A simple model for cholesterol accumulation on the artery wall near stagnation points

Autores
Gessaghi, Valeria Cristina; Tanoni, Debora; Perazzo, Carlos Alberto; Larreteguy, Axel Eduardo
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Cardiovascular diseases are one of the leading causes of death in the first world countries nowadays and atherosclerosis is the most relevant among them. It is a disease that affects medium and large size arteries, which causes the formation of plaques within the artery wall. These plaques, called athero- mas, develop due to the accumulation of fat, cholesterol, cell debris, smooth muscle cells and other cells and substances. Atheromas may cause temporary or definitive lack of blood sup ply to organs, such as the heart or the brain. This article proposes a model for choles terol accumulation and fatty streak formation, which are possible precursors of atheroma. The model is basically a mass balance of low density lipoproteins (LDL) in the intima. The inflow, outflow, oxidation, and consumption of LDL is modeled combining partial models and en dothelial LDL permeability correlations avail able in the literature. A simple zero-dimensional case was run for assessing the sensibility of the model to the ini- tial conditions. A more complex case of a two- dimensional flow in the vecinity of a stagnation point on a rigid wall was used for evaluating the influence of spatial variations of the wall-shear stresses. Blood ow was assumed as an steady flow of an homogeneous newtonian fluid, while blood pressure and LDL blood concentration values were assumed as physiologic. Results showing local LDL mass accumula- tion and intimal thickening evolution for the first case, and spatial distribution of the initial intimal growth rate for the second one, indicate that there is a very short initial transient behaviour of LDL mass accumulation and inti- mal thickeness, which may well be considered instantaneous compared to the usual periods involved in the lesion formation. This allows the use of simple quasi-steady solution in future computational implementations of more realistic applications involving 3D arterial geometries with wall remodelling, that will significantly reduce the computational effort.
Fil: Gessaghi, Valeria Cristina. Universidad Nacional de la Pampa. Facultad de Ingeniería; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Tanoni, Debora. Universidad Argentina de la Empresa. Facultad de Ingeniería y Ciencias Exactas; Argentina
Fil: Perazzo, Carlos Alberto. Universidad Favaloro; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Larreteguy, Axel Eduardo. Universidad Argentina de la Empresa. Facultad de Ingeniería y Ciencias Exactas; Argentina
Materia
Atherosclerosis
Hemodynamics
Cholesterol transport
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/195454

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spelling A simple model for cholesterol accumulation on the artery wall near stagnation pointsGessaghi, Valeria CristinaTanoni, DeboraPerazzo, Carlos AlbertoLarreteguy, Axel EduardoAtherosclerosisHemodynamicsCholesterol transporthttps://purl.org/becyt/ford/1.3https://purl.org/becyt/ford/1Cardiovascular diseases are one of the leading causes of death in the first world countries nowadays and atherosclerosis is the most relevant among them. It is a disease that affects medium and large size arteries, which causes the formation of plaques within the artery wall. These plaques, called athero- mas, develop due to the accumulation of fat, cholesterol, cell debris, smooth muscle cells and other cells and substances. Atheromas may cause temporary or definitive lack of blood sup ply to organs, such as the heart or the brain. This article proposes a model for choles terol accumulation and fatty streak formation, which are possible precursors of atheroma. The model is basically a mass balance of low density lipoproteins (LDL) in the intima. The inflow, outflow, oxidation, and consumption of LDL is modeled combining partial models and en dothelial LDL permeability correlations avail able in the literature. A simple zero-dimensional case was run for assessing the sensibility of the model to the ini- tial conditions. A more complex case of a two- dimensional flow in the vecinity of a stagnation point on a rigid wall was used for evaluating the influence of spatial variations of the wall-shear stresses. Blood ow was assumed as an steady flow of an homogeneous newtonian fluid, while blood pressure and LDL blood concentration values were assumed as physiologic. Results showing local LDL mass accumula- tion and intimal thickening evolution for the first case, and spatial distribution of the initial intimal growth rate for the second one, indicate that there is a very short initial transient behaviour of LDL mass accumulation and inti- mal thickeness, which may well be considered instantaneous compared to the usual periods involved in the lesion formation. This allows the use of simple quasi-steady solution in future computational implementations of more realistic applications involving 3D arterial geometries with wall remodelling, that will significantly reduce the computational effort.Fil: Gessaghi, Valeria Cristina. Universidad Nacional de la Pampa. Facultad de Ingeniería; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Tanoni, Debora. Universidad Argentina de la Empresa. Facultad de Ingeniería y Ciencias Exactas; ArgentinaFil: Perazzo, Carlos Alberto. Universidad Favaloro; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Larreteguy, Axel Eduardo. Universidad Argentina de la Empresa. Facultad de Ingeniería y Ciencias Exactas; ArgentinaPlanta Piloto de Ingeniería Química2012-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/195454Gessaghi, Valeria Cristina; Tanoni, Debora; Perazzo, Carlos Alberto; Larreteguy, Axel Eduardo; A simple model for cholesterol accumulation on the artery wall near stagnation points; Planta Piloto de Ingeniería Química; Latin American Applied Research; 42; 4-2012; 1-90327-07931851-8796CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.scielo.org.ar/scielo.php?script=sci_arttext&pid=S0327-07932012000100001info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-17T11:37:35Zoai:ri.conicet.gov.ar:11336/195454instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-17 11:37:35.418CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv A simple model for cholesterol accumulation on the artery wall near stagnation points
