The Localized Hemodynamics [6].

However, LST may also be promoted by the nonphysiological

hemodynamics of stented vessels, in conjunction with these
of Drug-Eluting Stents Are known risk factors [6].
These nonphysiological hemodynamics can arise due to the
Not Improved by the Presence obstructing presence of the stent struts, as can be seen in Fig. 1.
of Magnetic Struts Wall shear stresses (WSS)—the tangential stress imparted on the
vessel wall by the viscous drag of flowing blood—fall to low lev-
els in the recirculation zones which form adjacent to the struts.
P. R. S. Vijayaratnam Low WSS may promote LST by inhibiting the proliferation of
School of Mechanical and Manufacturing Engineering, anticoagulant-expressing endothelial cells and retarding the endo-
thelial coverage of arterial and strut surfaces [6,7]. High WSS
University of New South Wales,
peaks over the strut corners may further promote LST by activat-
Sydney 2052, Australia ing platelets to release platelet-aggregating factors, such as throm-
e-mail: p.vijayaratnam@unsw.edu.au boxane A2 and adenosine diphosphate [6,8]. These activated
platelets can subsequently enter downstream recirculation zones,
T. J. Barber as shown in Fig. 1, and reach high concentrations because of the
School of Mechanical and Manufacturing Engineering, nature of flow in separated regions [6]. This aggregation of plate-
University of New South Wales, lets, combined with the reduction of anticoagulant-expressing
endothelial cells in low WSS regions, may trigger thrombus
Sydney 2052, Australia
formation [6].
e-mail: t.barber@unsw.edu.au The feasibility of implementing magnetic DES struts to allevi-
ate these prothrombotic hemodynamics is assessed in this numeri-
J. A. Reizes cal study from a fluid dynamics perspective. Blood, a biomagnetic
School of Mechanical and Manufacturing Engineering, fluid, experiences two forces when in the vicinity of magnets: (1)
University of New South Wales, magnetization forces which reorient red blood cells to align with
Sydney 2052, Australia the magnetic field and (2) Lorentz forces which oppose the flow
of blood [9]. The aim of this study is to investigate whether these
e-mail: j.reizes@unsw.edu.au
forces can locally affect blood flow in a manner that alleviates the
nonphysiological WSS which precipitate LST.

The feasibility of implementing magnetic struts into drug-eluting Methods

stents (DESs) to mitigate the adverse hemodynamics which pre-
cipitate stent thrombosis is examined. These adverse hemodynam- Geometry. To investigate these aims, a series of two-
ics include platelet-activating high wall shear stresses (WSS) and dimensional computational fluid dynamics (CFD) simulations
endothelial dysfunction-inducing low wall shear stresses. By mag- were performed using the idealized stented-vessel geometry
netizing the stent struts, two forces are induced on the surround- depicted in Fig. 2. In this geometry, the vessel lumen was modeled
ing blood: (1) magnetization forces which reorient red blood cells as a 3-mm tall fluid domain with a single 0.1-mm square cross
to align with the magnetic field and (2) Lorentz forces which
oppose the motion of the conducting fluid. The aim of this study
was to investigate whether these forces can be used to locally
alter blood flow in a manner that alleviates the thrombogenicity of
stented vessels. Two-dimensional steady-state computational fluid
dynamics (CFD) simulations were used to numerically model
blood flow over a single magnetic drug-eluting stent strut with a
square cross section. The effects of magnet orientation and mag-
netic flux density on the hemodynamics of the stented vessel were
elucidated in vessels transporting oxygenated and deoxygenated
blood. The simulations are compared in terms of the size of sepa-
rated flow regions. The results indicate that unrealistically strong
magnets would be required to achieve even modest hemodynamic
improvements and that the magnetic strut concept is ill-suited to
mitigate stent thrombosis. [DOI: 10.1115/1.4035263]
Fig. 1 The prothrombotic effects of nonphysiological wall
Introduction shear stresses
Despite the success of drug-eluting stents (DESs) in restoring
blood flow to arteries occluded by plaque, the issue of late stent
thrombosis (LST) has continued to cause concerns over the long-
term safety of these devices. The likelihood of LST—typically
defined as thrombus formation in a stented artery more than 30
days after stent implantation [1]—is rare and occurs in just
0.2–0.7% of DES patients [2–4]; however, mortality rates as high
as 45% and an additional nonfatal myocardial infarction rate of
30–40% have been associated with this disease [2,5]. The cause of
LST is multifactorial, with documented risk factors including
patient factors such as diabetes mellitus, as well as procedural and
stent factors such as stent undersizing and delayed arterial healing
Fig. 2 Geometry and boundary conditions. A single 0.1-mm
square cross section DES strut was positioned halfway
Manuscript received April 17, 2016; final manuscript received November 4, between the inlet and outlet with one side of the strut in direct
2016; published online November 30, 2016. Assoc. Editor: Ram Devireddy. contact with the vessel wall.

