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An agent-based model of the response to angioplasty and bare-metal stent deployment in an atherosclerotic blood vessel
Authors
A Facoetti
AA Alsheikh-Ali
+75 more
AD Blann
AG Touchard
AL Stahl
Antonia E. Curtin
AR Pries
AS Go
BN Brown
BP Murphy
C Cerletti
C Pappas
CA Dinarello
CI Seye
D Chamie
D Stoeckel
DJ Grainger
DL Fischman
DW Muller
F Otsuka
F Zhang
FD Kolodgie
FG Welt
GS Ashcroft
H Friedman
H Hamid
H Noma
HM Heikkila
HR Poorhosseini
IF Charo
J Pillay
JM Anderson
K Chitkara
K Groschel
K Wasser
KH Lee
Leming Zhou
M Daigneault
M Drakopoulou
M Gawaz
M Homoncik
M Niazi
M Schillinger
M Wildgruber
MA Costa
MP Rodero
MR Ward
MS Chen
MW Majesky
NY Li
P Rangamani
PA DiMilla
PA Suwanabol
PS Monraats
PW Serruys
R Hoffmann
R Virmani
RA Stefanescu
RM Botnar
S Gordon
S Heidenreich
S Mohan
S Tsai
S Waxman
SM Opal
SM Sagnella
SP Karas
SR Mulukutla
T Ferkol
T Kimura
T Kondo
T Thim
TA Meadows
Timothy W. Secomb
V Subban
VL Roger
Y Najean
Publication date
1 January 2014
Publisher
'Public Library of Science (PLoS)'
Doi
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on
PubMed
Abstract
Purpose: While animal models are widely used to investigate the development of restenosis in blood vessels following an intervention, computational models offer another means for investigating this phenomenon. A computational model of the response of a treated vessel would allow investigators to assess the effects of altering certain vessel- and stent-related variables. The authors aimed to develop a novel computational model of restenosis development following an angioplasty and bare-metal stent implantation in an atherosclerotic vessel using agent-based modeling techniques. The presented model is intended to demonstrate the body's response to the intervention and to explore how different vessel geometries or stent arrangements may affect restenosis development. Methods: The model was created on a two-dimensional grid space. It utilizes the post-procedural vessel lumen diameter and stent information as its input parameters. The simulation starting point of the model is an atherosclerotic vessel after an angioplasty and stent implantation procedure. The model subsequently generates the final lumen diameter, percent change in lumen cross-sectional area, time to lumen diameter stabilization, and local concentrations of inflammatory cytokines upon simulation completion. Simulation results were directly compared with the results from serial imaging studies and cytokine levels studies in atherosclerotic patients from the relevant literature. Results: The final lumen diameter results were all within one standard deviation of the mean lumen diameters reported in the comparison studies. The overlapping-stent simulations yielded results that matched published trends. The cytokine levels remained within the range of physiological levels throughout the simulations. Conclusion: We developed a novel computational model that successfully simulated the development of restenosis in a blood vessel following an angioplasty and bare-metal stent deployment based on the characteristics of the vessel crosssection and stent. A further development of this model could ultimately be used as a predictive tool to depict patient outcomes and inform treatment options. © 2014 Curtin, Zhou
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