gradient can rupture the tional in silico investigations can predict stenosis locations and aneu-
arterial lining, leading to dilation, thrombus formation, and vessel rysm rupture sites at early stages. Long et al.21 confirmed the validity
bulging, characteristics of an aneurysm.6–8 Medical studies9–13 report of such approaches, reporting a strong correlation between MRI

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-1

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

velocity measurements and numerical predictions. Hemodynamic time average wall shear stress (TAWSS), oscillatory shear index (OSI),
analysis through computational fluid dynamics (CFD) has been exten- relative residence time (RRT), and endothelial cell activation potential
sively used for simulating blood flow. However, past studies have pre- (ECAP),35–38 are evaluated to enhance understanding of disease pro-
dominantly treated arterial walls as rigid structures, overlooking the gression and its implications.
dynamic interaction between blood flow and arterial wall behavior, To address the research gaps, idealized models combining steno-
which plays a crucial role in hemodynamics. sis with a downstream aneurysm were developed to represent a range
Fluid–structure interaction (FSI) combines CFD with finite ele- of pathological conditions. These models include three symmetric
ment analysis (FEA) to account for the mutual influence between cases, case 1, case 2, and case 3, with varying stenosis severities of
blood flow and arterial walls, providing a more realistic simulation 50%–90% constriction, and an additional asymmetric case, case 4, fea-
approach.22 With advancements in computational power, FSI has been turing 70% stenosis with degree of eccentricity being 0.75, respectively.
applied to study blood flow in healthy and diseased vessels.23–26 Unlike An in silico investigation used physiologically relevant pulsatile inlet
rigid wall models, which can overestimate WSS by up to 50%, FSI velocity and outlet pressure profiles. Velocity patterns were first ana-
allows for the modeling of deformable arterial walls, offering greater lyzed, followed by vorticity snapshots and three-dimensional vortical
accuracy in simulating blood dynamics.15,27 By incorporating vessel structures obtained using the Q-criterion along longitudinal and trans-
elasticity, FSI provides valuable insights into blood flow mechanics and verse planes of the model. Subsequently, hemodynamic parameters
aids in patient-specific treatment decisions. Key factors in solving FSI were derived to understand the complex flow dynamics comprehen-
problems include arterial wall thickness and material properties, which sively. A one-way FSI analysis, incorporating a nonlinear viscoelastic
are crucial for accurate vascular simulations.28 arterial wall model, was conducted to simulate blood flow interaction
Limited studies have explored FSI analysis in cardiovascular sys- with the arterial wall, closely mimicking biological conditions. The
tems. Scotti et al.29 demonstrated that asymmetry and wall thickness study focused on total deformation and von Mises stress on the arterial
in abdominal aortic aneurysms (AAAs) significantly affect stress distri- wall to analyze structural responses. The objective was to investigate
bution, though their assumption of linear elasticity for arterial walls structural and flow alterations across varying stenosis levels, providing
limits clinical applicability. Philip et al.30 used FSI simulations to study a realistic and detailed understanding of arterial biomechanics.
AAA growth with six shape indexes but oversimplified the hyperelastic This study establishes a correlation between hemodynamics and
nature of aneurysms by assuming linear elasticity, potentially overlook- arterial wall biomechanics, highlighting how stenosis severity and
ing rupture and thrombus risks. Lone et al.31 investigated supra geometry influence disease progression. The findings offer valuable
valvular aortic stenosis using FSI, developing a model to predict trans- insights into vascular complications such as thrombus formation and
stenotic pressure drops and highlighting the effects of aortic wall aneurysmal rupture by emphasizing the interconnected relationship
elasticity and stenosis severity. However, they did not consider the pul- between hemodynamics and biomechanics in arteries with multiple
satile nature of blood flow, which is essential for exploring hemody- pathologies. The one-way FSI approach provides a comprehensive
namics. Nandakumar et al.32 studied blood flow in a stenosed 2D understanding of how fluid forces affect wall stress and deformation,
channel, observing higher WSS with a dilatant blood model compared which is crucial for assessing disease progression, guiding therapeutic
to Navier–Stokes equations. Still, their rigid-walled and steady-flow interventions, and optimizing stent designs. These insights enhance
assumptions reduced physiological relevance. Pincombe and diagnostic strategies and inform the development of more effective
Mazumdar33 examined the impact of blood vessel stenosis and dila- treatments.
tions on reactance impedance using the Bingham model, while
Abdelwahab et al.34 investigated electro-osmotic forces in micropolar II. METHODOLOGY
blood flow through stenotic and aneurysmal carotid arteries. Accurate FSI simulations require patient-specific geometries, realis-
The above studies reveal that assuming linear elasticity for arterial tic boundary conditions, and arterial wall material properties. However,
walls in FSI simulations does not fully capture the physical behavior of idealizations and assumptions are necessary to simplify the complexity
arteries, addressing significant gaps in prior research. A stenosed artery of modeling cellular-level activities mathematically. The in silico investi-
manifesting an aneurysm downstream introduces additional complexi- gation of stenosis with a downstream aneurysm using FSI employs a
ties, necessitating accurate arterial elasticity and transient blood flow detailed computational approach to understand the fluid–solid interac-
modeling for a deeper understanding of hemodynamics. Incorporating tions within the combined diseased regions.14,17,31,39,40
stenosis and aneurysm in idealized models is a baseline study for devel-
oping patient-specific fluid flow models that accurately represent these A. Model description
standard vascular features. This study investigates the hemodynamic As stenosis contributes to the development of fusiform aneur-
and structural interactions in arteries with multiple pathologies, focus- ysms,13 this study developed four three-dimensional idealized models
ing on the combined effects of stenosis severity and arterial wall visco- manifesting stenosis and an aneurysm placed downstream to analyze
elasticity. The study addresses key challenges in cardiovascular hemodynamics. These models represent varying degrees of stenosis
modeling, including (a) the lack of comprehensive FSI analyses for (DOS): 50%, 70%, and 90% (cases 1–3), respectively, as shown in
coexisting pathologies, such as stenosis and downstream aneurysms, Fig. 1(a). The degree of eccentricity (e) in a stenosed vessel quantifies
that are often investigated in isolation and (b) the predominant reli- how asymmetrically the stenosis is distributed within the lumen. It is
ance on linear elastic models for arterial walls, overlooking their realis- often defined based on the minimum and
tic non-linear behavior. Following the study, critical hemodynamic
maximumdiameters of the
parameters such as high oscillatory low magnitude shear (HOLMES) residual lumen at the stenosed section e ¼ 1 – Dmin
Dmax .41 In the eccen-
and wall shear stress gradient (WSSG), alongside standard metrics like tric model, the stenosis axis was offset by 0.05 D, where D is the inlet

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-2

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 1. CAD modeling of idealized mod-

els: (a) symmetric cases showing ideal-
ized stenosis and aneurysm geometries,
represented by curvature functions F1, F2,
F3, and F4, demonstrating variations in
stenosis and aneurysm dimensions,
respectively. The parameters include the
maximum projection of stenosis h and the
length of the stenotic and aneurysmal
regions. (b) Asymmetric case highlighting
the effect of eccentricity F5, with the new
projection length h1 incorporated to model
asymmetry due to eccentricity. (c) The
three-dimensional flow domain illustrates
the complete arterial model, with S-1
marking the medial plane for hemody-
namic and biomechanical analysis.

diameter of the vessel, as shown in Table I, to reflect the asymmetrical equations, accurately defined from computed tomography (CT) and
development of stenosis over time. This was applied to the 70% steno- MRI measurements,42,43 with details provided in this section.
sis model, case 4, with an eccentricity e of 0.75 to evaluate the impact The spline function for stenosis (Fs), as in Eq. (1), is defined based
of asymmetry on flow dynamics. A 50% aneurysm was included in all on the undeformed section radius (r), the maximum projection of ste-
models to account for distensibility. The total vessel length was nosis from the centerline (h), and the length of the stenotic region (ls).
366.6 mm, with inlet and outlet section lengths of 100 mm each. Similarly, the spline function for aneurysms (Fa) depends on the artery
Computer aided design (CAD) models were created using spline diameter (D), the aneurysm maximum diameter (Dmax), and the
length of the aneurysmal region (la). Detailed values used in this study
TABLE I. Details of measurement of geometrical models (all dimensions in mm). are provided in Table I. These models aim to replicate the hemody-
namic and biomechanical conditions associated with cardiovascular
Stenosis pathologies such as atherosclerosis and arterial remodeling,44–46
 
px
Case 1 (50% constriction) D ¼ 20 h¼5 ls ¼ 40 Fs ¼ r ðx1 Þ ¼ r – h  sin : (1)
ls
Case 2 (70% constriction) D ¼ 20 h¼7 ls ¼ 40
Case 3 (90% constriction) D ¼ 20 h¼9 ls ¼ 40 In Eq. (1), r(x1) is the radius of stenosis, r is the radius of the
Case 4 (70% constriction) with a D ¼ 20 h1 ¼ 8 ls ¼ 40 artery, h is the maximum projection of the stenosis into the lumen,
degree of eccentricity, e ¼ 0.75 and ls is the length of the stenosis region.
Aneurysm The eccentricity in stenosis shape significantly affects arterial
Cases 1–4 (50% dilation) D ¼ 20 Dmax ¼ 30 lA ¼ 66.6 hemodynamics, influencing flow direction, pressure drop, and recircu-
lation zones. Timofeeva et al.19 highlighted the importance of (e) using

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-3

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

numerical simulations but assumed steady flow, neglecting the pulsa- The complex eigenvalues of the velocity gradient tensor (rv f) are par-
tile nature of blood. In this study, a degree of eccentricity being 0.75 ticularly useful for studying vortical structures, especially in regions
with 70% stenosis [Fig. 1(b)] is analyzed to correlate arterial wall where streamlines exhibit circular or spiral patterns.55 The tensor
responses with eccentricity. The aneurysm curvature (Fa) is based on (rv f) can be decomposed into two components: a symmetric part,
the diameter-to-high ratio (DHR), defined as Dmax/lA, with a severity e(v f), representing the strain rate tensor, and an asymmetric part, Xv,
level of 0.45 for 50% aneurysms, adapted from Philip et al.30 The cur- representing the vorticity tensor, as expressed as
vature equation [Eq. (3)] is adapted from an earlier study,46
    rvf ¼ eðvf Þ þ Xv : (6)
ðDmax  DÞ 2px p D
Fa ¼ r ðx2 Þ ¼ 1 þ sin  þ : (2) The characteristic equation of eigenvalues, k, of rvf is given by
4 la 2 2
In Eq. (2), r(x2) represents the lumen radius as a function of axial k3 þ Pk2 þ Qk þ R ¼ 0: (7)
length. The study suggests that indices derived from patient-specific For an incompressible flow, P ¼ r:v, the first invariant is therefore
CT or MR images can be translated into size, shape, or curvature-
zero. The second and third invariants, Q and R, are defined as
based metrics.46 The overall three-dimensional flow domain is illus-


trated in Fig. 1(c). 1
Q¼ kXv k2  keðvf Þk2 ; (8)
2
  
B. Mathematical formulation R ¼  det rvf : (9)
This section presents the governing equations for the fluid and
The Q-criterion, defined in Eq. (9) and derived from the characteristic
solid domains, including their coupling through FSI. It also details the
equation in Eq. (8), is analyzed in this study to examine the formation
boundary conditions, arterial wall modeling, and hemodynamic indi-
and dynamics of vortical structures. Its correlation with wall shear
cators to understand the disease progression. Furthermore, the section
stress (WSS) and various hemodynamic parameters is also
discusses the biomechanical responses of the artery and provides a
comprehensive description of the simulation setup. investigated.

b. Solid domain. The governing equation for the solid domain is

1. Governing equations
the balance equation, adapted from Ref. 54, as described as
This section outlines the governing equations for the fluid and  s 
solid domains and explains the FSI coupling scheme. @v
qs þ ðr  vs Þvs  f  r  rs ¼ 0 Xst : (10)
@t
a. Fluid domain. The fluid is modeled as a Newtonian, incom- In Eq. (10) qs is the density of the solid, f represents the external body
pressible flow governed by the Navier–Stokes equations, as defined as force acting on the structure, and rs is the Cauchy stress tensor, where
  subscript s denotes solid.54 Displacement u describes the configuration of
@v f
qf þ v  rv  r  rf ¼ 0; r  v ¼ 0 Xt : (3) the solid with velocity field, vs ¼ @u
s
@t . In the Lagrangian form, the above
@t
Eq. (11) with respect to some fixed reference state can be written as
In Eq. (4), the fluid density (qf) is considered constant, and v repre-  2 s 
sents the fluid velocity. External forces, such as body forces due to @ u   
qs  f  r  Ss F T Þ1 ¼ 0; Xs : (11)
gravity or human motion, are assumed to be negligible. Although @t 2
blood exhibits non-Newtonian behavior, it is modeled as a Newtonian
In Eq. (12) is the equation of elastodynamics, where Ss is the second
fluid in this study due to the deformation dynamics of corpuscles in
large vessels (radius > 5.0 mm), where large velocities and shear rates Piola–Kirchoff tensor, which is defined as Ss ¼ F T RS ¼ JF 1 rs F T ,
dominate.47–49 Moreover, in such regions, the shear rates typically Rs is the first Piola–Kirchoff tensor defined as Rs ¼ Jrs F T , where J
exceed 100 s1, where non-Newtonian effects become negligible. denotes the determinant of the deformation gradient tensor, and F is
Furthermore, this approximation simplifies simulations without sub- defined as F ¼ I þ rus . Here, I is the identity tensor.
stantially compromising accuracy in the bulk flow characteristics.49–53
Additionally, the kinematic viscosity remains nearly constant in vessels c. Fluid–solid interaction. The boundary conditions on the fluid–
with radii exceeding 5 mm, justifying the neglect of non-Newtonian solid interface are assumed to be
effects54
rf n ¼ rs n; v f ¼ vs ; on C0t : (12)
r ¼ q I þ 2leðvf Þ:
f f
(4)
In Eq. (12), n is the standard unit vector to interface. C0t .
This implies
The constitutive relation of the stress tensor is given in Eq. (4); here, l that the no-slip condition for the flow and the force on the interface
is the dynamic viscosity of the fluid, qf represents the Lagrange multi- are in balance.54
plier associated with the incompressibility constraint, and eðvf Þ is the Furthermore, the detailed methodology of FSI coupling is illus-
strain rate tensor, as revealed by trated in Fig. 2, which outlines the simulation process using a fully cou-

 pled segregated algorithm. The process begins with the fluid solver
1 T calculating velocity and pressure. The interaction between blood flow
eðv f Þ ¼ rvf þ ðrvf Þ : (5)
2 and the arterial wall is then passed to the structural solver, where the

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-4

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 2. Flowchart of the FSI coupling pro-

cess using a segregated algorithm. The
fluid solver calculates velocity and pres-
sure fields, transferring wall traction to the
structural solver to compute displacement.
The mesh is updated iteratively until the
relative displacement error falls below a
predefined tolerance (105), ensuring
convergence and stability.

momentum equation is solved to determine wall displacement. The average Reynolds number is 267, the peak Reynolds number is
The updated displacement is used to modify the computational mesh. 3011, and the Womersley number of the flow is 15.25 with a pulsatility
The iteration terminates if the relative displacement error is less than a index of 7.57. A non-dimensional pressure profile (p/P) is employed at
predefined tolerance (105). Otherwise, the algorithm updates the the outlet, where p is the instantaneous pressure, and P is the peak
mesh and repeats the loop until convergence, ensuring a stable and pressure, corresponding to the inlet velocity profile. The inlet and out-
accurate solution for the coupled system. It may  that C in the
 be noted let profiles are illustrated in Fig. 3. In this study, a velocity-inlet and
given below flow chart is the same as C0t i.e., C ¼ C0t . pressure-outlet boundary condition was employed.