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 section DES strut positioned halfway between the inlet and outlet.
One side of the strut was in direct contact with the vessel wall,
while the other three sides were exposed to luminal blood flow.
The dimensions used were consistent with those used in our prior
analysis of stent-based drug therapy in the renal vasculature [10],
reflecting the current clinical interest in noncoronary vessels
[11–14]. Furthermore, the square-edged, two-dimensional nature
of the geometry enabled the modeling of a worst-case scenario in
which the flow is perpendicular to the strut and in which flow dis-
turbances are maximized. This made it the ideal geometry for
studying the validity of the magnetic DES concept.
negative magnetic susceptibility [18], voxyg ¼ 6.6  107.
Conversely, deoxygenated blood is paramagnetic, signifying that
it is attracted toward the direction of increasing magnetic field
intensity; thus, it has a positive magnetic susceptibility [19],
vdeoxyg ¼ 3.5  106. Both v values were implemented to broaden
the range of stented-vessel environments in which the feasibility
of the magnetic DES concept was evaluated. Finally, the magnet-
ization field and the magnetic field were assumed to be parallel,
enabling the magnetization force in Eq. (2) to be rewritten as
FM ¼ l0 MrH (9)

where M ¼ |M| and H ¼ |H|.

Mathematical Model. The blood flowing through this ideal- The solution of Eqs. (1)–(9) was accomplished through the
ized geometry was modeled using a combination of the continuity use of the finite volume solver ANSYS FLUENT 14.5 (ANSYS, Inc.,
(Eq. (1)), momentum (Eq. (2)), and Maxwell equations Canonsburg, PA). A semi-implicit (SIMPLEC) algorithm coupled
(Eqs. (3)–(7)) the pressure and velocity, while a second-order central differenc-
ing scheme spatially discretized the pressure and momentum vari-
$V¼0 (1) ables. A second-order upwind scheme was used to discretize the
1" # Cartesian components of the induced magnetic field vector. The
ðV  $ÞV ¼ $2 V þ $P þ J|fflffl 0 ðM  $ÞH
q ffl} þ l
{zfflB |fflfflfflfflfflfflffl
ffl{zfflfflfflfflfflfflfflffl}
(2) inbuilt magnetohydrodynamics module of ANSYS FLUENT 14.5 was
FL M
used to calculate the Lorentz body force, while the magnetization
F
body force was implemented into the solver using user-defined
$  B ¼ $  ½l0 ðH þ MÞ ¼ 0 (3) functions.
$J¼0 (4)
Boundary Conditions. In the process of resolving these body
$H¼J (5) forces, the magnetic fields surrounding the stent strut boundary
were defined in the same way as the fields surrounding infinitely
J ¼ rðE þ V  BÞ ¼ rðrU þ V  BÞ (6)
long permanent rectangular magnets. The intensity of these mag-
2 netic fields, H, is related to the magnetic flux density, B, by the
$ U ¼ $  ðV  BÞ (7)
equation B ¼ l0 (M þ H); however, as M  H, the simplified
V is the velocity vector of blood in the lumen (m/s) and $ is the form, B ¼ l0H, was used in this analysis. Two magnetic flux den-
