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
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e2f1393b60c94b3bb8dba15bdf8cb9d1
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spelling	oai:doaj.org-article:e2f1393b60c94b3bb8dba15bdf8cb9d12021-11-11T06:44:14ZNumerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation1932-6203https://doaj.org/article/e2f1393b60c94b3bb8dba15bdf8cb9d12021-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8565790/?tool=EBIhttps://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 (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/e2f1393b60c94b3bb8dba15bdf8cb9d1
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Numerical modelling of blood rheology and platelet activation through a stenosed left coronary artery bifurcation

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