2. Boundary conditions
3. Viscoelastic artery wall modeling
In this study, transient laminar Newtonian flow is modeled to
investigate blood flow in pathological arterial conditions. Blood The viscoelastic nature of artery walls, arising from their complex
is treated as a Newtonian fluid, as the non-Newtonian effects are sig- structure of elastic fibers, collagen fibers, smooth muscle cells, and
nificant only in small-diameter arteries (d < 5 mm). The blood proper- ground substance, enables them to adapt dynamically to changes in
ties are defined with a viscosity of 0.003 45 Pa s and a density of blood pressure and flow. This dual elastic and viscous behavior ensures
1060 kg/m3.56 A non-dimensional velocity profile (v/V) is applied at efficient circulation and protection against mechanical damage.58–60 In
the inlet, where v is the instantaneous velocity, V is the peak velocity, t silico modeling relies on spring and dashpot elements to capture these
is the instantaneous time, and T is the time of one cardiac cycle. properties, which are essential for mimicking physiological functions
This profile, adapted from Usmani and Muralidhar,57 was and ensuring durability under dynamic blood flow. The generalized
decomposed into eight harmonics for the inflow boundary condition. Maxwell model, represented by a spring and dashpot in series, plays a

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-5

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 3. Time variation of (a) non-dimensional velocity and (b) non-dimensional pressure. The velocity profile (red) exhibits an initial peak followed by oscillations, while the pres-
sure profile (black) shows fluctuations over time, indicating the dynamic nature of the flow.

key role in fluid–structure interaction modeling, with its constitutive The generalized Maxwell model was chosen for its close resem-
equation defined as blance to the natural viscoelastic properties of arterial tissue and its
g superior ability to capture time-dependent stress and deformation
r þ r_ ¼ g_e : (13) behavior.61
E
In Eq. (13), r is the Cauchy stress tensor, g is the damping coefficient, 4. Hemodynamics indicators
E is the elastic modulus, and e_ is the strain rate tensor. The viscoelastic
behavior of soft tissues is modeled using the generalized Maxwell Past studies have employed hemodynamic indicators to analyze
approach,61 where the relaxation modulus is expressed through the physiological conditions such as atherosclerosis, mycotic aneurysm
Prony series, as defined as infections, and hypoxia, with most focusing on wall interactions. These
" # critical parameters, strongly linked to the initiation, progression, and
XN
E ¼ E1 1 þ ba eðsaÞ : pathogenesis of stenosis and aneurysms, are reviewed in this section.
1
(14)
a¼1 Key indicators,35 including TAWSS, OSI, RRT, ECAP, WSSG, and
HOLMES, have been evaluated.
In Eq. (15), N is the number of Maxwell elements, E1 is the long-term Among them, mean-WSS, defined as the time-averaged magni-
elastic modulus, Ea is the elastic coefficient, ba is the viscoelastic tude of the WSS vector over a cardiac cycle, is pivotal in identifying
parameter, and sa is the relaxation time. ba and E1 are determined zones prone to atherosclerosis development. While multiple patholo-
using Eqs. (15) and (16), respectively. The values of ba and sa are pro- gies involve various biological factors and spatiotemporal scales, these
vided in Table II, are often observed at bifurcations, curvatures, and constrictions within
Ea the human vasculature. These hemodynamic indicators are evaluated
ba ¼ ; (15) as follows: TAWSS62 is an index defined by
E1
ð
XN 1 T !
E1 ¼1 Ea : (16) TAWSS ¼ sw dt: (17)
T 0
a¼1

TABLE II. Artery wall material models.

Viscoelastic (Maxwell model) based on the Prony shear relaxation

Density (kg/m3) Young modulus (MPa) Poisson ratio Relative shear modulus (b) Relaxation time (s) References

2000 2.7 0.45 b1 ¼ 0.353 s1 ¼ 0.001 Salman and Yazicioglu61

b2 ¼ 0.286 s2 ¼ 0.01
b3 ¼ 0.298 s3 ¼ 0.10
b4 ¼ 0.285 s4 ¼ 1.00
b5 ¼ 0.348 s5 ¼ 10.0

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-6

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

TAWSS (1–7 Pa) supports vascular homeostasis, with low

(<1 Pa) linked to atherosclerosis and high (>7 Pa) to endothelial dam-
age and aneurysms. OSI, ranging from 0 (unidirectional WSS) to 0.5
(oscillating WSS), quantifies WSS deviation, as defined in Eq. (18).
0 1
ðT
B !
sw dt C
B C
B
OSI ¼ 0:5B1  ð T
0 C:
C (18)
@ ! A
sw dt
0
63
WSSG influences vascular pathology, with high values promot-
ing atherosclerosis and low or oscillatory values linked to aneurysms,
and is defined as
0 ðT 1
ð !
sw dt C
1 T BB C
WSSG ¼ B~n  ð0 C dt: (19)
T 0 B T C
@ s! dt A w
0

RRT, proposed by Himburg et al.,64 quantifies blood particle stag-

nation near the arterial wall. High RRT, linked to low or oscillatory
WSS, promotes endothelial dysfunction, inflammation, and plaque
formation, aiding in diagnosing vascular diseases and optimizing inter-
ventions. It is defined as
 
1
RRT ¼ : (20)
ð1  2OSI Þ  TAWSS FIG. 4. Computational mesh for (a) fluid and (b) solid domains.
HOLMES and ECAP are critical indicators. HOLMES, intro-
duced by Alimohammadi et al.,65 identifies regions with low TAWSS (2.40 GHz) was used for numerical simulations, featuring 64 GB of
and high OSI, indicating disturbed hemodynamics. It aids in identify- RAM and 40 cores.
ing high-risk arterial zones and designing interventions like stents or The GIT and time independence test (TIT) were conducted to
grafts to restore standard shear stress patterns. HOLMES is defined as ensure the accuracy and efficiency of the numerical simulations, as
HOLMES ¼ TAWSSð0:5  OSIÞ: (21) shown in Fig. 5. The GIT, performed on case 1, analyzed three mesh
sizes: coarse M1 (2 mm), medium M2 (1 mm), and fine M3 (0.66 mm),
On the other hand, ECAP, defined in Eq. (22), quantifies the risk calculated based on the inlet diameter (D) as M1 ¼ D/10, M2 ¼ D/20,
of endothelial activation under hemodynamic stress. High ECAP val- and M3 ¼ D/30. Mesh statistics are detailed in Table III. Velocity pro-
ues, linked to low or oscillatory WSS, predict inflammation-prone files at the longitudinal plane S-1 were plotted against flow time for
regions and plaque formation these mesh sizes. As shown in Fig. 5(b), the velocity changes between
  M2 and M3 were negligible, making M2 the optimal choice for achiev-
OSI
ECAP ¼ : (22) ing numerical convergence while reducing computational costs. The
TAWSS selected mesh size (M2) and boundary conditions, consistent across all
cases, confirm that the GIT results are applicable to all other cases.
The TIT determined the optimal time step size (T/2) using the
5. Numerical simulations
following equation:
uDt
Meshing was performed separately for the fluid and solid CFL ¼ : (23)
domains, as illustrated in Fig. 4. A grid independence test (GIT), as dis- Dx
cussed in this section (refer to Fig. 5), was conducted to ensure mesh Here, u is the flow velocity, Dt is the time step, and Dx is the char-
size. Tetrahedral mesh elements were utilized for both the fluid and acteristic mesh cell size. TIT was performed with three time step sizes
solid domains. A face sizing of 0.75 mm was applied to accurately cap- (T, T/2, and T/4), and velocity profiles at the longitudinal plane S-1
ture the geometric changes at the stenosis and aneurysm regions, as were plotted against flow time for the time step sizes, as shown in
shown in Fig. 4(a). For the solid domain, an artery wall thickness of Fig. 5(b), the velocity changes between T/2 and T/4 were negligible,
2.5 mm was selected, as depicted in Fig. 4(b). Additionally, to accu- making T/2 the optimal choice for achieving the balance of accuracy
rately capture flow conditions at the fluid domain boundaries, six infla- and computational efficiency.
tion layers were incorporated into the fluid domain mesh. A Flow stabilization was achieved using a time step size of 0.0065
workstation equipped with two IntelV XeonV Silver 4210R processors
R R
with 923 steps (equivalent to six cardiac cycles) and 45 iterations per

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-7

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 5. (a) Computational three-dimensional domain with S-1 longitudinal section, (b) grid independence test (GIT) comparing velocity magnitudes at section S1 for M1, M2, and
M3, showing negligible differences between M2 and M3, making M2 optimal; and (c) time independence test (TIT) at section S1 comparing time steps T (0.013 s), T/2 (0.0065 s),
and T/4 (0.003 25 s), with T/2 selected for accuracy and efficiency.

step. Numerical schemes included the SIMPLE (semi-implicit method A steady flow with a peak Reynolds number (Re ¼ 1350) through
for pressure-linked equations) scheme for fluid analysis and the a symmetric tubular bulge was simulated and validated against experi-
Galerkin-based finite element method (FEM) for structural analysis. A mental results from Patel et al.20 Fluid properties, including a density
second-order upwind scheme minimized numerical diffusion, and a of 1156 kg/m3 and a kinematic viscosity of 7.39  106 m2/s, were
second-order implicit method improved temporal accuracy, while matched to those used in their experiments. A uniform velocity profile
Rhie–Chow interpolation stabilized pressure–velocity coupling. was applied at the inlet, while a constant pressure (p ¼ 0) was imposed
III. VALIDATION at the outlet using a zero-gradient condition. The three-dimensional
flow field was simulated using incompressible Navier–Stokes equations
The numerical solver was validated against experimental work by in a finite-volume framework. Velocity profiles were analyzed at three
Patel et al.20 on abdominal aortic aneurysms. An idealized computa- sections (S-1 to S-3) within the aneurysm, located at dimensionless dis-
tional model was developed based on the geometry used in their parti- tances y/L ¼ 0.2, 0.5, and 0.8, as shown in Fig. 6(b). The comparison of
cle image velocimetry (PIV) experiments.20,66 The model features an axial velocity against radial distance shows strong agreement between
inlet diameter (d1) and outlet diameter (do) of 1.6 cm each. The aneu- experimental and computational results [Fig. 5(c)].
rysm, characterized as fusiform and axisymmetric, has a maximum
diameter (Dmax) and length (L), with a dilation ratio (Dmax/d1) of 2.5 IV. RESULTS AND DISCUSSION
and an elongation ratio (L/d1) of 4. Inlet and outlet sections are 9 cm This section discusses the velocity magnitude, vorticity, and
long, allowing the flow to fully develop before reaching the aneurysm. Q-criterion, respectively. Additionally, critical hemodynamic indices
The computational domain was discretized with tetrahedral mesh ele- (e.g., TAWSS, OSI, RRT, ECAP) and biomechanical responses, such as
ments, comprising 444 652 nodes and 1 873 123 elements, as illustrated total deformation and von Mises stress on the arterial wall, are ana-
in Fig. 6(a). lyzed and correlated with pathological conditions to provide a compre-
hensive understanding of blood flow dynamics in an artery
TABLE III. Details of mesh statics for the grid-independent study. incorporating multiple pathologies.

Fluid Solid Total A. Flow dynamics in artery manifesting multiple

Mesh Size elements elements elements pathologies
Coarse (M1) 2 mm 225 084 99 627 324 711 Geometrical parameters are critical in blood flow dynamics, espe-
Medium (M2) 1 mm 1 842 033 729 566 2 571 599 cially for classifying cardiovascular conditions. This section examines
Fine (M3) 0.66 mm 7 511 516 2 453 254 9 964 770 hemodynamic parameters such as velocity magnitude, vorticity, and
Q-criterion across one longitudinal plane (S-1) and seven transverse

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-8

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 6. (a) Computational domain of the abdominal aortic aneurysm (AAA), (b) sections (S-1 to S-3) at which non-dimensional axial velocity profiles are compared, and (c) com-
parison of numerical and experimental axial velocity profiles are selected sections. The solver was validated by comparing velocity profiles at sections S1, S2, and S3 against
experimental results from Patel et al.,20 demonstrating strong agreement and confirming the reliability of the numerical approach.

planes (S-2 to S-8). The timing of the cardiac cycle is crucial in hemo- S-7) causes flow separation and the formation of recirculation zones
dynamic analysis, as the different phases of the cycle result in signifi- characterized by reduced velocities. At T-3, during peak systole, the
cant variations in the flow field. To capture these variations, we velocity magnitude reaches its maximum at S-3, where a strong jet
analyzed the hemodynamic parameters at distinct cardiac phases, forms and propagates downstream, crossing S-4. This jet is driven by
labeled as T-1 to T-7, corresponding to the fifth cardiac cycle of the the pressure difference across the stenosis and is disrupted by the
solution time. These phases represent the following stages of the car- abrupt expansion of the artery, generating recirculation zones. In the
diac cycle: early systole (T-1), mid-systole (T-2), peak systole (T-3), aneurysmal region (S-6 to S-8), the jet dissipates, velocities decrease,
deceleration phase (T-4), early diastole (T-5), peak diastole (T-6), and and the flow becomes more distributed due to the larger cross-
late diastole (T-7). sectional area. At T-4, as cardiac output decreases, the jet weakens, and
a noticeable deflection in the flow path is observed at S-5, indicating
1. Velocity distribution the onset of three-dimensional flow patterns. Recirculation zones near
the aneurysm remain prominent as flow decelerates further. During
Velocity magnitude variation across the seven cardiac phases T-5, early diastole brings reverse flow in the post-stenotic region, par-
(T-1 to T-7) on the longitudinal plane (S-1) and transverse planes (S-2 ticularly in S-1, driven by the negative pressure gradient. Although
to S-8) for all cases, as shown in Fig. 7 (Multimedia view). Figure 7(a) velocities are low, the disturbed flow is evident in cross-sectional planes
illustrates the blood flow behavior in an artery with 50% stenosis fol- (S-4 and S-5), where recirculation regions persist. At T-6, reverse flow
lowed by a 50% aneurysm, i.e., case 1, over seven cardiac phases (T-1 strengthens between S-4 and S-6 as the pressure gradient continues to
to T-7). At T-1, during early systole, the velocity is nearly uniform, decrease. Velocities drop further in the stenotic region, and flow dis-
with a slight pressure gradient forming between the pre-stenotic (S-2) turbances dominate the post-stenotic and aneurysmal areas. By T-7,
and post-stenotic (S-4) regions. Low cardiac output results in reduced reverse flow peaks, with prominent disturbances and low velocities in
velocities downstream (S-4 to S-8). At T-2, as cardiac output increases, the post-stenotic region (S-4 to S-6). The flow stabilizes slightly down-
flow accelerates through the stenotic region (S-3), creating a high- stream in the aneurysmal region (S-7 to S-8), where the velocities are
velocity jet downstream at S-4. The sharp pressure gradient drives this more evenly distributed. Figure 7(b) illustrates the velocity variations
acceleration, while the sudden expansion at the aneurysm onset (S-6 to across sections S-1 to S-8 for a 70% stenosis, i.e., followed by an