gradient operator. In the momentum equation, q is the blood sity field configurations were studied: the first with poles at the
density (kg/m3),  is the kinematic viscosity of blood (m2/s), P is top and bottom of the strut and the second with poles facing fore
the thermodynamic pressure (Pa), and t is the time (s). The two and aft of the strut. The x- and y-components of the first configura-
additional body forces, FL (N/m3) and FM (N/m3), act on the tion are described [20] as
blood due to interactions with the magnetic field; FL is the Lor-
entz force, which opposes the motion of electrically conducting Bx ð x; yÞ
8 " # " #9
fluids in an imposed magnetic fields, and FM is the magnetization
force, which is an attractive or repulsive response to magnetic l0 MS < ð x þ wÞ2 þ ð y  hÞ2 ð x  wÞ2 þ ð y  hÞ2 =
¼ ln  ln
field gradients. In the Maxwell equations, J, B, M, E, and H are 4p : ð x þ wÞ2 þ ð y þ hÞ2 ð x  wÞ2 þ ð y þ hÞ2 ;
the total current density (A/m2), magnetic flux density (T), mag-
netization (A/m), electric field intensity (V/m), and magnetic field (10)
intensity (A/m), respectively. l0 is the permeability of free space
and
(H/m), r is the electrical conductivity of blood (S/m), and finally,
U is an electric potential field (V) resulting from the movement of By ð x;yÞ
blood within the magnetic field. 8 ! !9
Several assumptions were used to simplify this hemodynamic l0 MS < 1 2hð xþwÞ 2h ð xw Þ =
model. Blood was modeled with a uniform density, q ¼ 1060 ¼ tan 2
tan1 2
2p : ð xþwÞ þy2 h2 ð xwÞ þy2 h2 ;
kg/m3, and laminar flow conditions were assumed due to the low
Reynolds numbers (Re < 1300 [15]) in the renal vasculature. A (11)
constant viscosity of  ¼ 3.3  106 m2/s, based on blood’s lowest
viscosity limit, was ascribed to the blood as it yields more exag- while the components of the second configuration are described
gerated recirculating flow regions than other blood rheological [20] as
models [10]. Furthermore, blood was modeled as a conducting
fluid with a constant electrical conductivity of r ¼ 0.8 S/m. This
Bx ð x;yÞ
conductivity has been measured to be 0.7 S/m in stationary blood ( ! !)
[16] and increases by 10% when subjected to medium shear l0 MS 1 2wð yþhÞ 1 2wð yhÞ
rates as viscous forces alter erythrocyte orientation [17]. Conduc- ¼ tan tan
2p ð yþhÞ2 þx2 w2 ð yhÞ2 þx2 w2
tivity is also dependent on temperature and hematocrit, although
these effects and the effect of shear rate were neglected for (12)
simplicity. Additionally, a simplified magnetization model was
implemented in which temperature and density dependencies and
were neglected. In this model,
By ð x; yÞ
M ¼ vH (8) ( " # " #)
l MS ð y þ hÞ2 þ ð x  wÞ2 ð y  hÞ2 þ ð x  wÞ2
where v is the magnetic susceptibility of blood. Oxygenated blood ¼ 0 ln 2
 ln 2
4p ð y þ hÞ2 þ ð x þ wÞ ð y  hÞ2 þ ð x þ wÞ
is diamagnetic, indicating that it is repelled away from the direc-
tion of increasing magnetic field intensity, so that it possesses a (13)

