Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.

Coronary bifurcations are prone to atherosclerotic plaque growth, experiencing regions of reduced wall shear stress (WSS) and increased platelet adhesion. This study compares effects across different rheological approaches on hemodynamics, combined with a shear stress exposure history model of plate...

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Autores principales: David G Owen, Diana C de Oliveira, Emma K Neale, Duncan E T Shepherd, Daniel M Espino
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Publicado: Public Library of Science (PLoS) 2021
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Acceso en línea:https://doaj.org/article/78522bf3f9d64a0181c2588f4fb2afea
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spelling oai:doaj.org-article:78522bf3f9d64a0181c2588f4fb2afea2021-12-02T20:04:29ZNumerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.1932-620310.1371/journal.pone.0259196https://doaj.org/article/78522bf3f9d64a0181c2588f4fb2afea2021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0259196https://doaj.org/toc/1932-6203Coronary bifurcations are prone to atherosclerotic plaque growth, experiencing regions of reduced wall shear stress (WSS) and increased platelet adhesion. This study compares effects across different rheological approaches on hemodynamics, combined with a shear stress exposure history model of platelets within a stenosed porcine bifurcation. Simulations used both single/multiphase blood models to determine which approach best predicts phenomena associated with atherosclerosis and atherothrombosis. A novel Lagrangian platelet tracking model was used to evaluate residence time and shear history of platelets indicating likely regions of thrombus formation. Results show a decrease in area of regions with pathologically low time-averaged WSS with the use of multiphase models, particularly in a stenotic bifurcation. Significant non-Newtonian effects were observed due to low-shear and varying hematocrit levels found on the outer walls of the bifurcation and distal to the stenosis. Platelet residence time increased 11% in the stenosed artery, with exposure times to low-shear sufficient for red blood cell aggregation (>1.5 s). increasing the risk of thrombosis. This shows stenotic artery hemodynamics are inherently non-Newtonian and multiphase, with variations in hematocrit (0.163-0.617) and elevated vorticity distal to stenosis (+15%) impairing the function of the endothelium via reduced time-averaged WSS regions, rheological properties and platelet activation/adhesion.David G OwenDiana C de OliveiraEmma K NealeDuncan E T ShepherdDaniel M EspinoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 11, p e0259196 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
David G Owen
Diana C de Oliveira
Emma K Neale
Duncan E T Shepherd
Daniel M Espino
Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.
description Coronary bifurcations are prone to atherosclerotic plaque growth, experiencing regions of reduced wall shear stress (WSS) and increased platelet adhesion. This study compares effects across different rheological approaches on hemodynamics, combined with a shear stress exposure history model of platelets within a stenosed porcine bifurcation. Simulations used both single/multiphase blood models to determine which approach best predicts phenomena associated with atherosclerosis and atherothrombosis. A novel Lagrangian platelet tracking model was used to evaluate residence time and shear history of platelets indicating likely regions of thrombus formation. Results show a decrease in area of regions with pathologically low time-averaged WSS with the use of multiphase models, particularly in a stenotic bifurcation. Significant non-Newtonian effects were observed due to low-shear and varying hematocrit levels found on the outer walls of the bifurcation and distal to the stenosis. Platelet residence time increased 11% in the stenosed artery, with exposure times to low-shear sufficient for red blood cell aggregation (>1.5 s). increasing the risk of thrombosis. This shows stenotic artery hemodynamics are inherently non-Newtonian and multiphase, with variations in hematocrit (0.163-0.617) and elevated vorticity distal to stenosis (+15%) impairing the function of the endothelium via reduced time-averaged WSS regions, rheological properties and platelet activation/adhesion.
format article
author David G Owen
Diana C de Oliveira
Emma K Neale
Duncan E T Shepherd
Daniel M Espino
author_facet David G Owen
Diana C de Oliveira
Emma K Neale
Duncan E T Shepherd
Daniel M Espino
author_sort David G Owen
title Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.
title_short Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.
title_full Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.
title_fullStr Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.
title_full_unstemmed Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.
title_sort numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/78522bf3f9d64a0181c2588f4fb2afea
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