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-9

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

S-8 as it adapts to the aneurysmal geometry. At T-2, velocity increases

significantly due to the pressure gradient across the stenosis, forming a
high-speed jet at S-3 that extends to S-4. Small recirculation zones
appear downstream of S-3 while the jet dissipates toward S-5. In the
aneurysmal region, velocity reduces sharply, with S-7 exhibiting the
lowest values due to the sudden expansion. At T-3, during peak systole,
the jet extends further downstream to S-6, with strong recirculation
zones forming at S-5 and S-6 due to abrupt expansion. In the aneurys-
mal region, the jet diminishes, and velocity drops significantly at S-7
and S-8. At T-4, as cardiac output decreases, the jet weakens but
extends into the aneurysmal region, where a deflection occurs due to
asymmetrical geometry and interactions with recirculation zones. At
T-5, the jet influence persists, with the core-dominated flow at S-5 and
S-6, while three-dimensional flow patterns emerge at S-7 and S-8.
These disturbances highlight the complexity of the flow as it propa-
gates through the aneurysm. At T-6, reverse flow begins downstream
of the stenosis, with a reverse jet originating at S-3. This interacts with
recirculation zones at S-5 and S-6, leading to oscillatory patterns near
the aneurysm wall at S-7. Flow becomes disorganized further down-
stream at S-8. At T-7, reverse flow dominates, reducing velocity
gradients and causing flow separation at S-2 and recirculation zones at
S-4 to S-6. Within the aneurysmal region, the reverse flow interacts
with the walls at S-7 before stabilizing downstream at S-8.
Figure 7(c) illustrates velocity variations across sections S-1 to S-8
for a 90% stenosis followed by an aneurysm (case 3) during the cardiac
cycle. At T-1, a weak jet forms upstream of the stenosis, with velocities
slightly more prominent than in cases 1 and 2, driven by the develop-
ing pressure gradient. Velocity peaks at the stenotic throat (S-3) due to
the extreme narrowing, creating a short high-speed jet. The flow
remains relatively uniform downstream (S-4 to S-8), with no signifi-
cant recirculation zones observed. At T-2, cardiac output increases sig-
nificantly, producing a fully developed high-speed jet that extends
from S-3 to S-5. This jet causes recirculation zones to form in the post-
stenotic region, particularly at S-4, and grow toward S-5 as momentum
decreases. The jet dissipates in the aneurysmal region (S-6 to S-8), and
velocity decreases sharply due to the geometric expansion.
Recirculation zones dominate at S-7, where low velocities increase the
potential for thrombus formation. During T-3, at peak systole,
the velocity jet reaches its maximum intensity at S-3 and extends into
the aneurysmal region (S-6). Flow three-dimensionality emerges in the
cross-planes of S-6 to S-8, with complex velocity patterns dominating.
Recirculation zones in the post-stenotic regions (S-4 to S-5) expand,
while in the aneurysm, disturbances increase at S-7 and reduce by S-8
as velocity stabilizes slightly. At T-4, the jet weakens as cardiac output
decreases but extends into the aneurysm. Three-dimensional flow per-
FIG. 7. Velocity magnitude (m/s) variation across the seven cardiac phases (T-1 to sists in S-6 to S-8, with disturbances intensifying at S-7 due to interac-
T-7) on the longitudinal plane (S-1) and transverse planes (S-2 to S-8) for all cases: tions with recirculation zones. At T-5, as velocity continues to decline,
(a) case 1 (50% stenosis), (b) case 2 (70% stenosis), (c) case 3 (90% stenosis), and the jet diminishes at S-3 but still influences flow up to the aneurysmal
(d) case 4 (degree of eccentricity 0.75% and 70% stenosis). The flow patterns illus- region. In the post-stenotic segments (S-4 to S-5), recirculation zones
trate differences in jet formation, recirculation zones, and post-stenotic flow behavior
persist, while in the aneurysm (S-6 to S-8), three-dimensionality
[Case 1–4: min and max Vel range: 0.01 to 0.8 m/s]. Multimedia available online.
remains visible but begins to decrease, with cross-plane velocities
reducing at S-7 and S-8. At T-6, reverse flow develops, originating at
aneurysm, i.e., case 2 over seven cardiac phases (T-1 to T-7). At T-1, a S-1 and propagating downstream. A central high-velocity jet appears
weak jet originates upstream of the stenosis due to the dominance of at S-3, while reverse flow intensifies in the post-stenotic region (S-4 to
the reverse flow portion from the previous cardiac cycle. Velocity S-5). In the aneurysmal region, disturbances reduce compared to ear-
increases gradually at S-3, but minimal flow separation is observed lier phases, and flow begins to stabilize. By T-7, reverse flow dominates,
downstream due to low incoming energy. Flow stabilizes from S-5 to with low velocities and minimal recirculation zones across S-4 to S-8.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-10

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

In the aneurysm (S-6 to S-8), three-dimensional effects subside, and S-6 to S-8. In case 4 (degree of eccentricity 0.75), the jet influence is
flow becomes uniform downstream. Thus, case 3 reveals the pro- similar to case 2, but eccentricity shifts flow asymmetrically, introduc-
nounced impact of a 90% stenosis, characterized by stronger velocity ing earlier three-dimensionality at S-4 and enhancing disturbances in
jets, extensive recirculation zones, and persistent three-dimensional the post-stenotic region. Thus, stenosis severity increases jet length
flow in the aneurysmal region. To reinforce the Newtonian assumption and complexity while eccentricity shifts and amplifies flow
for case 3, additional simulations using a non-Newtonian Carreau disturbances.
model were performed and included in the multimedia view. Some dif- Velocity magnitude contours (Fig. 7) provide spatial insights into
ferences were observed during diastole, with enhanced velocity magni- flow behavior, but they do not capture the temporal evolution of veloc-
tudes and three-dimensional flow in the post-stenotic region. ity at specific locations. To analyze how velocity changes over time at
However, during systole, the overall flow patterns remained similar, different sections of the artery, velocity traces are drawn at S-1 to S-
with only a slight increase in jet penetration length in the non- 8 for all cases. These traces across different sections (S-1 to S-8) are
Newtonian model. influenced by the pulsatile inlet velocity profile, with variations arising
Figure 7(d) illustrates velocity variations across sections S-1 to due to jet formation, flow separation, pressure gradients, and flow dis-
S-8 for stenosis with 0.75 degree of eccentricity, i.e., case 4 followed by turbances in the post-stenotic and aneurysmal regions. At S-1
an aneurysm over seven cardiac phases (T-1 to T-7). At T-1, recircula- [Fig. 8(a)], the velocity profile closely follows the inlet velocity for all
tion zones are observed near the walls in the pre-stenotic region (S-2), cases, with case 3 exhibiting the highest velocity magnitude due to the
while the flow is uniform with low velocity elsewhere. Velocity significant acceleration caused by severe stenosis. Case 4 has slightly
increases at S-3 due to narrowing, but recirculation persists. lower values than case 3 but is comparable to case 2, as eccentricity
Downstream (S-4 to S-6), velocity is low and uniform, and in the aneu- affects the velocity distribution rather than peak values. At S-2
rysmal region (S-7 to S-8), flow disturbances appear with further veloc- [Fig. 8(b)], a slight phase shift appears, and the profile no longer per-
ity reduction. At T-2, a high-speed jet forms at S-3 as flow accelerates, fectly matches the inlet, indicating the influence of a developing pres-
peaking in velocity at the stenotic throat. The eccentricity shifts the jet sure gradient. Case 3 continues to show the strongest acceleration,
asymmetrically toward the arterial wall, with flow three- while case 4 exhibits a shift in velocity distribution due to the asymme-
dimensionality becoming visible at S-4 only. Recirculation zones try of the stenosis. Moving to S-3 [Fig. 8(c)], where the stenotic throat
develop downstream at S-4, diminish by S-5, and vanish by S-6 as the is located, the profile closely matches the inlet, but the velocity magni-
jet dissipates. In the aneurysmal region, velocity decreases sharply at tudes are significantly higher due to the narrowing-induced accelera-
S-7 due to expansion, slightly increasing at S-8 as flow redistributes. At tion. Case 3 reaches the highest velocity peak, forming a strong and
T-3, during peak systole, the jet reaches maximum intensity at S-3 and well-defined high-speed jet, while case 4 displays an asymmetric peak,
extends to S-6. Three-dimensionality at S-4 disrupts jet uniformity, indicating a non-uniform velocity distribution. In S-4 [Fig. 8(d)],
with recirculation zones intensifying downstream at S-5. In the aneu- where the jet exits into the post-stenotic region, the systolic phase still
rysm, disturbances dominate at S-7 but reduce at S-8 as flow velocities follows the inlet, but the diastolic portion is missing due to jet dissipa-
decrease. At T-4, the jet weakens at S-3, while recirculation zones tion and changes in flow structure. Case 3 maintains a strong jet influ-
expand in the post-stenotic region (S-4 to S-5). In the aneurysmal ence, with flow extending downstream, whereas case 4 exhibits earlier
region, high velocity is concentrated at the center of S-7, with weaker flow disturbances, contributing to three-dimensional effects at this
circulation zones near the walls, while flow stabilizes at S-8. Along T-5, location. At S-5 [Fig. 8(e)], velocity magnitudes further reduce, and
the jet dissipates completely at S-3, and flow separation intensifies at S- recirculation zones develop, leading to disturbances in the velocity pro-
4, with disturbances increasing in the post-stenotic region (S-5 to S-6). file. Case 3 continues to exhibit a strong influence of the jet, while case
In the aneurysmal region, velocity decreases further at S-7 with distur- 4 shows moderate but asymmetric variations, indicating a non-
bances persisting. At T-6, reverse flow develops, and a small high- uniform transition of flow patterns. At S-6 [Fig. 8(f)], as the flow
speed jet is visible at S-3. Recirculation zones dominate downstream in transitions into the aneurysm, velocity reduces significantly as the
the post-stenotic region (S-5 to S-6), while flow separation persists in expansion alters flow conditions. Case 3 shows a strong jet influence
the aneurysm at S-7, stabilizing toward S-8. Along T-7, disturbances persisting in this region, while case 4 exhibits non-uniform velocity
occur upstream at S-1, and flow velocity increases at S-3, with an distributions due to asymmetric flow development. In S-7 [Fig. 8(g)],
asymmetric shift toward one side of the artery. Flow separation is inside the aneurysm, velocity magnitudes decrease significantly, with
prominent at S-4, where three-dimensionality is most evident. In the continued disturbances in cases 3 and 4. Case 3 exhibits significant var-
post-stenotic region (S-5 to S-6), disturbances persist, while in the iations due to residual jet influence, while case 4 continues to show
aneurysmal region (S-7 to S-8), velocities reduce further. A multimedia asymmetric flow features. Case 2 demonstrates minor fluctuations,
file (Video 1), which is an integral part of Fig. 7, is available online. It whereas case 1 has the most uniform profile, indicating a smoother
illustrates the variation in velocity magnitudes for each case (1–4) flow transition. Finally, at S-8 [Fig. 8(h)], as the flow exits the aneu-
during the sixth cardiac cycle, from T-1 to T-7. rysm, velocity stabilizes across all cases. However, case 3 still exhibits
Overall, as stenosis severity and eccentricity increase from cases residual fluctuations due to the prolonged effect of the high-speed jet
1–4, jet influence length, flow three-dimensionality, and recirculation and earlier disturbances. Case 1 has the most uniform velocity distri-
zones become more pronounced. In case 1 (50% stenosis), the jet influ- bution, while case 4 retains slight asymmetries as the effects of eccen-
ence is short, ending at S-4, with no three-dimensionality. Case 2, i.e., tricity persist.
70% stenosis, sees the jet extending to S-6, with three-dimensionality Overall, S-1 to S-3 closely follow the inlet velocity trend, but post-
in the aneurysm (S-6 to S-8). In case 3 (90% stenosis), the jet influence stenotic regions (S-4 to S-6) exhibit variations due to jet dissipation,
reaches S-8, with strong recirculation and three-dimensionality from pressure recovery, and disturbances from recirculation effects. The

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-11

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 8. Velocity traces for all cases—1 to 4 at the longitudinal and transverse sections: (a) S-1, (b) S-2, (c) S-3, (d) S-4, (e) S-5, (f) S-6, (g) S-7, and (h) S-8. These plots repre-
sent the temporal velocity variations at different locations along the artery, illustrating the effects of stenosis severity and eccentricity on jet formation, recirculation, and flow dis-
turbances. The schematic diagram in the bottom right corner indicates the probing locations.

aneurysmal regions (S-7 to S-8) show the most prominent fluctuations structures appear along S-3, with the fluid core moving toward the
in case 3, reflecting the prolonged effect of the jet. The severity of ste- center, while at S-4, it moves outward. The pressure gradient causes
nosis determines the jet length and velocity magnitude, while eccen- mild acceleration, but convective effects are not yet dominant, ensuring
tricity in case 4 alters the onset of disturbances, introducing earlier attached flow along the walls. By T-3, shear layers extend beyond S-4,
three-dimensional effects and asymmetric velocity variations. Overall, with recirculation zones forming in the stenosis concavity, as seen in
velocity traces follow the inlet profile at S-1 but deviate downstream Fig. 9(a). The shear layers remain attached without fully detached vor-
due to jet formation, flow separation, and recirculation. Case 3 shows tices. At T-4, localized disturbances emerge between S-4 and S-5, with
the highest velocity and most extended jet influence, reaching S-8, increasing convective effects downstream. At T-5, the adverse pressure
while case 4 exhibits earlier asymmetry at S-4. Velocity reduces in the gradient leads to recirculation zones from S-4 to S-6, evident in
post-stenotic region (S-5 to S-6) and decreases further in the aneurysm Fig. 9(a), with superimposed streamlines highlighting multiple small
(S-7 to S-8), where case 3 retains the most disturbances, and case 1 zones at S-4 and S-5. Along T-6, recirculation zones develop on both
shows the least variations. Stenosis severity affects jet length, while sides of the stenosis at S-3, shifting toward the aneurysmal wall at S-6.
eccentricity alters flow distribution and early disturbances.
However, the flow remains attached upstream, where viscous effects
persist. At T-7, recirculation zones continue, showing asymmetry,
2. Spatio-temporal vorticity evolution while flow attachment is maintained near the walls upstream.
Figure 9 (Multimedia view) shows the variation of spatiotemporal Throughout the cycle, the flow exhibits localized disturbances and
vorticity at selected cycle phases T-1 to T-7 on planes S1 and S2–S8, recirculation zones.
respectively. This analysis highlights regions of rotational flow and sep- Figure 9(b) illustrates the vorticity distribution in case-2 over
aration, offering key insights into vortex dynamics and recirculation seven cardiac phases, where the stenosis results in a 70% reduction in
zones, particularly in the post-stenotic and aneurysmal regions. diameter. At T-1, the flow remains fully attached to the walls upstream
In case-1, with a 50% diameter reduction due to stenosis, the flow and downstream of the stenosis, with a moderate pressure gradient
exhibits distinct behavior over time, as shown in Fig. 9(a). At T-1 and maintaining a smooth profile. The influence of wall effects prevents
T-2, the flow remains attached to the walls, with shear layers confined significant flow separation, ensuring an organized flow structure at this
to the boundary layer from S-2 to S-4. At T-2, symmetrical shear layer stage.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-12

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 9. Vorticity (s1) contours over the longitudinal plane (S-1) and transverse planes (S-2 to S-8) at seven cardiac phases (T-1 to T-7) for all cases: (a) case-1, (b) case-2,
(c) case-3, and (d) case-4. The visualizations include streamlines, illustrating the evolution of flow structures, vortex formation, and post-stenotic disturbances, with variations
influenced by stenosis severity and eccentricity. Multimedia available online.

At T-2, initial shear layers begin to form at the stenosis, as seen further downstream, and recirculation zones begin to appear in the
on S-1. These layers remain confined near the walls, with fluid moving post-stenotic region on S-1. Attached vortical structures develop along
toward the center on S-2 and S-3 and outward on S-4. As the flow the walls from S-3 to S-6, with a recirculation zone forming just after
accelerates near the stenosis, the convective effects increase, marking S-3, becoming more evident at S-4 and reaching its peak at S-5 before
the early transition in flow behavior. By T-3, the shear layers extend dissipating by S-6. The increasing adverse pressure gradient drives the