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Fig. 3 Magnetic flux density contours of the magnetic DES
strut used in this study. The magnet has been modeled as an
infinitely long permanent rectangular magnet with height
2h 5 70 lm and width 2w 5 70 lm. The cases in which Bmax 5 1
T are depicted for the configurations in which the poles are (a)
on the top and bottom strut faces and (b) on the fore and aft
strut faces. Note that the positions of the north and south poles
are interchangeable in each case and do not affect the results.
On the assumption of a coating thickness of 15 lm, the height and
width of the infinitely long permanent rectangular magnet in both
configurations were 2h ¼ 2w ¼ 70 lm. The value of MS was varied
in order to yield peak magnetic flux densities of Bmax ¼ 0 T, 4 T,
and 8 T at the strut surface. The magnetic flux density fields of the
top–bottom pole configuration and the fore–aft pole configuration
are visualized in Figs. 3(a) and 3(b), respectively, for a case where
Bmax ¼ 1 T.
Except these changes in magnet strength and orientation, all the
hemodynamic boundary conditions remained the same in each
Fig. 4 The magnetically altered hemodynamics of oxygenated blood in a vessel with a well-
apposed DES strut: (a) top–bottom and (b) fore–aft
Journal of Biomechanical Engineering
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simulation. A steady, fully developed inlet velocity profile corre-
sponding to a Reynolds number of 427 was used, consistent with
mean flow conditions in the renal vasculature [21]. A uniform,
zero gauge pressure boundary condition was specified at the out-
let, while no-slip conditions were assigned to the strut–lumen and
lumen–tissue interfaces. A symmetry boundary condition was also
specified at the top of the lumen domain, as shown in Fig. 2.
Finally, the arterial wall was treated as rigid and electrically insu-
lating (i.e., @U/@n ¼ 0, where n is the direction normal to the
wall), while zero-induced magnetic flux density at the inlet and
outlet was also specified.
Grid Description. These same boundary conditions, sans mag-
netic fields, were also used in a series of mesh independence stud-
ies, performed to ensure the reliability of the subsequent magnetic
DES cases. The mesh densities used in these studies were greatest
in the regions closest to the stent strut and also near the arterial
wall. This enabled the resolution of thin boundary layers along the
strut and arterial walls. The flow was deemed to be resolved once
the grid convergence indexes (GCI) corresponding to the lengths
of recirculation zones fell below 2%. This GCI was defined as [22]
 
 ffine  fcoarse 

3 
ffine 
GCIfine grid ¼ (14)
rp  1
where ffine and fcoarse refer to either the proximal or distal recircu-
lation length (mm) for a fine and coarse mesh, respectively; r is
the refinement factor; and p is the order of accuracy of the solu-
tion. Using values of r ¼ 2 and p ¼ 2, the blood flow around the
strut was found to be adequately resolved with a mesh containing
225,064 elements.
JANUARY 2017, Vol. 139 / 014502-3
 Fig. 5 The magnetically altered hemodynamics of deoxygenated blood in a vessel with a
well-apposed DES strut: (a) top–bottom and (b) fore–aft

Table 1 The effect of magnetic flux density and orientation on recirculation length in oxygenated and deoxygenated blood

Magnet orientation Bmax (T) Lproximal (mm) % change Ldistal (mm) % change

Nonmagnetic strut
n/a 0 0.065 n/a 0.115 n/a
Magnetic strut in oxygenated blood
Top–bottom 4.0 0.065 0 0.115 0
Top–bottom 8.0 0.065 0 0.115 0
Fore–aft 4.0 0.065 0 0.116 0.9
Fore–aft 8.0 0.065 0 0.116 0.9
Magnetic strut in deoxygenated blood
Top–bottom 4.0 0.065 0 0.115 0
Top–bottom 8.0 0.064 1.5 0.115 0
Fore–aft 4.0 0.065 0 0.114 0.9
Fore–aft 8.0 0.065 0 0.112 2.6

Results and Discussion
The results obtained using this mesh can be seen in Figs. 4
and 5, respectively. It can be seen in Fig. 4 that oxygenated blood
is only noticeably affected by the presence of the magnetic strut
when the top–bottom configuration magnet is used and when
Bmax ¼ 8 T. This configuration, shown in Fig. 4(a)-(iii), yielded a
slightly taller proximal recirculation zone and an enlarged second-
ary vortex within this zone. Similarly, it can be seen in Fig. 5 that
deoxygenated blood is only noticeably affected by the presence of
a magnetic strut when a top–bottom configuration magnet is
used and when Bmax  4 T. This configuration yielded a proximal
recirculation zone with reduced height and an enlarged secondary
vortex within the distal recirculation zone, as can be seen in
Figs. 5(a)-(ii) and 5(a)-(iii). In contrast, the fore–aft magnet con-
figuration had negligible impact on the hemodynamics of the
stented vessel in either oxygenated or deoxygenated blood.
The differences between Figs. 4 and 5 are due to the different
magnetic susceptibilities of oxygenated and deoxygenated blood,
whereas oxygenated blood is repelled away from the direction of
increasing magnetic flux density, deoxygenated blood accelerates
toward this direction. Hence, as oxygenated blood within the
proximal recirculation zone moves down the strut face—in the
same direction that magnetic flux density increases for the
top–bottom configuration magnet—the blood decelerates. When
the magnet is strong enough, as shown in Fig. 4(a)-(iii), the fluid

