Developing Pulsatile Flow in a Deployed Coronary Stent
Author(s) -
Divakar Rajamohan,
Rupak K. Banerjee,
L. H. Back,
Ashraf Ibrahim,
Milind A. Jog
Publication year - 2005
Publication title -
journal of biomechanical engineering
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 126
eISSN - 1528-8951
pISSN - 0148-0731
DOI - 10.1115/1.2194067
Subject(s) - shear stress , pulsatile flow , restenosis , stent , hemodynamics , shear (geology) , cardiology , materials science , mechanics , medicine , composite material , physics
A major consequence of stent implantation is restenosis that occurs due to neointimal formation. This patho-physiologic process of tissue growth may not be completely eliminated. Recent evidence suggests that there are several factors such as geometry and size of vessel, and stent design that alter hemodynamic parameters, including local wall shear stress distributions, all of which influence the restenosis process. The present three-dimensional analysis of developing pulsatile flow in a deployed coronary stent quantifies hemodynamic parameters and illustrates the changes in local wall shear stress distributions and their impact on restenosis. The present model evaluates the effect of entrance flow, where the stent is placed at the entrance region of a branched coronary artery. Stent geometry showed a complex three-dimensional variation of wall shear stress distributions within the stented region. Higher order of magnitude of wall shear stress of 530 dyn/cm2 is observed on the surface of cross-link intersections at the entrance of the stent. A low positive wall shear stress of 10 dyn/cm2 and a negative wall shear stress of -10 dyn/cm2 are seen at the immediate upstream and downstream regions of strut intersections, respectively. Modified oscillatory shear index is calculated which showed persistent recirculation at the downstream region of each strut intersection. The portions of the vessel where there is low and negative wall shear stress may represent locations of thrombus formation and platelet accumulation. The present results indicate that the immediate downstream regions of strut intersections are areas highly susceptible to restenosis, whereas a high shear stress at the strut intersection may cause platelet activation and free emboli formation.
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