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-13

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

growth of these structures, while the effects along the walls attempt to evolve. The previously formed recirculation zones increase in size,
maintain flow attachment. At T-4, as the flow enters the aneurysm, it influenced by the changing pressure conditions within the aneurysm.
decelerates, causing the shear layers to extend beyond S-6 and recircu- Beyond S-6, the flow remains disturbed, with no clearly defined shear
lation zones to grow in size, as shown on S-1. The interaction between layer structures, leading to persistent irregular motion throughout the
opposing shear layers causes the core jet to shift between the distal aneurysmal region. At T-5, the negative flow direction disrupts the
walls of the aneurysm. Recirculation zones begin to form at S-3, grow shear layers, creating a disturbed flow. The jet emerging from the ste-
more prominent at S-4, and fully develop at S-5, with an increasing nosis is significantly weakened, extending only a few diameters down-
number from S-6 to S-7. The changing momentum within the aneu- stream, as observed on S-1. While convective forces are diminished,
rysm leads to complex flow behavior, though no fully detached vortices the unsteady nature of the flow remains pronounced, contributing to
are observed. At T-5, the shear layers extend further from S-6, and the breakup of the shear layers. In the stenotic region, a single recircu-
irregular flow patterns emerge within the aneurysm, as seen on S-1. lation zone forms due to the weak reverse jet, as seen on S-3. In the
The recirculation zones become more dispersed at S-6, S-7, and S-8 aneurysmal region, the number of recirculation zones increases from
due to increased convective effects. The adverse pressure gradient S-6 to S-7 but becomes less pronounced at S-8. At T-6, strong shear
results in localized flow reversal, and the interaction between recircu- layers form upstream of the stenosis, reflecting the persistence of
lating flow and shear layers leads to significant variations in flow direc- adverse pressure gradients, while downstream disturbances persist but
tion. At this stage, the negative flow direction intensifies these effects, with reduced intensity, as observed on S-1. Compared to earlier instan-
further weakening the shear layers and allowing complex flow struc- ces, the intensity of the disturbances has diminished, with viscous
tures to persist. By T-6, the negative flow direction becomes dominant, forces playing a more significant role in stabilizing the flow. In the pre-
weakening the shear layers further. The flow within the aneurysm stenotic region along S-2, no prominent recirculation zones are
remains irregular, with recirculation zones continuing to evolve, as observed, whereas a single strong recirculation zone is visible at S-3.
seen on S-7 and S-8. Small shear layers are observed in the stenotic The number of recirculation zones increases progressively from S-4 to
region at S-3 due to peak reversal flow. Vortical structures are present S-5. Finally, at T-7, the upstream shear layers weaken considerably as
both upstream and downstream of the stenosis, though they exhibit the convective forces subsided, as observed on S-1. The flow begins to
asymmetry due to interactions between the recirculating zones and stabilize, with reduced disturbances in the aneurysm and weaker recir-
shear layers. At T-7, weak traces of vorticity appear upstream of the culation zones. The viscous forces play a more prominent role in
stenosis, reflecting the effects of earlier flow alterations. These traces dampening the remaining instabilities, and the flow begins to reattach
indicate that while the flow remains structured in certain regions, dis- to the walls.
turbances persist. The shear layers are more diffused, and the flow In case-4, characterized by 0.75 of eccentricity and 70% constric-
within the aneurysm continues to exhibit minor fluctuations. tion, the flow dynamics around the asymmetry evolve from T-1 to
In case-3, with a 90% reduction in diameter due to the stenosis, T-7, as described in Fig. 9(d). At T-1, weak shear layers persist due to
the flow dynamics are significantly more unstable, with strong shear remnants from the previous cardiac cycle, as observed on S-1. At T-2,
layer interactions observed across time instances T-1 to T-7, as strong shear layers begin along mid-stenosis at S-3, extending to S-4. A
described in Fig. 9(c). At T-1, weak shear layers are seen arising single recirculation zone emerges at S-3, driven by the increased
upstream of the stenosis, remnants from the previous cycle due to the adverse pressure gradient and sudden 70% constriction, disappearing
negative portion of the flow as observed on S-1. These remnants are a by S-4. At T-3, shear layers extend to the aneurysm, as seen on S-1,
result of the adverse pressure gradient and convective forces from the exhibiting asymmetry compared to symmetrical cases. The adverse
earlier cycle. The viscous forces are not sufficient to dampen these pressure gradient leads to recirculation zone development on one side
structures entirely, so they persist upstream. At T-2, the upstream of the post-stenotic region, clearly depicted with superimposed stream-
shear layers break apart, indicating disturbed flow as their remnants lines on vorticity maps. Recirculation zones increase from S-3 to S-4
interact with the forward flow. Strong shear layers form at the stenosis and diminish by S-6. At T-4, shear layer breakdown occurs in the
due to the pressure gradient, with vortices observed nestled within the post-stenotic region due to unstable velocity gradients and an
concavity of the stenosis along S-3. These vortices arise from the inter- increased adverse pressure gradient, as observed on S-1. This leads to
play between convective forces and the adverse pressure gradient. The flow disturbances in the post-stenotic region, which are carried for-
development of recirculation zones begins at S-4, and two partially ward in the aneurysm. Recirculation zones begin developing from S-3,
developed zones are observed on S-5. These zones diminish as the flow initially forming asymmetrically along the artery wall. By S-4, a more
progresses and completely disappear by S-6. At T-3, the shear layers prominent recirculation zone appears on one side of the arterial wall,
extend into the aneurysm but weaken beyond S-7. In this region, the indicating asymmetry. The number of recirculation zones increases
interaction between opposing shear layers becomes more noticeable, from S-5 through S-8. At T-5, due to the start of the reversal flow, the
leading to the formation of small recirculation zones. These interac- disturbance in the flow is decreased in the post-stenotic region, as
tions cause localized variations in flow direction, with fluid shifting observed on S-1. However, the disturbed nature of the flow with a
between adjacent shear layers rather than forming a continuous struc- small recirculation zone still exists on S-4 to S-7. At T-6, a weak reverse
ture. As a result, the flow exhibits a more complex distribution of jet develops in the stenotic region, directed upstream, as observed on
smaller recirculation zones instead of large, well-defined regions. At S-1. Disturbances in the shear layers become more pronounced on S-4
T-4, the shear layers remain strong up to S-5, maintaining their influ- and S-5. By T-7, the shear layers weaken, and the flow disturbances
ence on the flow structure. However, beyond S-5, they begin to spread increase, resulting in weak recirculation zones, as seen on S-1.
within the aneurysm. This distribution results in the confinement of These observations are consistent with studies indicating that in
recirculation zones to the post-stenotic region, where they continue to stenosed arteries, shear layers can become unstable, leading to the

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-14

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

formation of several recirculation zones downstream of the stenosis.

These observations indicate that post-stenotic regions are prone to
flow disturbances and recirculation zones due to shear layer break-
down and adverse pressure gradients. It can enhance flow recirculation
and shear rates in arteries, contributing to complex hemodynamic pat-
terns. A multimedia file (Video 2), which is an integral part of Fig. 9, is
available online. It illustrates the variation in outplane vorticity for
each case (1–4) during the cardiac cycle from T-1 to T-7 is provided.

3. Three-dimensional vortical structures

The spatiotemporal evolution of vortices is visualized in three
dimensions using the Q-criterion [Fig. 10 (Multimedia view)],
highlighting their location and movement to provide insights into wall
loading. Vortical structures are plotted at six cardiac phases (T-2 to
T-7), capturing significant development from T-2 onwards, with vor-
ticity structures and streamlines enhancing clarity.
The formation of vortical structures at the above-mentioned car-
diac phases for case 1 with 50% constriction is mentioned in Fig. 10(a).
In case 1, the vortical structures forming around the stenosis at T-2 are
due to the sharp pressure gradient and acceleration as it moves
through the narrowed region. At T-3, a ring-like structure emerges in
the post-stenotic region due to the flow expansion sudden downstream
of stenosis. This expansion leads to flow separation driven by velocity
gradients and shear layer formation. The dominance of the convective
forces over viscous forces contributes to the development of recircula-
tion zones near the artery wall downstream of the stenotic region, as
seen in a dashed rectangle at phase T3. At T-4, as the flow decelerates,
the ring structure progresses downstream. It begins to breakup into
smaller structures, reflecting how the reduced flow velocity allows the
shear layers to interact and disrupt the coherent vortex while the vis-
cous term starts to play a more prominent role in dissipating energy.
There is an asymmetry in the streamlines, particularly at T-4. At T-5,
during the onset of negative flow, the interaction of opposing flow
causes the vortical structures to shift along the right walls, as flow
reversal enhances shear layer interactions, and the pressure gradient
becomes negative. By T-6, these structures progress downstream at the
aneurysm inlet, where inertial forces push the vortices through.
Furthermore, they begin to weaken as viscous forces increase, and by
T-7, the vortices lose their strength due to the dominance of viscous
effects, leading to their breakdown.
In case 2, with 70% stenosis, and case 3, with 90% stenosis, arte-
rial narrowing leads to the formation of vortex rings, with the severity
of stenosis causing distinct flow characteristics in each case. The vorti-
cal structures for case 2 are illustrated using the Q-criterion in
Fig. 10(b). In case 2, the vortex ring forms early at T-2 near the stenotic
region due to the pressure gradient and strong acceleration of the flow
through the stenosis. This ring is then pushed downstream into the
post-stenotic region by T-3, settling near the aneurysmal inlet as con- FIG. 10. Three-dimensional vortical structures using the Q-criterion across six car-
vective forces dominate. diac phases (T-2 to T-7), with detailed correlations to shear layers and streamlines
By T-5, as the negative flow begins, the weakening of shear layers on S-1 plane highlighted within black dashed boxes: (a) case 1, (b) case 2, (c) case
3, and (d) case 4. Multimedia available online.
and flow reversal causes the vortex ring to disintegrate, with new vorti-
cal structures forming along the aneurysmal wall occupying the distal
portion and further extending along the outlet. From T-6 to T-7, vis- increased narrowing results in a stronger flow acceleration. At T-2, the
cous forces dominate, gradually dissipating the vortical structures and ring vortex is shifted further downstream into the post-stenotic region
reducing the overall flow complexity. compared to case 2—see dashed rectangle at phase T-2. By T-3, a series
The vortical structure variation at six cardiac phases for case 3 of ring-like structures extend from the post-stenotic region into the
has been mentioned in Fig. 10(c). In case 3, with 90% stenosis, the aneurysmal domain, driven by the intense core flow originating from

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-15

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

the stenosis. The initial ring remains attached to the distal aneurysmal Overall, the comparison of vortex dynamics across the four
wall, enveloping the trailing vortex structures. Shear layers form at the cases—50% stenosis (case 1), 70% symmetric stenosis (case 2), 90%
onset of the aneurysm and begin to break down at its inlet, as shown in stenosis (case 3), and 70% eccentric stenosis with an eccentricity of
the vorticity snapshot at T-3. The interaction of these shear layers in the 0.75 (case 4) reveals that both the severity of stenosis and the degree of
distal aneurysmal region leads to the persistence of strong vortical struc- eccentricity significantly influence flow behavior. In case 1, with mild
tures. During T-4, the deceleration phase leads to the strengthening of stenosis, vortical structures are weak, transient, and confined to the
shear layers and the intensification of vortex trails, with vortical struc- immediate post-stenotic region, dissipating quickly due to limited flow
tures expanding to occupy the entire aneurysmal region. As negative disturbances. Case 2 shows more organized, symmetric vortices that
flow sets in at T-5, the shear layers begin to break down, causing the vor- form earlier and persist longer than in case 1 with ring-like structures
tical structures to weaken and shift upstream along the post-stenotic centered along the centerline. However, they gradually weaken during
region. Despite this upstream shift, vortical structures persist within the the deceleration and flow reversal phases. In contrast, case 3, with
aneurysm, evident as distributed zones of higher vorticity in the vorticity severe stenosis, exhibits the strongest and most spatially extensive vor-
snapshots. At T-6 and T-7, vortical structures in case 3 remain stronger tical structures, both downstream and upstream of the stenosis, driven
and more widespread compared to case 2 despite ongoing viscous dissi- by intense flow acceleration and reverse flow that sustains complex
pation during the flow reversal phase. These structures persist through- vortex dynamics even during late diastolic phases. Case 4 demonstrates
out the aneurysm and extend upstream due to strong reverse flow, how eccentricity alters vortex behavior, introducing asymmetry that
which also triggers additional vortical structures upstream of the steno- causes vortices to migrate toward the model walls, particularly the right
sis—that otherwise are missing in cases 1 and 2, respectively. The inter- wall, and persist longer compared to the symmetric case. The vortical
action between residual forward flow and reverse flow sustains flow structures in case 4 are stronger, more asymmetric, and occupy a
disturbances, leading to complex vortex dynamics. While weakening broader post-stenotic region, with additional cylindrical vortices form-
over time, these vortices remain prominent, highlighting the impact of ing around the central rings due to enhanced shear layer interactions.
severe stenosis on prolonged flow disturbances. Thus, increasing stenosis severity amplifies vortex strength, spatial dis-
In case 4, which features a 70% eccentric stenosis with a degree of tribution, and flow disturbances, while eccentricity introduces asym-
eccentricity 0.75, the evolution of vortical structures is dynamic and metry, wall interactions, and persistent vortical structures, highlighting
significantly influenced by the asymmetry of the stenosis. During the their combined impact on post-stenotic hemodynamics. Although the
T-1 phase, vortical structures begin to form downstream of the steno- peak Reynolds number reaches 3011, the cycle-averaged Reynolds
sis, with well-organized shear layers indicating early vortex develop- number remains around 267, indicating a weakly transitional regime.
ment due to flow separation caused by eccentric narrowing. At T-2, a In this range, the flow lacks sustained energy cascading, and shear layer
distinct ring-like vortical structure forms just downstream of the steno- instabilities are better captured using a laminar model. Turbulence
sis. This ring is the result of strong rotational flow caused by high- models, by contrast, were unable to resolve these transitional features
velocity gradients at the exit of the stenosis. Surrounding this ring, effectively in our comparative analysis, further supporting the use of a
additional cylindrical vortical structures develop, interacting with the laminar approach in this study. A multimedia file (Video 3), which is
ring due to flow disturbances introduced by the eccentric geometry. an integral part of Fig. 10, is available online. It illustrates the variation
These cylindrical structures appear as sheath-like vortices enveloping in three-dimensional vortical structures for each case (1–4) during the
sixth cardiac cycle from T-1 to T-7.
the central ring. Moving into the T-3 phase, the ring structure formed
earlier progresses forward into the post-stenotic region. Owing to the
eccentric nature of the stenosis, the shear layers start interacting asym- 4. Influence of multiple pathologies on hemodynamics
metrically, causing the vortical structures to shift toward the right wall. In case 3, representing severe stenosis, high-velocity magnitudes,
This shift occurs due to uneven velocity distribution, with higher and the extended high-speed jet significantly contribute to aneurysm
velocities on one side enhancing vortex strength and promoting migra- progression and increase the risk of rupture. In cases 2 and 4, signifi-
tion toward the wall. During the T-4 phase, flow deceleration weakens cant constriction also promotes aneurysm progression and rupture.
the shear layers, leading to the breakdown of previously coherent vorti- Case 4 further highlights the effect of eccentricity, with flow deviation
cal structures. These fragmented vortices distribute along both the left observed in the post-stenotic region. In contrast, mild stenosis in case
and right walls. At the same time, the ring structure formed earlier at 1 shows minimal impact on aneurysm behavior. The rotational behav-
T-2 continues to advance into the aneurysmal region, particularly ior of blood and recirculation zones is most prominent in case 3, where
along the proximal side, due to inertia. At T-5 (early diastolic phase), intensified recirculation and shear layer breakdown begin at T-3 and
the vortical structures continue to weaken, yet the ring structure persist through T-5, primarily in the aneurysm region. In case 2, shear
remains visible, now appearing attached along the right distal aneurys- layer breakdown starts at T-4 and continues until T-5, with stable
mal wall. This attachment is driven by the persistent asymmetric flow recirculation zones up to T-4, followed by a more randomized devel-
pattern and vortex-wall interactions. In the T-6 phase, the vortical opment of recirculation zones. In case 4, due to eccentricity, shear layer
structures further decay, and a new ring-like structure forms upstream breakdown initiates at T-3 and progresses asymmetrically toward the
of the stenosis, a result of flow reversal and recirculation zones typical arterial wall in the post-stenotic region, lasting until T-5.
during diastole in eccentric geometries. Finally, during T-7, the ring In contrast, for mild stenosis in case 1, shear layer breakdown
structure formed at T-6 advances toward the right wall upstream of starts at T-4 and continues through T-5, with lower recirculation
the stenosis. This movement is once again influenced by the eccentric- intensity and disturbances confined to the region before the aneurysm
ity, that causes preferential flow pathways and asymmetric vortex prior to S-6. Three-dimensional vortical structure formation and
migration. behavior are strongly influenced by stenosis severity and arterial

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-16

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

geometry. In cases 2 and 3, vortex rings form due to arterial narrowing, interplay of flow characteristics like vorticity, shear layers, and 3D vor-
with case 3 showing accelerated formation and faster downstream tex formation, particularly in regions of constricted blood flow.
propagation compared to case 2, where vortex displacement occurs in A comprehensive examination of TAWSS for every case, as
the post-stenotic region during peak systolic phases, followed by break- shown in Fig. 11, gives valuable details about the severity of stenosis.
down in the aneurysm region during the deceleration phase. In case 4, The maximum TAWSS values are consistently observed in the stenotic
eccentricity causes vortex rings to shift toward the artery wall during region across all cases, highlighted by the red circles in Fig. 11. This ele-
mid-systolic phases with breakdown occurring in the post-stenotic vation in TAWSS is directly linked to the narrowing of the artery,
region during the peak systolic phase and propagating into the aneu- which accelerates blood flow within the stenotic region. The resulting
rysm region. In contrast, case 1, with mild stenosis, exhibits limited increase in velocity generates higher shear forces on the vessel walls,
vortex formation, with breakdown confined to the post-stenotic particularly in the stenotic area, emphasizing the critical relationship
region, not extending into the aneurysm. These observations highlight between vascular narrowing and elevated shear stress. Generally, the
the critical role of stenosis severity and geometry in determining vortex TAWSS value for the healthy artery varies between 1 and– 2.5 Pa.67
dynamics, which significantly influence arterial biomechanics and dis- The maximum values of TAWSS at the stenotic region are 3.5, 14, 200,
ease progression. and 20 Pa for case 1 to case 4, respectively. The analysis of TAWSS
across varying stenosis models reveals significant insights into the
B. Hemodynamics indicators interplay between fluid dynamics and vascular pathophysiology. In
In the present study, six hemodynamic indicators—TAWSS, OSI, case 1, TAWSS indicates flow characterized by localized and weak vor-
RRT, ECAP, WSSG, and HOLMES—were computed. These indicators tices, as observed in Fig. 11(a). This low TAWSS suggests minimal risk
were analyzed across four cases that include diseased scenarios with for endothelial damage and atherogenesis, as the viscous forces effec-
varying stenosis levels being 50%, 70%, and 90% degree of stenosis and tively dampen any disturbances in the blood flow.68
one case featuring degree of eccentricity as 0.75 combined with a 70% In case 2, there is an elevation in TAWSS magnitude, as observed
degree of stenosis, with all cases exhibiting an aneurysmal dilation of in Fig. 11(b), which reflects the emergence of more pronounced shear
50%, respectively. layers and vorticity downstream [refer to Figs. 9(b) and 10(b)], raising
concerns about potential endothelial injury and the risk of plaque for-
mation due to the heightened localized wall stress.69 In case 3, TAWSS
1. Time average wall shear stress
shows a significant increase, as depicted in Fig. 11(c). This increase is
The distribution of TAWSS across all cases with varying stenosis caused by considerable flow acceleration and high-pressure gradients
severity and eccentricity highlights the significant influence on hemo- within the stenotic region, as confirmed by Figs. 8(c), 9(c), and 10(c).
dynamics that directly correlates with pathophysiological changes. The formation of strong vortices and disturbed flow dynamics further
Also, it serves as a critical marker for vascular wall stress, reflecting the amplifies the risk of aneurysm rupture and thrombosis, posing a