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 velocity reduces to zero along the strut face and causes the flow to r¼ refinement factor
separate from that surface. This accounts for the enlarged second- Re ¼ Reynolds number
ary recirculation zone within the proximal recirculation zone of t¼ time, s
Fig. 4(a)-(iii). Similarly, as deoxygenated blood within the distal V¼ velocity vector of blood in the lumen, m/s
recirculation zone moves up the strut face—in the same direction w¼ half-width of an infinitely long permanent rectangular
that magnetic flux density decreases in the top–bottom configura- magnet, m
tion magnet—it decelerates. When the magnet is strong enough, WSS ¼ wall shear stress, Pa
as shown in Fig. 5(a)-(iii), flow separation occurs, establishing the D¼ gradient operator, m1
large secondary vortex within the distal recirculation zone. l0 ¼ permeability of free space, H/m
The differences in height of the proximal recirculation zones in ¼ kinematic viscosity, m2/s
cases involving the top–bottom configuration magnet can simi- q¼ blood density, kg/m3
larly be explained by the differences in magnetic susceptibility. r¼ electrical conductivity of blood, S/m
The magnet causes deoxygenated blood flowing along the top of U¼ electric potential field, V
the proximal recirculation zone to be accelerated toward the strut, v¼ magnetic susceptibility of blood
thereby flattening the recirculation zone. On the other hand, oxy- vdeoxyg ¼ magnetic susceptibility of deoxygenated blood
genated blood flowing along the top of the proximal recirculation voxyg ¼ magnetic susceptibility of oxygenated blood
zone is repelled, thereby extending the height of this recirculation
zone. However, as shown in Table 1, no major reductions to the
proximal or distal recirculation lengths along the lumen were References
observed with either top–bottom or fore–aft pole configurations, [1] Joner, M., Finn, A. V., Farb, A., Mont, E. K., Kolodgie, F. D., Ladich, E.,
in both oxygenated and deoxygenated blood. Hence, the localized Kutys, R., Skorjia, K., Gold, H. K., and Virmani, R., 2006, “Pathology
hemodynamics of drug-eluting stents are not improved by the of Drug-Eluting Stents in Humans,” J. Am. Coll. Cardiol., 48(1),
presence of magnetic struts. pp. 193–202.
[2] Iakovou, I., Schmidt, T., Bonizzoni, E., Ge, L., Sangiorgi, G. M., Stankovic, G.,
Airoldi, F., Chieffo, A., Montorfano, M., Carlino, M., Michev, I., Corvaja, N.,
Conclusion Briguori, C., Gerckens, U., Grube, E., and Colombo, A., 2005, “Incidence,
Predictors, and Outcomes of Thrombosis After Successful Implantation of
In this CFD study, the feasibility of using magnetic DES struts Drug-Eluting Stents,” JAMA, 293(17), pp. 2126–2130.
to mitigate the adverse hemodynamics which precipitate stent [3] Moreno, R., Fernandez, C., Hernandez, R., Alfonso, F., Angiolillo, D. J.,
thrombosis was studied. However, even at unrealistically strong Sabate, M., Escaned, J., Ba~ nuelos, C., Fernandez-Ortiz, A., and Macaya, C.,
magnetic flux densities of 8.0 T, this magnetic strut concept only 2005, “Drug-Eluting Stent Thrombosis: Results From a Pooled
Analysis Including 10 Randomized Studies,” J. Am. Coll. Cardiol., 45(6),
minimally affected the length of the low WSS-producing recircu- pp. 954–959.
lation zones adjacent to the strut. Hence, the magnetic strut [4] Ong, A. T., McFadden, E. P., Regar, E., de Jaegere, P. P., van Domburg, R. T.,
concept was determined to be unsuitable for mitigating the non- and Serruys, P. W., 2005, “Late Angiographic Stent Thrombosis (LAST)
physiological shear stresses that precipitate LST. Events With Drug-Eluting Stents,” J. Am. Coll. Cardiol., 45(12),
pp. 2088–2092.
[5] Pfisterer, M., Brunner-La Rocca, H. P., Buser, P. T., Rickenbacher, P., Hun-
Acknowledgment ziker, P., Mueller, C., Jeger, R., Bader, F., Osswald, S., and Kaiser, C., 2006,
“Late Clinical Events After Clopidogrel Discontinuation May Limit the Benefit