FIG. 11. Distribution of time-averaged wall shear stress (TAWSS) across four distinct cases, highlighting regions of maximum TAWSS with red circles for better visualization.
The color scale represents the magnitude of TAWSS, with maximum and minimum values clearly projected: (a) case 1, (b) case 2, (c) case 3, and (d) case 4.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-17

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

serious threat to vascular integrity.70 Conversely, in case 4, the intro- likelihood of vascular complications such as plaque rupture or local-
duction of asymmetry modifies the flow dynamics, distributing wall ized aneurysmal weakening.71,72
shear stresses more evenly and preventing sharp concentration in a
single area, as observed in Fig. 11(d). This alteration helps to mitigate
the risks associated with high TAWSS, suggesting that while stenosis 2. Oscillatory shear index
severity poses inherent dangers, mild asymmetry can positively influ- The oscillatory shear index (OSI) is a dimensionless parameter
ence hemodynamic parameters.
that quantifies the directional changes in wall shear stress over a car-
TAWSS across the aneurysm is always low, which suggests that
diac cycle, indicating the extent of shear stress oscillation and is shown
the vessel wall is under less shear stress, especially in the dilated area. A
in Fig. 12. The maximum value of OSI is 0.5, which indicates areas of
characteristic of aneurysmal dilatation is the reduction in shear stress,
significant wall shear stress fluctuation, suggesting a pathological envi-
which results from altered flow dynamics that reduce shear forces
ronment where endothelial function may be compromised.73 Each
inside the aneurysm sac. The increased TAWSS resulting from the
interaction of multiple pathologies, such as stenosis and aneurysms, case illustrates how variations in stenosis severity and geometric eccen-
highlights the progressive impact of stenosis severity on the risk of tricity influence flow dynamics, leading to distinct pathophysiological
aneurysm rupture. A mild increase in TAWSS observed in the case of responses with significant changes in the OSI distribution. In case 1,
mild stenosis with 50% narrowing, case 1, does not pose a significant OSI reaches a maximum value of 0.5, with significant fluctuations
threat to aneurysmal or overall vascular health, as the wall shear stress observed in the post-stenotic region, progressing toward the aneurysm,
remains within a physiologically tolerable range. However, in moderate refer to Fig. 12(a). These fluctuations indicate an oscillatory flow pat-
stenosis with 70% narrowing, case 2, there is a substantial rise in tern due to the mild 50% stenosis, where the shear stress fluctuates in
TAWSS, which can significantly impact the aneurysm by promoting response to the constricted geometry. The instability in shear stress
endothelial dysfunction and potentially accelerating aneurysmal contributes to a fluctuating shear environment and may initiate
growth. In cases of severe stenosis with 90% narrowing, in case 3, inflammatory responses in the endothelium. In case 2, the OSI distri-
TAWSS becomes excessively high, markedly increasing the risk of bution exhibits similar fluctuations but with an extended region of
endothelial injury, aneurysm rupture, and thrombosis due to localized fluctuation compared to case 1, refer to Fig. 12(b). This change corre-
shear stress concentrations. The introduction of asymmetry in the vas- lates with the moderate 70% stenosis, which enhances the severity of
cular geometry, case 4, leads to a more effective redistribution of the flow disturbances downstream of the stenosis. The increased length
stresses, reducing sharp stress gradients and mitigating the risks associ- of the oscillation region reflects the greater instability in the flow, lead-
ated with high TAWSS. This stress redistribution helps to alleviate ing to prolonged exposure of the endothelium to oscillatory shear
focal mechanical loading on the arterial wall, potentially lowering the conditions.

FIG. 12. Distribution of oscillatory shear index (OSI) across four distinct cases, highlighting regions of the maximum distribution of OSI with red circles for better visualization.
The color scale represents the magnitude of OSI, with maximum and minimum values clearly projected: (a) case 1, (b) case 2, (c) case 3, and (d) case 4.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-18

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

In case 3, the fluctuations in OSI are pronounced throughout the In case 1, the maximum magnitude of RRT is 10 Pa1, observed
length from the pre-stenotic region to the aneurysm region, refer to in the region before the stenosis and over the aneurysmal region,
Fig. 12(c). The severe 90% stenosis case significantly alters the flow which is highlighted using red circles, as illustrated in Fig. 13(a). In
characteristics with strong oscillatory behavior. This severe constric- case 2, the distribution of relative residence of particles is in the region
tion creates a disturbed environment with high-velocity gradients, between stenosis and aneurysm as well as over the aneurysm with a
leading to intense shear stress fluctuations. The prolonged exposure to magnitude of 10 Pa1, as shown in Fig. 13(b). In case 3, the distribu-
these conditions can severely damage the endothelium, increasing the tion of the relative residence of particles are in the pre-stenotic, post-
likelihood of thrombosis and plaque rupture, emphasizing the patho- stenotic, and distal end of the post-aneurysmal region with a magni-
logical implications of high OSI in severely stenosed regions. In case 4, tude of 10 Pa1, as shown in Fig. 13(c). In case 4, the distribution of
with the introduction of eccentricity with a degree of eccentricity of the relative residence of particles is over the aneurysmal region with a
0.75 in a moderate 70% reflects a decrease in the pathological stress on magnitude of 10 Pa1, as shown in Fig. 13(d). The distribution is well
the endothelium, potentially mitigating risks associated with thrombus correlated with OSI and TAWSS results (refer to Figs. 11 and 12), as in
formation, even though the underlying stenosis remains severe. In the those regions, high OSI and low TAWSS can be observed for all four
stenosis case, the severity of flow fluctuations decreases, as in cases. In case 1, the flow dynamics exhibit minimal fluctuations due to
Fig. 12(d). mild stenosis, resulting in a smooth and consistent flow pattern.
The OSI distribution indicates reduced oscillatory behavior, pri- However, even in this scenario, the presence of flow stagnation near
marily between the proximal part of the stenosis and the distal part of the aneurysm results in oscillatory flow patterns that increase OSI and
the aneurysm. The eccentric geometry alters the flow dynamics, redis- decrease TAWSS. This combination of high residence time and low
tributing shear stress more evenly and reducing the magnitude of shear stress contributes to the risk of thrombus formation, as particles
fluctuations. reside in the stagnant regions, heightening the likelihood of coagula-
tion. In case 2, moderate stenosis leads to more pronounced flow dis-
3. Relative residence time turbances and oscillations. The flow separation behind the stenotic
region intensifies stagnation, resulting in a high OSI and low TAWSS.
Relative residence time (RRT) is a crucial hemodynamic parame- The stagnation regions create an environment where blood cells can
ter as it reflects the relationship between TAWSS, OSI, and flow stag- remain longer, fostering conditions conducive to thrombus formation.
nation regions. High OSI and low shear stress in these regions lead to In case 3, a severe narrowing of 90% intensifies flow acceleration,
increased flow oscillation, resulting in prolonged residence time of par- resulting in high shear stresses in the central stenotic region. However,
ticles, i.e., platelets, and promoting thrombus formation.74 The RRT downstream effects include significant flow separation and disturbance
variation with the stenosis severity and eccentricity has been men- in flow, leading to areas of low shear and high RRT. The presence of
tioned in Fig. 13. stagnation here indicates that while the flow is rapid through the

FIG. 13. Relative residence time (RRT) variations across all four cases and highlighting the maximum RRT regions in red circles for better visualization. The color scale repre-
sents the magnitude of RRT, with maximum and minimum values clearly projected: (a) case 1, (b) case 2, (c) case 3, and (d) case 4.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-19

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

stenosis, the highly disturbed vorticity downstream creates pockets Figure 14 depicts the fluctuations in ECAP over rising stenosis severi-
where platelets can reside, further increasing thrombus risk, illustrating ties, as well as the interaction of an aneurysm downstream of the ste-
the severity of stenosis can compromise vascular integrity and promote nosis. A red circle highlights the region with the highest ECAP.
pathological changes.75 In case 4, the eccentric geometry alters the flow The variation within the post-stenotic region reveals the effects of
dynamics significantly, redistributing flow patterns and promoting altered flow patterns on endothelial health and vascular stability. In
more uniform shear distribution across the vessel walls. While high case 1, maximum ECAP is concentrated on the central part of the
RRT is still observed over the aneurysmal region, the asymmetrical aneurysm, reaching a peak of 2.5 Pa1, refer to Fig. 14(a). This high
flow minimizes stagnation effects by allowing for better dispersion of ECAP indicates substantial endothelial activation in the aneurysmal
shear stresses. This reduction in peak RRT suggests a moderated risk region due to oscillatory flow and low TAWSS in this area [Figs. 11(a)
of thrombus formation compared to the fully symmetric scenario. and 12(a)]. The low shear stress paired with high OSI reflects dis-
However, the complexity of the flow patterns still presents a potential turbed, swirling flow that aggravates endothelial dysfunction, poten-
risk for localized pathological changes, underscoring the importance of tially leading to inflammation and aneurysm progression. This case
understanding flow characteristics in managing vascular health. demonstrates how even mild stenosis and aneurysms can create local-
In case 1, mild stenosis promotes flow stagnation near the aneu- ized flow disturbances that pose risks to vascular health. In case 2,
rysm, increases OSI, and decreases TAWSS, promoting thrombus for- ECAP is highest on the distal side of the stenosis, with a magnitude of
mation. Cases 2 and 3 show worsened flow disturbances, high OSI, 2 Pa1, refer to Fig. 14(b).
and low TAWSS, with severe narrowing causing a high disturbance in This region of elevated ECAP results from high OSI and low
the downstream and thrombus risk. In case 4, eccentric geometry TAWSS, indicative of flow acceleration through the stenosis followed
redistributes shear stresses, reducing stagnation but retaining localized by shear stress drops downstream [Figs. 11(b) and 12(b)]. The high
thrombus risk, emphasizing the role of flow dynamics in vascular ECAP in this area suggests that flow recirculation and low shear stress
health. in post-stenosis contribute to increased endothelial activation and
inflammation in the downstream segment, potentially weakening the
4. Endothelial cell activation potential arterial wall in the distal region and promoting disease progression. In
case 3, the maximum ECAP is observed in the pre-stenotic region,
Endothelial cell activation potential (ECAP) serves as a crucial reaching 2.0 Pa1, refer to Fig. 14(c). Here, the severe narrowing causes
hemodynamic marker that indicates endothelial cell activation due to flow to stagnate upstream, creating high OSI relative to TAWSS before
flow-induced shear stress. Elevated ECAP signifies regions of disturbed the constriction [Figs. 11(c) and 12(c)]. This environment fosters
flow and oscillating shear stress relative to low TAWSS, that can lead endothelial activation upstream of the stenosis, where increased
to inflammatory responses and secretion of nitric oxide, potentially inflammatory signaling can lead to early arterial wall degradation. The
contributing to vascular inflammation and disease progression.76 high ECAP in this pre-stenotic region illustrates the risks posed by

FIG. 14. Endothelial cell activation potential (ECAP) variations across all four cases and highlighting the maximum ECAP regions in red circles for better visualization. The color
scale represents the magnitude of ECAP, with maximum and minimum values clearly projected: (a) case 1, (b) case 2, (c) case 3, and (d) case 4.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-20

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

extreme narrowing, as it initiates inflammatory pathways prior to the value was 7 Pa, which is in the stenotic region and has some low varia-
constriction that can accelerate vascular disease and weaken the vessel tion downstream of the stenosis, as observed in Fig. 15(b). The oscilla-
wall.77 In case 4, the highest ECAP is observed along the inlet, as tions in shear stress amplify due to more substantial flow separation
shown in Fig. 14(d). The eccentricity, in this case, causes asymmetrical and reversal zones [Figs. 7(b) and 9(b)].
flow patterns, creating uneven shear stresses and oscillatory flows at This condition of 70% narrowing is a key hemodynamic factor in
the inlet where flow disturbance begins. This results in high OSI rela- promoting the aneurysm progression. In case 3, with severe narrowing
tive to TAWSS, triggering early endothelial activation and inflamma- at 90%, a significant rise in flow velocity through the stenosis induces
tion.78 The distribution of ECAP along the inlet illustrates how disturbances in the flow, particularly in the post-stenotic region
asymmetry amplifies flow disturbance, increasing the likelihood of [Fig. 7(c)]. The maximum value of HOLMES was observed at 90 Pa in
endothelial dysfunction and possibly promoting vascular inflammation the stenotic region, as described in Fig. 15(c). This extreme condition
and wall degradation.79 leads to rapid endothelial degradation, accelerating aneurysm progres-
sion and increasing the risk of rupture. In case 4, due to the significant
5. High oscillatory low magnitude shears eccentricity with 70% constriction, the maximum HOLMES was
observed at 6 Pa in the stenotic region, as described in Fig. 15(d).
High oscillatory low magnitude shears (HOLMES) is a critical In cases 1 and 2, where stenosis severity is mild and moderate,
hemodynamic parameter that represents the extent of oscillation of respectively, the constriction at the stenosis neck causes the flow to
flow-induced shear stress with less magnitude. The stenotic regions accelerate and decelerate rapidly, creating oscillatory shear stresses of
create regions with oscillatory and low-magnitude shear stress, which low magnitude. This phenomenon is more pronounced in case 3 due
are critical in promoting endothelial dysfunction and plaque progres- to the increased severity of stenosis, resulting in higher HOLMES val-
sion.80 Figure 15 shows the distribution and variation of HOLMES for ues. From a pathophysiological standpoint, high HOLMES regions are
all cases, as well as the highest region of HOLMES, which is indicated detrimental to the arterial wall, as the oscillatory shear stress can dam-
by the red circles. age endothelial cell alignment, leading to endothelial dysfunction.81
In case 1, with 50% constriction, a maximum magnitude of This dysfunction contributes to the weakening of the arterial wall,
HOLMES 1.6 Pa was found in the stenotic zone, as illustrated in making it more susceptible to rupture and thrombus formation, partic-
Fig. 15(a). Regardless of the mild level of stenosis, oscillatory shear ularly in stenotic regions where oscillatory shear is quite intense.
stress develops around the stenosis and downstream. Despite their
small size, these regions can have an impact on endothelial cell align-
6. Wall shear stress gradient
ment and function. In case 2, significant narrowing causes a notable
increase in flow velocity through the stenosis and larger recirculation Wall shear stress gradient (WSSG) serves as a hemodynamic
zones downstream [Figs. 7(b) and 9(b)]. The maximum HOLMES marker, highlighting the spatial distribution of shear stress and its

FIG. 15. High oscillatory low magnitude shear (HOLMES) variations across all four cases and highlighting the maximum HOLMES regions in red circles for better visualization.
The color scale represents the magnitude of HOLMES, with maximum and minimum values clearly projected: (a) case 1, (b) case 2, (c) case 3, and (d) case 4.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-21

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

impact on endothelial health. High WSSG, influenced by stenotic WSSG pattern suggests concentrated endothelial stress in the regions
severity and arterial geometry, indicates rapid changes in wall shear, of maximum flow separation, which could promote inflammatory
correlating with flow acceleration, deceleration, and reattachment pathways and weaken the vessel wall. The heightened WSSG around
zones. Elevated WSSG is biologically significant, increasing endothelial the aneurysmal region increases the likelihood of endothelial dysfunc-
stress and contributing to inflammation, vascular remodeling, plaque tion and localized vascular remodeling, heightening the risk of aneu-
formation, or aneurysm progression.7 Figure 16 shows WSSG varia- rysm progression. In case 4, with a maximum WSSG of 14 Pa, the
tions across all cases, with maximum WSSG regions marked by red spatial gradient is observed primarily between the stenosis and the
circles. aneurysm, as illustrated in Fig. 16(d). The introduction of eccentricity
In case 1, the maximum magnitude of WSSG reaches 12 Pa, con- redistributes the high-shear gradients, reducing the concentration of
centrated primarily between the neck of the stenosis and the aneurys- shear forces at a single point. The altered flow pathway due to eccen-
mal region, as illustrated in Fig. 16(a). This spatial shear gradient is tricity results in a more diffuse distribution of WSSG, mitigating
indicative of flow separation and reattachment zones, which generate extreme shear fluctuations. This reduced, more spread-out WSSG pat-
shear fluctuations that could potentially lead to endothelial stress. The tern decreases concentrated endothelial stress, suggesting a potentially
localized elevation in WSSG, in this case, signifies an increased risk for reduced risk of endothelial injury and inflammatory response,
vascular remodeling and endothelial damage that can stimulate although the asymmetric distribution still creates complex flow pat-
inflammatory responses. In case 2, WSSG is distributed more evenly terns warranting further monitoring.78
along the axial length of the artery, reaching a maximum of 14 Pa, as
illustrated in Fig. 16(b). The broader distribution of WSSG reflects C. Mechanical response of the arterial wall
more sustained gradients due to enhanced flow acceleration through Analyzing the biomechanical response is crucial for understand-
the stenosis. The relatively uniform shear gradients suggest a more dis- ing artery wall mechanics, especially concerning the interaction
persed endothelial stress pattern along the artery wall, contributing to between multiple pathologies. This analysis helps assess how the inter-
an elevated risk of endothelial activation across a wider area. This dis- action of multiple pathologies responds to pulsatile flow conditions,
tributed WSSG pattern implies a heightened potential for atherogene- providing insights into both the mechanical integrity of the arterial
sis throughout the arterial segment, as the gradual shear transitions wall and potential sites of failure. According to the literature,17,22,27,82
increase vulnerability to endothelial inflammation. For case 3, WSSG there is still limited research on biomechanical response assessment,
peaks at 14 Pa, concentrated in the neck of the stenosis and around the and understanding the changes due to diseased conditions remains a
aneurysmal region, like case 2, as illustrated in Fig. 16(c). The severe challenge. Therefore, we conducted a comprehensive biomechanical
constriction generates intense localized gradients due to extreme flow analysis using FSI to compare changes in the artery wall affected by
acceleration and deceleration around the stenosis and aneurysm. This multiple pathologies. This section details the total deformation of the

FIG. 16. Wall shear stress gradient (WSSG) variations across all four cases and highlighting the maximum WSSG regions in red circles for better visualization. The color scale
represents the magnitude of WSSG, with maximum and minimum values clearly projected: (a) case 1, (b) case 2, (c) case 3, and (d) case 4.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-22

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

artery wall, von Mises stresses on the wall, and structural changes in Figure 17 (Multimedia view) illustrates the total deformation of the
stenosis and aneurysm regions with respect to cardiac phases. artery wall across all cases over the end of one cardiac cycle. It includes
a comparison between undeformed and deformed models, along with
1. Total deformation of the arterial wall a comparison graph relative to the cases.
Figures 17(a)–17(e) show the total deformation contours calcu-
Total deformation of the arterial wall is caused by the traction at lated over the end of the cardiac cycle, illustrating deformation pat-
the fluid–solid interface, which is exerted due to the wall pressure on terns at the end of the cycle and a time-dependent analysis provided in
the inner walls of the artery due to the pulsatile nature of blood flow. the upcoming section (Sec. IV C 3). In case 1, the maximum

FIG. 17. Total deformation on the artery wall, including the whole-body view and XY cross-sectional view with deformation vectors at the stenosis and aneurysm: (a) case 1, (b)
case 2, (c) case 3, (d) case 4, (e) comparison of deformation between deformed and undeformed models, and (f) graph showing total deformation vs solution time for all four
cases. Multimedia available online.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-23

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

deformation occurs in the pre-stenotic region due to stiffness caused surfaces of the artery is nearly identical, with the exception of the mid-
by the constriction, as clearly observed in the XY cross section in stenotic region, where stress is higher on the inner surface than the
Fig. 17(a), where the vector progression contours also illustrate the outer surface, as shown in Fig. 18(a). In case 2, the artery exhibits
deformation progression in both the stenosis and aneurysm regions. greater stiffness than in the previous case, resulting in maximum stress
Similarly, in case 2, total deformation is lower at the region of interest occurring at the downstream edges of the stenosis. Minimum stress is
(ROI) compared to case 1 due to increased stiffness in the stenotic observed in the stenotic region, particularly on the outer surface, due
region. In contrast, the maximum deformation still occurs in the pre- to the high stiffness of the stenosis, as shown in Fig. 18(b). For case 3,
stenotic area, with deformation vectors directed toward this region, as where the constriction reaches 90%, maximum stress is concentrated
shown in Fig. 17(b). In case 3, the increased stiffness at the stenosis at the downstream edge of the stenosis, similar to the previous cases, as
results in maximum deformation at the pre-stenotic region. In con- the artery stiffness is considerably higher than in all other cases, as
trast, deformation is reduced in the ROI. Here, vectors are oriented shown in Fig. 18(c). Minimum stress is observed at the stenotic region,
toward the medial side in stenosis and moving laterally on the aneu- where the constriction is greatest. In case 4, due to the effect of eccen-
rysm, as shown in Fig. 17(c). For case 4, eccentricity effects cause maxi- tricity, maximum stress shifts further downstream from the stenosis
mum deformation between the aneurysm and stenosis in the ROI, rather than being concentrated at the edge of the stenosis. Minimum
clearly visible in the XY cross section, creating a band along the artery stress is located within the stenotic region. The inner and outer stress
orientation, as shown in Fig. 17(e). The vectors at the stenosis, in this distributions show significant variation in this case, with maximum-
case, shift toward its lateral side, and the same is true for aneurysm, as stress observed at the edges of the aneurysm on the inner surface and
depicted in Fig. 17(d). The changes in the total deformation at the start moderate stress on the outer surface, as shown in Fig. 18(d).
and end of the cardiac cycle have been compared, as shown in Maximum von Mises stress induced in the arterial wall is caused by
Fig. 17(e). In cases 1 to 3, constriction occurs at the stenosis region. At the deformation of the arterial wall under the wall pressure exerted
the same time, expansion is observed at the aneurysm. In case 3, a due to fluid flow.
slight bend is observed from the upstream to downstream regions of The temporal variation of von Mises stress over one complete
the stenosis due to the maximum constriction being 90%, with the cardiac cycle for the inner and outer surfaces of the artery is shown in
bend directed toward the medial side. In case 4, a significant bend is Figs. 18(e) and 18(f). The maximum stress on the inner surface is 5,
observed due to the presence of asymmetric stenosis, with the bend 4.8, 4.7, and 6.8 kPa for cases 1–4, respectively. In cases 1–3, maximum
directed toward the lateral side. The maximum deformations are 0.35, stress occurs at peak systole, while in case 4, it peaks at early systole, as
0.09, 0.17, and 1.9 mm for cases 1–4, respectively, as shown in shown in Fig. 18(e). On the outer surface, maximum stress values are
Fig. 17(f). The graph indicates that the maximum deformation in cases 4.9, 4.7, 4.2, and 8.8 kPa for cases 1–4, respectively. For the outer sur-
1, 2, and 3 occurs between 0.0 and 0.20 s of flow time, from early sys- face, the maximum stress occurs at early systole for cases 1, 2, and 4,
tole to peak systole. In contrast, in case 4, the maximum deformation while in case 3, it peaks after peak systole, as shown in Fig. 18(f).
occurs between 0.6 and 0.8 s, from peak diastole to late diastole. Over Overall, case 4 experiences the highest stress, while cases 1–3 exhibit
one cardiac cycle, case 4 exhibits the highest overall maximum defor- moderate stress levels.
mation, followed by case 1, while cases 2 and 3 show overlapping Further, the elevated von Mises stress observed in the eccentric
slopes of total deformation. The maximum deformation observed in
stenosis configuration (case 4), peaking at 8.8 kPa, is primarily driven
case 4 is attributed to the eccentricity that causes a bend, which is
by asymmetries in the flow field resulting from the off-centered geom-
clearly visible in Fig. 17(e). The relatively high deformation in case 1 is
etry. In symmetric stenosis (case 3), the flow remains aligned along the
due to moderate stiffness at the stenosis compared to cases 2 and 3.
centerline, forming symmetric shear layers and vortices downstream
Total deformation can become significant based on the pathological
[Fig. 10(c)]. In contrast, the eccentric narrowing in case-4 [Fig. 10(d)]
situation of the stenotic shape. A multimedia file (Video 4), which is
causes jet deflection toward the thinner side of the arterial wall, leading
an integral part of Fig. 17, is available online. It illustrates the variation
to highly asymmetric shear layers and unbalanced vortex formation.
in total deformation of the artery wall for each case (1–4) during the
These large-scale vortices impinge more forcefully on specific regions
sixth cardiac cycle from T-1 to T-7.
of the wall, especially downstream of the eccentric throat. The asym-
metrical shear layer breakdown promotes localized regions of elevated
2. Stresses on the arterial wall
vorticity and pressure fluctuations, which directly translate into non-
von Mises stress is highly significant in arterial mechanics, as it uniform surface forces acting on the vessel wall.
provides a critical measure for understanding how the artery wall Structurally, this asymmetric loading leads to uneven deforma-
responds to the pulsatile nature of blood flow. Figure 18 (Multimedia tion, with the thinner side of the wall undergoing significantly more
view) illustrates von Mises stress over one cardiac cycle across all cases, displacement than the thicker region. This differential deformation
with a correlation of stress distribution between the inner and outer produces stress concentration zones, particularly near the transition
surfaces of the artery wall. Finally, a comparative graph of stress gener- between thick and thin wall segments. The spatial redistribution of
ation on the inner and outer surfaces has been plotted to analyze stress stress is further intensified by the unsteady, skewed pressure fields gen-
variation under different case conditions. erated by flow separation and recirculation zones, which are more pro-
In case 1, maximum von Mises stress is observed downstream of nounced in the eccentric case. As a result, the von Mises stress
the stenosis, resulting from the 50% constriction inflow and increased accumulates in regions subjected to both high curvature and concen-
stiffness of the stenotic region. High-stress concentrations occur at the trated fluid forces. This combined effect of flow-induced asymmetry
edges of the stenosis where the stiffer region meets the more compliant and geometric eccentricity explains the higher wall stress observed in
section of the artery. The stress distribution on the inner and outer case 4 and highlights the complex fluid–structure interactions that

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-24

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 18. von Mises stresses on the arterial wall, including the whole-body view and XY cross-sectional view with inner and outer stress distributions: (a) case 1, (b) case 2, (c)
case 3, (d) case 4, (e) graph showing maximum von Mises stress at the inner surface of the artery over one cardiac cycle for all cases, and (f) graph showing von Mises stress
at the outer surface of the artery over one cardiac cycle for all cases. Multimedia available online.

emerge in eccentric vascular pathologies. A multimedia file (Video 5), mechanical environment in the stenotic region, aiding in the predic-
which is an integral part of Fig. 18, is available online. It illustrates the tion of disease progression and guiding therapeutic interventions.
variation in von Mises stress on the arterial wall for each case (1–4) In case 1, at T-3, stress levels are moderate, and the deformation
during the sixth cardiac cycle from T-1 to T-7. vector is directed toward the distal side due to the peak systolic phase.
At T-4, stress decreases compared to T-3 due to the deceleration phase
of the cardiac cycle, and the deformation vector shifts toward the prox-
3. Temporal variations in deformation and stress of
imal side or upstream of the stenosis. At T-5, stress reaches its mini-
artery wall
mum, and the deformation vector moves laterally toward the stenosis
wall at the start and medially from the wall at the end of the stenosis.
Deformation and stress at five cardiac phases, T-3 to T-7, in the At T-6, stress levels are moderate, and the deformation vector is
stenotic region are shown in Fig. 19 (Multimedia view). Total deforma- aligned toward the proximal side with moderate magnitude. At T-7,
tion and von Mises stress offer a—comprehensive view of the stress increases compared to T-6, and the vectors align toward the

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-25

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 19. Temporal evolution of stress distribution and deformation vectors in the stenotic region, illustrated through XY cross-sectional contours across five cardiac phases (T-3
to T-7). Each row represents different cases: (a) case 1, (b) case 2, (c) case 3, and (d) case 4. The visualizations highlight the dynamic changes in mechanical behavior, show-
casing variations in stress concentration and deformation patterns influenced by pathological severity during the cardiac cycle. Multimedia available online.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-26

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

proximal side with a higher magnitude, as shown in Fig. 19(a). Due to reaches a minimum, and deformation vectors move downstream of
the 50% constriction, the von Mises stress combines stress acting on the aneurysm in the distal direction with increased magnitude. At T-6,
the arterial wall and elevated stress in the stenotic region, indicating stress rises, and the deformation vectors shift upstream toward the
high mechanical loading, which are more significant risk of rupture or proximal direction with increased magnitude. At T-7, stress remains
structural damage. In case 2, at T-3, stress is moderate and evenly dis- elevated, and the deformation vectors continue moving upstream of
tributed along the length of the stenosis, with deformation vectors the aneurysm in the proximal direction. Figure 20(c) shows the tempo-
directed downstream of the stenosis in the distal direction. At T-4, ral changes in stress and deformation for case 3. At T-3, stress is high-
stress decreases compared to T-3, and the deformation vectors shift est at the beginning of the aneurysm, with deformation vectors
upstream toward the proximal direction. At T-5, stress reaches a mini- moving downstream of the aneurysm in the distal direction with mod-
mum across the stenosis, with deformation vectors directed laterally at erate magnitude. At T-4, stress decreases, and the deformation vectors
the beginning of the stenosis and toward the distal side at the end. shift laterally toward the aneurysm wall with reduced magnitude. At
At T-6, stress is moderate, and the deformation vectors align T-5, stress reaches its minimum, and the deformation vectors move
upstream toward the proximal side with moderate magnitude. At T-7, distally with increased magnitude. At T-6, stress rises, and the defor-
stress slightly increases compared to T-6, and deformation vectors mation vectors shift toward the proximal direction. At T-7, stress fur-
move upstream with maximum magnitude in the proximal direction, ther increases compared to T-6, with deformation vectors moving
as shown in Fig. 19(b). In case 3, with maximum constriction of 90% upstream of the aneurysm in the proximal direction with high magni-
and significantly higher stiffness than in all other cases, stress at T-3 is tude. Figure 20(d) illustrates the temporal changes in stress and defor-
moderate, and the deformation vector is directed downstream of the mation at the aneurysm for case 4. At T-3, stress is at its maximum,
stenosis in the distal direction. At T-4, stress decreases, and the defor- and deformation vectors move toward the aneurysm wall in the medial
mation vector shifts laterally toward the stenosis wall with low magni- direction with low magnitude. At T-4, stress decreases, and the defor-
tude. At T-5, stress remains low, and the deformation vector changes mation vectors shift laterally. At T-5, stress reaches its minimum, with
direction toward the downstream side of the stenosis in the distal deformation vectors continuing to move in the lateral direction. At T-
direction with increased magnitude. At T-6, stress rises in the stenosis, 6, stress increases, and the deformation vectors move laterally with
and the deformation vector changes direction toward the upstream increased magnitude. At T-7, stress further rises from T-6, and the
side in the proximal direction. At T-7, stress remains high, and the deformation vectors continue moving laterally with high magnitude. A
deformation vector moves toward the proximal side with high magni- multimedia file (Video 7), which is an integral part of Fig. 20, is avail-
tude, as shown in Fig. 19(c). In case 4, with asymmetric stenosis, stress able online. It illustrates the variation in total deformation vector varia-
at T-3 is moderate, and the deformation vector is directed medially tion at aneurysm for each case (1–4) during the sixth cardiac cycle
with low magnitude. At T-4, stress decreases while the deformation from T-1 to T-7.
vector shifts laterally with increased magnitude. At T-5, stress remains
low in the stenosis, and the deformation vector maintains the same 4. Hemodynamics and biomechanical interactions
direction as at T-4. At T-6, stress increases, and the deformation vector
shifts laterally with further increased magnitude. The FSI investigation offers practical implications for clinical
At T-7, behavior is like that observed at T-6, as shown in decision-making, particularly for identifying rupture risk as atheroscle-
Fig. 19(d). A multimedia file (Video 6), which is an integral part of rotic constrictions in the arterial flow path create an adverse pressure
Fig. 19, is available online. It illustrates the variation in total deforma- gradient downstream of the stenosis, promoting the formation of
tion vector variation at stenosis for each case (1–4) during the sixth eddies and vorticity. This high flow increases wall shear stress on the
cardiac cycle from T-1 to T-7. arterial walls in the downstream region, leading to endothelial layer
Temporal changes in stress and deformation for aneurysm at five thinning, which can result in rupture and thrombus formation. In all
cardiac phases (T-3 to T-7) for all cases have been illustrated in Fig. 20 cases showing heightened stress or significant total deformation, inter-
(Multimedia view). In case 1, at T-3, the stress is maximum at the start ventional measures such as stenting or arterial wall reinforcement may
of the aneurysm, and deformation vectors are moving downstream of be prioritized to counter localized peak stresses. Areas with pro-
the aneurysm in the distal direction [Fig. 20(a)]. At T-4, stress is less at nounced gradients of WSS or elevated RRT underscore regions at risk
the aneurysm region compared to T-3, and the deformation vector for pathophysiological changes like thrombus formation, guiding early
moves toward the proximal to the distal direction at the aneurysmal intervention. By identifying high-risk zones and their underlying
region. At T-5, stress is minimum, and the deformation vector moves dynamics, FSI serves as an indispensable tool for developing patient-
toward the downstream stenosis with a low magnitude direction change specific strategies that improve surgical outcomes and minimize rup-
from lateral to distal. At T-6, the stress is increased, and the deformation ture risks through an accurate understanding of arterial biomechanics.
vector moves upstream of the aneurysm toward the proximal direction In case 1, total deformation reaches 0.35 mm, attaining a peak
with moderate magnitude. At T-7, stress increased at the aneurysmal early in the cardiac cycle. Here, moderate WSS is observed, and while
region, and the deformation vector moved toward the proximal direc- vorticity forms primarily downstream, the vortices remain weak and
tion with high magnitude. Figure 20(b) illustrates the temporal changes localized due to lower stenosis severity. This localized flow pattern sus-
in stress and deformation for case 2. At T-3, stress is high at the start of tains stable WSS levels, preventing extreme stress concentrations on
the aneurysm, and deformation vectors move downstream of the steno- the wall. Despite the presence of vortices and oscillatory shear in this
sis in the distal direction with moderate magnitude. moderate stenosis, von Mises stress is notably higher than in more
At T-4, stress decreases, and the deformation vectors shift later- severe cases, causing sustained less distributed wall loading. The result
ally toward the aneurysm wall with low magnitude. At T-5, stress is a gradual build-up of stress along the artery, especially in the neck