P.V. was supported by an Australian Postgraduate Award schol- of Drug-Eluting Stents: An Observational Study of Drug-Eluting Versus Bare-
arship from the Australian Government Department of Education Metal Stents,” J. Am. Coll. Cardiol., 48(12), pp. 2584–2591.
[6] Koskinas, K. C., Chatzizisis, Y. S., Antoniadis, A. P., and Giannoglou, G. D.,
and Training.1 The funders had no role in the study design, data 2012, “Role of Endothelial Shear Stress in Stent Restenosis and Thrombosis:
collection and analysis, decision to publish, or preparation of the Pathophysiologic Mechanisms and Implications for Clinical Translation,”
manuscript. J. Am. Coll. Cardiol., 59(15), pp. 1337–1349.
[7] Akagawa, E., Ookawa, K., and Ohshima, N., 2004, “Endovascular Stent Con-
figuration Affects Intraluminal Flow Dynamics and In Vitro
Endothelialization,” Biorheology, 41(6), pp. 665–680.
[8] Holme, P. A., Ørvim, U., Hamers, M. J. A. G., Solum, N. O., Brosstad, F. R.,
Nomenclature Barstad, R. M., and Sakariassen, K. S., 1997, “Shear-Induced Platelet Activa-
B¼ magnetic flux density, T tion and Platelet Microparticle Formation at Blood Flow Conditions as in
Arteries With a Severe Stenosis,” Arterioscler. Thromb. Vasc. Biol., 17(4),
Bx ¼ the x-component of the magnetic flux density field, T pp. 646–653.
By ¼ the y-component of the magnetic flux density field, T [9] Tzirtzilakis, E. E., 2005, “A Mathematical Model for Blood Flow in Magnetic
CFD ¼ computational fluid dynamics Field,” Phys. Fluids, 17(7), p. 077103.
DES ¼ drug-eluting stent [10] Vijayaratnam, P. R. S., O’Brien, C. C., Reizes, J. A., Barber, T. J., and
Edelman, E. R., 2015, “The Impact of Blood Rheology on Drug Transport in
E¼ electric field intensity, V/m Stented Arteries: Steady Simulations,” PLoS One, 10(6), p. e0128178.
fcoarse ¼ coarse-grid solution [11] Van Jaarsveld, B. C., Krijnen, P., Pieterman, H., Derkx, F. H. M., Deinum, J.,
ffine ¼ fine-grid solution Postma, C. T., Dees, A., Woittiez, A. J., Bartelink, A. K., Man in ’t Veld, A. J.,
FL ¼ Lorentz force, N/m3 and Schalekamp, M. A., 2000, “The Effect of Balloon Angioplasty on Hyper-
tension in Atherosclerotic Renal-Artery Stenosis,” N. Engl. J. Med., 342(14),
FM ¼ magnetization force, N/m3 pp. 1007–1014.
GCI ¼ grid convergence index [12] White, C. J., Ramee, S. R., Collins, T. J., Jenkins, J. S., Escobar, A., and Shaw,
h¼ half-height of an infinitely long permanent rectangular D., 1997, “Renal Artery Stent Placement: Utility in Lesions Difficult to Treat
magnet, m With Balloon Angioplasty,” J. Am. Coll. Cardiol., 30(6), pp. 1445–1450.
[13] Rocha-Singh, K., Jaff, M. R., and Rosenfeld, K., 2005, “ASPIRE-2 Trial Inves-
H¼ magnetic field intensity, A/m tigators Evaluation of the Safety and Effectiveness of Renal Artery Stenting
J¼ total current density, A/m2 After Unsuccessful Balloon Angioplasty: The ASPIRE-2 Study,” J. Am. Coll.
Ldistal ¼ length of the distal recirculation zone, mm Cardiol., 46(5), pp. 776–783.
Lproximal ¼ length of the proximal recirculation zone, mm [14] Dorros, G., Prince, C., and Mathiak, L., 1993, “Stenting of a Renal Artery Ste-
nosis Achieves Better Relief of the Obstructive Lesion Than Balloon
LST ¼ late stent thrombosis Angioplasty,” Catheterization Cardiovasc. Diagn., 29(3), pp. 191–198.
M¼ magnetization of blood, A/m [15] Yamamoto, T., Ogasawara, Y., Kimura, A., Tanaka, H., Hiramatsu, O.,
MS ¼ magnetization of magnet, A/m Tsujioka, K., Lever, M. J., Parker, K. H., Jones, C. J., Caro, C. G., and Kajiya,
p¼ order of accuracy of the solution F., 1996, “Blood Velocity Profiles in the Human Renal Artery by Doppler
Ultrasound and Their Relationship to Atherosclerosis,” Arterioscler. Thromb.
P¼ the thermodynamic pressure, Pa Vasc. Biol., 16(1), pp. 172–177.
[16] Gabriel, S., Lau, R. W., and Gabriel, C., 1996, “The Dielectric Properties of
Biological Tissues—III: Parametric Models for the Dielectric Spectrum of
1
https://education.gov.au/australian-postgraduate-awards Tissues,” Phys. Med. Biol., 41(11), pp. 2271–2293.