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-27

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

FIG. 20. Temporal progression of stress

distribution and deformation vectors in the
aneurysmal region, depicted through XY
cross-sectional contours across five car-
diac phases (T-3 to T-7). Each row corre-
sponds to different cases: (a) case 1, (b)
case 2, (c) case 3, and (d) case 4. The
illustrations highlight dynamic variations in
stress concentration and deformation
behavior influenced by pathological
changes during the cardiac cycle, offering
insights into the mechanical response of
the arterial wall. Multimedia available
online.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-28

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

and aneurysmal region, indicating a low yet more negligible risk for represent blood flow behavior across varying shear rate regimes.
potential vascular remodeling. Furthermore, the use of idealized geometries in the current study
Case 2 exhibits increased WSS and more pronounced vorticity, presents another limitation in terms of human anatomy. The future
with a total deformation of 0.09 mm. The more significant stenosis scope aims to conduct fully coupled two-way FSI simulations across a
constriction accelerates the blood flow, amplifying the Q-criterion val- broader range of pathological scenarios, incorporating layer-specific
ues and enhancing vortex formation just beyond the stenotic region. arterial wall models, patient-specific models, material properties, and
This high-shear flow exerts elevated WSS gradients along the arterial physiologically relevant boundary conditions. These efforts are
wall, intensifying the shear oscillations near the aneurysm. These oscil- expected to enhance the accuracy and clinical relevance of hemody-
lations propagate more strongly here than in case 1, increasing the like- namic analyses in future cardiovascular modeling studies and treat-
lihood of endothelial damage and further inflammation. This ment planning.
constriction raises von Mises stress to nearly the same level as in case 1
but with more spatial fluctuation, suggesting a focused yet periodically VI. CONCLUSIONS
high-loading pattern that could intensify arterial stiffness over time. This study investigates the interplay between hemodynamics and
Case 3, with its significant constriction to 90%, leads to an even biomechanics in arteries with coexisting stenosis and aneurysms using
more pronounced hemodynamic and structural response. Total defor- one-way FSI. The findings highlight the significant impact of stenosis
mation, though relatively low at 0.17 mm, is marked by sharply ele- severity and geometry on flow dynamics and arterial mechanics, shap-
vated WSS values and substantial flow acceleration. The Q-criterion ing disease progression. The key outcomes from this analysis are sum-
identifies high vortex trails, especially in the post-stenotic region, indi- marized as follows:
cating significant flow disturbance. These disturbed vorticity regions
1. Stenosis severity and eccentricity greatly influence vortical
create high WSS and OSI fluctuations, amplifying wall stresses across
dynamics. For stenosis 70%, vortices are weak and transient.
the stenotic region and extending distally, with von Mises stress reach-
However, stenosis >70% (case 3–4) leads to intense, persistent
ing near-maximum levels at 3.5 kPa. The severe flow disruption from
vortices due to strong flow disturbances. Eccentric stenosis adds
these vortices not only affects the endothelial lining but also promotes
localized strain within the wall, correlating with regions of high asymmetry, causing wall-adjacent vortex migration and pro-
TAWSS and potentially signaling areas prone to aneurysmal progres- longed disturbances. Overall, stenosis beyond 70% and eccentric-
sion with rupture risk. ity significantly amplify vortex strength, complexity, and
In case 4, introducing eccentricity of degree 0.75 with 70% steno- asymmetry.
sis exhibits unique dynamics that shift stress profiles despite the sever- 2. Increasing stenosis severity (>70%) significantly elevates hemo-
ity of stenosis. Here, total deformation surges to 1.9 mm, notably dynamic indicators—OSI, RRT, ECAP, HOLMES, and WSSG,
delayed to the later part of the cardiac cycle, an effect resulting from indicating greater flow disturbances, thrombus risk, and aneu-
flow redistribution due to the asymmetry. The eccentricity mitigates rysm progression, especially in 90% stenosis (case 3). Eccentricity
WSS overshoot by redistributing shear forces along a broader surface redistributes shear stress, reducing localized stress, but maintains
area and dissipating intense vortices that otherwise localize in symmet- complex flow patterns, influencing aneurysm dynamics (case 4).
ric models. This diffused stress pattern lowers peak von Mises stress to While eccentricity moderates risks, severe stenosis still drives
8.8 kPa, effectively distributing wall stress and minimizing the risk of pronounced pathological changes.
abrupt failure. However, OSI remains elevated along asymmetrically 3. FSI reveals pulsatile flow dynamics significantly influence arterial
concentrated flow zones, creating sustained low-shear, high-residence wall deformation, with stenosis severity and geometry playing
areas that may still contribute to thrombus developments. key roles. Eccentric stenosis (case 4) exhibits the highest defor-
mation of 1.9 mm due to asymmetric flow patterns causing
V. LIMITATIONS AND FUTURE SCOPE uneven wall loading and bending stresses, while severe symmet-
This study focused on specific boundary and flow conditions rep- ric stenosis (case 3) shows lower deformation of 0.17 mm due to
resenting a particular physiological state, such as a defined heart rate increased wall stiffness. This highlights the role of flow asymme-
under certain activity levels for an individual with a specified age, sex, try in modulating arterial wall mechanics.
body mass index (BMI), and geographical background. One of the key 4. The interaction between disturbed flow and arterial structure
limitations of this study lies in the use of one-way fluid–structure inter- leads to localized stress concentrations, which is critical for
action (FSI), which, although significantly more computationally effi- assessing rupture risk. von Mises stress peaks in eccentric cases
cient than two-way FSI, may lead to an underestimation of certain being 8.8 kPa in case 4 due to redistributed shear forces from
hemodynamic parameters—particularly in regions experiencing large asymmetric flow, while severe symmetric stenosis (case 3) causes
wall deformations or complex fluid–solid interactions. While the one- highly localized stress regions linked to elevated OSI and WSSG.
way approach offers a practical trade-off between computational cost These stress concentrations, especially near stenosis and aneu-
and accuracy, it does not fully capture the bidirectional coupling rysm interfaces, increase the likelihood of endothelial damage,
between blood flow and arterial wall mechanics. Preliminary compari- vascular remodeling, and potential wall failure.
sons with two-way FSI demonstrate that the fully coupled model pro- 5. Biomedically, FSI modeling shows that severe stenosis (>70%),
vides a more realistic depiction of wall stress and deformation, especially 90% stenosis, greatly increases wall stress and rupture
especially in stenosed geometries. Additionally, while a non- risk, requiring urgent medical attention. While eccentric stenosis
Newtonian Carreau model was employed for selected simulations in reduces localized stress, it creates complex flow patterns that still
this study, future work will extend this analysis by incorporating a pose vascular risks. These insights support patient-specific
broader range of non-Newtonian rheological models to better assessments for targeted clinical interventions.

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-29

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

ACKNOWLEDGMENTS RRT Relative residence time

r Undeformed section radius
The authors acknowledge the financial support provided by
the Indian Council of Medical Research (ICMR), India (GIA/2019/ TAWSS Time average wall shear stress
000607/PRCGIA IRIS cell, ICMR, ID. No. 2020-9527) for carrying WSSG Wall shear stress gradient
out this research work. Xf Initial state
f
Xt Fluid domain
Xst Solid domain
AUTHOR DECLARATIONS
Conflict of Interest REFERENCES
The authors have no conflicts to disclose. 1
M. D. Cesare, H. Bixby, T. Gaziano, L. Hadeed, C. Kabudula, D. V. McGhie, J.
Mwangi, B. Pervan, P. Perel, D. Pi~ neiro, S. Taylor, and F. Pinto, World Heart
Ethics Approval Report 2023: Confronting the World’s Number One Killer (World Heart
Federation Geneva, Switzerland, 2023), pp. 1–52.
For this study, no ethical committee approval is required. 2
W. H. Gutstein and C. A. Perez, “Contribution of vasoconstriction to the origin
of atherosclerosis: A conceptual study,” Trends Cardiovasc. Med. 14(7), 257–
Author Contributions 261 (2004).
3
D. F. Young and F. Y. Tsai, “Flow characteristics in models of arterial steno-
Priyanshu Soni: Conceptualization (lead); Data curation (equal); sis—I. Steady flow,” J. Biomech. 6(4), 395–410 (1973).
Formal analysis (lead); Investigation (lead); Methodology (equal); 4
K. Jain, “The effect of varying degrees of stenosis on transition to turbulence in
Software (lead); Validation (equal); Visualization (lead); Writing – oscillatory flows,” Biomech. Model. Mechanobiol. 21(3), 1029–1041 (2022).
review & editing (lead). Abhra Bhattacharyya: Conceptualization
5
M. E. Boghosian and K. W. Cassel, “A pressure-gradient mechanism for vortex
shedding in constricted channels,” Phys. Fluids 25(12), 123603 (2013).
(equal); Investigation (equal); Methodology (equal); Software (equal); 6
G. Lippi, M. Franchini, and G. Targher, “Arterial thrombus formation in car-
Validation (equal); Writing – original draft (equal). Abdullah Y. diovascular disease,” Nat. Rev. Cardiol. 8(9), 502–512 (2011).
Usmani: Conceptualization (equal); Formal analysis (equal); 7
J. M. Dolan, J. Kolega, and H. Meng, “High wall shear stress and spatial gra-
Resources (equal); Supervision (equal); Visualization (equal); Writing dients in vascular pathology: A review,” Ann. Biomed. Eng. 41(7), 1411–1427
– review & editing (equal). Sanjay Kumar Rai: Funding acquisition (2013).
(equal); Project administration (equal); Resources (equal); Supervision
8
S. Choudhury, K. Anupindi, and B. S. V. Patnaik, “Influence of wall shear stress
(equal). B. V. Rathish Kumar: Formal analysis (equal); Project admin- and geometry on the lumen surface concentration of low density lipoprotein in
a model abdominal aortic aneurysm,” Phys. Fluids 31(1), 011901 (2019).
istration (equal); Supervision (equal); Writing – review & editing 9
S. Kumar, R. Subramanyan, K. Ravi Mandalam, V. R. K. Rao, A. K. Gupta, S.
(equal). Joseph, N. Madhavan Unni, and A. Sreenivasa Rao, “Aneurysmal form of aor-
toarteritis (Takayasu’s disease): Analysis of thirty cases,” Clin. Radiol. 42(5),
342–347 (1990).
DATA AVAILABILITY 10
M. Kalra, J. M. Panneton, J. M. Hofer, and J. C. Andrews, “Aneurysm and ste-
The data that support the findings of this study are available from nosis of the celiomesenteric trunk: A rare anomaly,” J. Vasc. Surg. 37(3), 679–
the corresponding author upon reasonable request. 682 (2003).
11
N. C. Ara ujo and C. S. Junqueira, “Combined aneurysm and infrahepatic steno-
sis of the inferior vena cava,” J. Diagn. Med. Sonography 28(6), 307–310 (2012).
12
K. Hassani, M. Navidbakhsh, and M. Rostami, “Modeling of the aorta artery
NOMENCLATURE aneurysms and renal artery stenosis using cardiovascular electronic system,”
Biomed. Eng. Online 6, 22 (2007).
AAAs Abdominal aortic aneurysms 13
G. S. Sangha, A. Busch, A. Acuna, A. G. Berman, E. H. Phillips, M. Trenner,
CAD Computer aided design H. H. Eckstein, L. Maegdefessel, and C. J. Goergen, “Effects of iliac stenosis on
CFD Computational fluid dynamics abdominal aortic aneurysm formation in mice and humans,” J. Vasc. Res.
CT Computed tomography 56(5), 217–229 (2019).
CVDs Cardiovascular diseases
14
M. N. Uddin, K. E. Hoque, and M. M. Billah, “The impact of multiple stenosis
and aneurysms on arterial diseases: A cardiovascular study,” Heliyon 10(5),
D Diameter of artery
e26889 (2024).
Dmax Maximum diameter 15
D. Balzani, A. Heinlein, A. Klawonn, O. Rheinbach, and J. Schr€ oder,
DHR Diameter to height ratio “Comparison of arterial wall models in fluid–structure interaction simulations,”
DOS Degree of stenosis Comput. Mech. 72(5), 949–965 (2023).
ECAP Endothelial cell activation potential 16
S. Kumar, S. K. Rai, B. V. R. Kumar, and O. Shankar, “The pulsatile 3D-
Fa Function of aneurysm Hemodynamics in a doubly afflicted human descending abdominal artery with
iliac branching,” Comput. Methods Biomech. Biomed. Eng. 26(6), 680–699
Fs Function of stenosis
(2022).
FEA Finite element analysis 17
P. M. Panchal, D. S. Hathi, N. K. Shah, and A. M. Lakdawala, “A numerical
FSI Fluid–structure interaction study on pulsatile non-Newtonian hemodynamics in double-fusiform abdomi-
HOLMES High oscillatory low magnitude shear nal aortic aneurysms,” Phys. Fluids 34(3), 031908 (2022).
h Maximum projection of stenosis from centerline 18
M. Timofeeva, A. Ooi, E. K. W. Poon, and P. Barlis, “Numerical simulation of
la Length of aneurysm the blood flow through the coronary artery stenosis: Effects of varying eccen-
ls Length of stenosis tricity,” Comput. Biol. Med. 146(February), 105672 (2022).
19
S. Patel, A. Y. Usmani, and K. Muralidhar, “Effect of aorto-iliac bifurcation and
MRI Magnetic resonance imaging iliac stenosis on flow dynamics in an abdominal aortic aneurysm,” Fluid Dyn.
OSI Oscillatory shear index Res. 49(3), 035513 (2017).