Journal of Biomechanical Engineering JANUARY 2017, Vol. 139 / 014502-5

Downloaded From: http://biomechanical.asmedigitalcollection.asme.org/pdfaccess.ashx?url=/data/journals/jbendy/935860/ on 02/25/2017 Terms of Use: http://www.asme.org/abo

 [17] Frewer, R. A., 1974, “The Electrical Conductivity of Flowing Blood,” Biomed.
Eng., 9(12), p. 552.
[18] Motta, M., Haik, Y., Gandhari, A., and Chen, C. J., 1998, “High Magnetic Field
Effects on Human Deoxygenated Hemoglobin Light Absorption,” Bioelectro-
chem. Bioenerg., 47(2), pp. 297–300.
[19] Haik, Y., Pai, V., and Chen, C. J., 1999, “Biomagnetic Fluid Dynamics,” Fluid
Dynamics at Interfaces, W. Shyy and R. Narayanan, eds., Cambridge
University Press, Cambridge, UK, pp. 439–452.
014502-6 / Vol. 139, JANUARY 2017
Downloaded From: http://biomechanical.asmedigitalcollection.asme.org/pdfaccess.ashx?url=/data/journals/jbendy/935860/ on 02/25/2017 Terms of Use: http://www.asme.org/abo
[20] Furlani, E. P., 2001, Permanent Magnet and Electromechanical Devices:
Materials, Analysis, and Applications, Academic Press, San Diego, CA,
Chap. 4.
[21] O’Brien, C. C., Kolachalama, V. B., Barber, T. J., Simmons, A., and Edelman,
E. R., 2013, “Impact of Flow Pulsatility on Arterial Drug Distribution in Stent-
Based Therapy,” J. Controlled Release, 168(2), pp. 115–124.
[22] Roache, P. J., 1997, “Quantification of Uncertainty in Computational Fluid
Dynamics,” Annu. Rev. Fluid Mech., 29(1), pp. 123–160.
Transactions of the ASME