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-30

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

20
K. Maruthi Prasad, “Effects of stenosis and post stenotic dilatation on Jeffrey 39
A. Hussain, M. N. Riaz Dar, and E. M. Tag-eldin, “Effects of stenosis and aneu-
fluid flow in arteries,” Int. J. Res. Eng. Technol. 04(13), 195–201 (2015). rysm on blood flow in stenotic-aneurysmal artery,” Heliyon 9(7), e17788
21
Q. Long, X. Y. Xu, U. K€ohler, M. B. Robertson, I. Marshall, and P. Hoskins, (2023).
“Quantitative comparison of CFD predicted and MRI measured velocity fields 40
M. A. U. Rehman and O. Ekici, “Comparative analysis of mechanical wall shear
in a carotid bifurcation phantom,” Biorheology 39(3–4), 467–474 (2002). stress and hemodynamics to study the influence of asymmetry in abdominal
22
P. N. Williamson, P. D. Docherty, S. G. Yazdi, A. Khanafer, N. Kabaliuk, M. aortic aneurysm and descending thoracic aortic aneurysm,” Phys. Fluids 36(7),
Jermy, and P. H. Geoghegan, “Review of the development of hemodynamic 071904 (2024).
modeling techniques to capture flow behavior in arteries affected by aneurysm, 41
S. S. Varghese, S. H. Frankel, and P. F. Fischer, “Modeling transition to turbu-
atherosclerosis, and stenting,” J. Biomech. Eng. 144(4), 1–13 (2022). lence in eccentric stenotic flows,” J. Biomech. Eng. 130(1), 1–7 (2008).
23 42
A. A. Nejad, Z. Talebi, D. Cheraghali, A. Shahbani-Zahiri, and M. Norouzi, J. Shum, G. Martufi, E. Di Martino, C. B. Washington, J. Grisafi, S. C. Muluk,
“Pulsatile flow of non-Newtonian blood fluid inside stenosed arteries: and E. A. Finol, “Quantitative assessment of abdominal aortic aneurysm geom-
Investigating the effects of viscoelastic and elastic walls, arteriosclerosis, and etry,” Ann. Biomed. Eng. 39(1), 277–286 (2011).
polycythemia diseases,” Comput. Methods Programs Biomed. 154, 109–122 43
T. K. Mittal and N. Marcus, “Imaging diagnosis of aortic stenosis,” Clin.
(2018). Radiol. 76(1), 3–14 (2021).
24
G. Lorenzini and A. Conti, “Numerical transient state analysis of partly 44
S. Kamangar, I. A. Badruddin, N. A. Ahamad, K. Govindaraju, N. Nik-Ghazali,
obstructed haemodynamics using FSI approach,” Cent. Eur. J. Eng. 3, 285–305 N. J. Salman Ahmed, A. Badarudin, and T. M. Yunus Khan, “The influence of
(2013). geometrical shapes of stenosis on the blood flow in stenosed artery,” Sains
25
C. M. Haggerty, M. Restrepo, E. Tang, D. A. De Zelicourt, K. S. Sundareswaran, Malays. 46(10), 1923–1933 (2017).
L. Mirabella, J. Bethel, K. K. Whitehead, M. A. Fogel, and A. P. Yoganathan, 45
R. K. Dash, G. Jayaraman, and K. N. Mehta, “Flow in a catheterized curved
“Fontan hemodynamics from 100 patient-specific cardiac magnetic resonance artery with stenosis,” J. Biomech. 32(1), 49–61 (1999).
studies: A computational fluid dynamics analysis,” J. Thorac. Cardiovasc. Surg. 46
G. Martufi, E. S. Di Martino, C. H. Amon, S. C. Muluk, and E. A. Finol, “Three-
148(4), 1481–1489 (2014). dimensional geometrical characterization of abdominal aortic aneurysms:
26
H. Kamada, M. Nakamura, H. Ota, S. Higuchi, and K. Takase, “Blood flow Image-based wall thickness distribution,” J. Biomech. Eng. 131(6), 1–11 (2009).
47
analysis with computational fluid dynamics and 4D-flow MRI for vascular dis- T. J. Pedley, The Fluid Mechanics of Large Blood Vessels (Cambridge University
eases,” J. Cardiol. 80(5), 386–396 (2022). Press, 1980).
27
A. A. Rostam-Alilou, H. R. Jarrah, A. Zolfagharian, and M. Bodaghi, “Fluid– 48
H. C. Huang, Z. H. Li, and A. S. Usmani, “Finite element analysis for transient
structure interaction (FSI) simulation for studying the impact of atherosclerosis non-Newtonian flow,” in Finite Element Analysis of Non-Newtonian Flow
on hemodynamics, arterial tissue remodeling, and initiation risk of intracranial (Springer London, 1999), pp. 95–128.
aneurysms,” Biomech. Model. Mechanobiol. 21(5), 1393–1406 (2022). 49
P. D. Ballyk, D. A. Steinman, and C. R. Ethier, “Simulation of non-Newtonian
28
E. Tang, Z. Wei, M. A. Fogel, A. Veneziani, and A. P. Yoganathan, “Fluid-struc- blood flow in an end-to-side anastomosis,” Biorheology 31(5), 565–586 (1994).
ture interaction simulation of an intra-atrial fontan connection,” Biology 9(12), 50
S. A. Berger and L. D. Jou, “Flows in stenotic vessels,” Annu. Rev. Fluid Mech.
412–420 (2020). 32(34), 347–382 (2000).
29
C. M. Scotti, A. D. Shkolnik, S. C. Muluk, and E. A. Finol, “Fluid-structure 51
B. M. Johnston, P. R. Johnston, S. Corney, and D. Kilpatrick, “Non-Newtonian
interaction in abdominal aortic aneurysms: Effects of asymmetry and wall blood flow in human right coronary arteries: Transient simulations,”
thickness,” Biomed. Eng. Online 4(1), 22 (2005). J. Biomech. 39(6), 1116–1128 (2006).
30
N. T. Philip, B. S. V. Patnaik, and B. J. Sudhir, “Hemodynamic simulation of 52
K. Perktold and M. Resch, “Numerical flow studies in human carotid artery
abdominal aortic aneurysm on idealised models: Investigation of stress param- bifurcations: Basic discussion of the geometric factor in atherogenesis,”
eters during disease progression,” Comput. Methods Programs Biomed. 213, J. Biomed. Eng. 12(2), 111–123 (1990).
106508 (2022). 53
V. Kannojiya, A. K. Das, and P. K. Das, “Simulation of blood as fluid: A review
31
T. Lone, A. Alday, and R. Zakerzadeh, “Numerical analysis of stenoses severity from rheological aspects,” IEEE Rev. Biomed. Eng. 14, 327–341 (2021).
54
and aortic wall mechanics in patients with supravalvular aortic stenosis,” M. Razzaq, S. Turek, J. Hron, J. F. Acker, F. Weichert, I. Q. Grunwald, C.
Comput. Biol. Med. 135(April), 104573 (2021). Roth, M. Wagner, and B. F. Romeike, “Numerical simulation and bench-
32
N. Nandakumar, K. C. Sahu, and M. Anand, “Pulsatile flow of a shear-thinning marking of fluid-structure interaction with application to hemodynamics,”
model for blood through a two-dimensional stenosed channel,” Eur. J. Mech. in Fundamental Trends in Fluid-Structure Interaction (World Scientific,
B/Fluids 49(Part A), 29–35 (2015). 2010), pp. 171–199.
33
B. Pincombe and J. Mazumdar, “The effects of post-stenotic dilatations on the 55
T. W. Secomb, “Hemodynamics,” Compr. Physiol. 6(2), 975–1003 (2016).
flow of a blood analogue through stenosed coronary arteries,” Math. Comput. 56
P. Soni, S. Kumar, B. R. Kumar, S. K. Rai, A. Verma, and O. Shankar, “A com-
Model. 25(6), 57–70 (1997). prehensive review on CFD simulations of left ventricle hemodynamics:
34
A. M. Abdelwahab, K. S. Mekheimer, K. K. Ali, A. El-Kholy, and N. S. Sweed, Numerical methods, experimental validation techniques, and emerging trends,”
“Numerical simulation of electroosmotic force on micropolar pulsatile blood- J. Braz. Soc. Mech. Sci. Eng. 46(5), 301 (2024).
stream through aneurysm and stenosis of carotid,” Waves Random Complex 57
A. Y. Usmani and K. Muralidhar, “Pulsatile flow in a compliant stenosed asym-
Medium 34(5), 4288–4319 (2024). metric model,” Exp. Fluids 57(12), 1–24 (2016).
35
O. Mutlu, H. E. Salman, H. Al-Thani, A. El-Menyar, U. A. Qidwai, and H. C. 58
W. Elliott, D. Guo, G. Veldtman, and W. Tan, “Effect of viscoelasticity on
Yalcin, “How does hemodynamics affect rupture tissue mechanics in abdomi- arterial-like pulsatile flow dynamics and energy,” J. Biomech. Eng. 142(4), 1–12
nal aortic aneurysm: Focus on wall shear stress derived parameters, time- (2020).
averaged wall shear stress, oscillatory shear index, endothelial cell activation 59
B. M. Learoyd and M. G. Taylor, “Alterations with age in the viscoelastic prop-
potential, and relative residence time,” Comput. Biol. Med. 154, 106609 (2023). erties of human arterial walls,” Circ. Res. 18(3), 278–292 (1966).
36
D. Adamopoulos, G. Rovas, N. Johner, H. M€ uller, and J. Deux, “Left atrial wall 60
W. Zhang, Y. Liu, and G. S. Kassab, “Viscoelasticity reduces the dynamic
shear stress distribution correlates with atrial endocardial electrogram voltage stresses and strains in the vessel wall: Implications for vessel fatigue,” Am. J.
fibrosis patients with atrial fibrillation,” medRxiv (2024). Physiol. Heart Circ. Physiol. 293(4), 2355–2360 (2007).
37
C. Trenti, M. Ziegler, N. Bjarnegård, T. Ebbers, M. Lindenberger, and P. 61
H. E. Salman and Y. Yazicioglu, “Computational analysis for non-invasive
Dyverfeldt, “Wall shear stress and relative residence time as potential risk factors detection of stenosis in peripheral arteries,” Med. Eng. Phys. 70, 39–50
for abdominal aortic aneurysms in males: A 4D flow cardiovascular magnetic (2019).
resonance case–control study,” J. Cardiovasc. Magn. Reson. 24(1), 1–12 (2022). 62
D. N. Ku, D. P. Giddens, C. K. Zarins, and S. Glagov, “Pulsatile flow and ath-
38
A. A. Soares, F. A. Carvalho, and A. Leite, “Wall shear stress-based hemody- erosclerosis in the human carotid bifurcation. Positive correlation between pla-
namic descriptors in the abdominal aorta bifurcation: Analysis of a case study,” que location and low and oscillating shear stress,” Arteriosclerosis 5(3), 293–
J. Appl. Fluid Mech. 14(6), 1657–1668 (2021). 302 (1985).

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-31

Published under an exclusive license by AIP Publishing
 Physics of Fluids ARTICLE pubs.aip.org/aip/pof

63
M. Lei, C. Kleinstreuer, and G. A. Truskey, “A focal stress gradient-dependent 72
P. K. Shah, “Plaque disruption and coronary thrombosis: New insight into
mass transfer mechanism for atherogenesis in branching arteries,” Med. Eng. pathogenesis and prevention,” Clin. Cardiol. 20(S2), 38–44 (1997).
Phys. 18(4), 326–332 (1996). 73
L. Chen, H. Qu, B. Liu, B.-C. Chen, Z. Yang, D.-Z. Shi, and Y. Zhang, “Low or
64
H. A. Himburg, D. M. Grzybowski, A. L. Hazel, J. A. LaMack, X. M. Li, and oscillatory shear stress and endothelial permeability in atherosclerosis,” Front.
M. H. Friedman, “Spatial comparison between wall shear stress measures and Physiol. 15(September), 1–11 (2024).
74
porcine arterial endothelial permeability,” Am. J. Physiol. Heart Circ. Physiol. V. L. Rayz, L. Boussel, L. Ge, J. R. Leach, A. J. Martin, M. T. Lawton, C.
286(5), 1916–1922 (2004). McCulloch, and D. Saloner, “Flow residence time and regions of intraluminal
65
M. Alimohammadi, C. Pichardo-Almarza, O. Agu, and V. Díaz-Zuccarini, thrombus deposition in intracranial aneurysms,” Ann. Biomed. Eng. 38(10),
“Development of a patient-specific multi-scale model to understand atheroscle- 3058–3069 (2010).
rosis and calcification locations: Comparison with in vivo data in an aortic dis- 75
Y. Asaad and N. Korin, “From weakly adhesive to highly thrombogenic: The
section,” Front. Physiol. 7(June), 1–15 (2016). shear gradient switch,” Haematologica 105(10), 2355–2357 (2020).
66 76
C. J. Egelhoff, R. S. Budwig, D. F. Elger, T. A. Khraishi, and K. H. Johansen, O. F. Barak, S. Mladinov, R. L. Hoiland, J. C. Tremblay, S. R. Thom, M. Yang, T.
“Model studies of the flow in abdominal aortic aneurysms during resting and Mijacika, and Z. Dujic, “Disturbed blood flow worsens endothelial dysfunction in
exercise conditions,” J. Biomech. 32(12), 1319–1329 (1999). moderate-severe chronic obstructive pulmonary disease,” Sci. Rep. 7(1), 1–10 (2017).
67
F. Gijsen, Y. Katagiri, P. Barlis, C. Bourantas, C. Collet, U. Coskun, J. Daemen, 77
M. A. Gimbrone and G. García-Carde~ na, “Endothelial cell dysfunction and the
J. Dijkstra, E. Edelman, P. Evans, K. Van Der Heiden, and R. Hose, “Expert rec- pathobiology of atherosclerosis,” Circ. Res. 118(4), 620–636 (2016).
78
ommendations on the assessment of wall shear stress in human coronary arter- M. Zhou, Y. Yu, R. Chen, X. Liu, Y. Hu, Z. Ma, L. Gao, W. Jian, and L. Wang,
ies: Existing methodologies, technical considerations, and clinical applications,” “Wall shear stress and its role in atherosclerosis,” Front. Cardiovasc. Med.
Eur. Heart J. 40, 3421–3433 (2019). 10(April), 1–11 (2023).
68
A. M. Shaaban and A. J. Duerinckx, “Wall shear stress and early atherosclero- 79
V. Peiffer, S. J. Sherwin, and P. D. Weinberg, “Does low and oscillatory wall
sis: A review,” Am. J. Roentgenol. 174(6), 1657–1665 (2000). shear stress correlate spatially with early atherosclerosis? A systematic review,”
69
H. Samady, P. Eshtehardi, M. C. McDaniel, J. Suo, S. S. Dhawan, C. Maynard, Cardiovasc. Res. 99(2), 242–250 (2013).
L. H. Timmins, A. A. Quyyumi, and D. P. Giddens, “Coronary artery wall shear 80
S. S. Dhawan, R. P. A. Nanjundappa, J. R. Branch, W. R. Taylor, A. A. Quyyumi,
stress is associated with progression and transformation of atherosclerotic pla- H. Jo, M. C. McDaniel, J. Suo, D. Giddens, and H. Samady, “Shear stress and pla-
que and arterial remodeling in patients with coronary artery disease,” que development,” Expert Rev. Cardiovasc. Ther. 8(4), 545–556 (2010).
81
Circulation 124(7), 779–788 (2011). T. Ziegler, K. Bouzourene, V. J. Harrison, H. R. Brunner, and D. Hayoz,
70
K. Sunderland, J. Jiang, and F. Zhao, “Disturbed flow’s impact on cellular “Influence of oscillatory and unidirectional flow environments on the expres-
changes indicative of vascular aneurysm initiation, expansion, and rupture: A sion of endothelin and nitric oxide synthase in cultured endothelial cells,”
pathological and methodological review,” J. Cell. Physiol. 237(1), 278–300 Arterioscler. Thromb. Vasc. Biol. 18(5), 686–692 (1998).
(2022). 82
D. Lopes, H. Puga, J. C. Teixeira, and S. F. Teixeira, “Influence of arterial
71
A. Sanyal and H. C. Han, “Artery buckling affects the mechanical stress in ath- mechanical properties on carotid blood flow: Comparison of CFD and FSI
erosclerotic plaques,” Biomed. Eng. Online 14(Suppl 1), S4 (2015). studies,” Int. J. Mech. Sci. 160(January), 209–218 (2019).

Phys. Fluids 37, 071913 (2025); doi: 10.1063/5.0263599 37, 071913-32

Published under an exclusive license by AIP Publishing