title A simple model for cholesterol accumulation on the artery wall near stagnation points
spellingShingle A simple model for cholesterol accumulation on the artery wall near stagnation points
Gessaghi, Valeria Cristina
Atherosclerosis
Hemodynamics
Cholesterol transport
title_short A simple model for cholesterol accumulation on the artery wall near stagnation points
title_full A simple model for cholesterol accumulation on the artery wall near stagnation points
title_fullStr A simple model for cholesterol accumulation on the artery wall near stagnation points
title_full_unstemmed A simple model for cholesterol accumulation on the artery wall near stagnation points
title_sort A simple model for cholesterol accumulation on the artery wall near stagnation points
dc.creator.none.fl_str_mv Gessaghi, Valeria Cristina
Tanoni, Debora
Perazzo, Carlos Alberto
Larreteguy, Axel Eduardo
author Gessaghi, Valeria Cristina
author_facet Gessaghi, Valeria Cristina
Tanoni, Debora
Perazzo, Carlos Alberto
Larreteguy, Axel Eduardo
author_role author
author2 Tanoni, Debora
Perazzo, Carlos Alberto
Larreteguy, Axel Eduardo
author2_role author
author
author
dc.subject.none.fl_str_mv Atherosclerosis
Hemodynamics
Cholesterol transport
topic Atherosclerosis
Hemodynamics
Cholesterol transport
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.3
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Cardiovascular diseases are one of the leading causes of death in the first world countries nowadays and atherosclerosis is the most relevant among them. It is a disease that affects medium and large size arteries, which causes the formation of plaques within the artery wall. These plaques, called athero- mas, develop due to the accumulation of fat, cholesterol, cell debris, smooth muscle cells and other cells and substances. Atheromas may cause temporary or definitive lack of blood sup ply to organs, such as the heart or the brain. This article proposes a model for choles terol accumulation and fatty streak formation, which are possible precursors of atheroma. The model is basically a mass balance of low density lipoproteins (LDL) in the intima. The inflow, outflow, oxidation, and consumption of LDL is modeled combining partial models and en dothelial LDL permeability correlations avail able in the literature. A simple zero-dimensional case was run for assessing the sensibility of the model to the ini- tial conditions. A more complex case of a two- dimensional flow in the vecinity of a stagnation point on a rigid wall was used for evaluating the influence of spatial variations of the wall-shear stresses. Blood ow was assumed as an steady flow of an homogeneous newtonian fluid, while blood pressure and LDL blood concentration values were assumed as physiologic. Results showing local LDL mass accumula- tion and intimal thickening evolution for the first case, and spatial distribution of the initial intimal growth rate for the second one, indicate that there is a very short initial transient behaviour of LDL mass accumulation and inti- mal thickeness, which may well be considered instantaneous compared to the usual periods involved in the lesion formation. This allows the use of simple quasi-steady solution in future computational implementations of more realistic applications involving 3D arterial geometries with wall remodelling, that will significantly reduce the computational effort.
Fil: Gessaghi, Valeria Cristina. Universidad Nacional de la Pampa. Facultad de Ingeniería; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Tanoni, Debora. Universidad Argentina de la Empresa. Facultad de Ingeniería y Ciencias Exactas; Argentina
Fil: Perazzo, Carlos Alberto. Universidad Favaloro; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Larreteguy, Axel Eduardo. Universidad Argentina de la Empresa. Facultad de Ingeniería y Ciencias Exactas; Argentina
description Cardiovascular diseases are one of the leading causes of death in the first world countries nowadays and atherosclerosis is the most relevant among them. It is a disease that affects medium and large size arteries, which causes the formation of plaques within the artery wall. These plaques, called athero- mas, develop due to the accumulation of fat, cholesterol, cell debris, smooth muscle cells and other cells and substances. Atheromas may cause temporary or definitive lack of blood sup ply to organs, such as the heart or the brain. This article proposes a model for choles terol accumulation and fatty streak formation, which are possible precursors of atheroma. The model is basically a mass balance of low density lipoproteins (LDL) in the intima. The inflow, outflow, oxidation, and consumption of LDL is modeled combining partial models and en dothelial LDL permeability correlations avail able in the literature. A simple zero-dimensional case was run for assessing the sensibility of the model to the ini- tial conditions. A more complex case of a two- dimensional flow in the vecinity of a stagnation point on a rigid wall was used for evaluating the influence of spatial variations of the wall-shear stresses. Blood ow was assumed as an steady flow of an homogeneous newtonian fluid, while blood pressure and LDL blood concentration values were assumed as physiologic. Results showing local LDL mass accumula- tion and intimal thickening evolution for the first case, and spatial distribution of the initial intimal growth rate for the second one, indicate that there is a very short initial transient behaviour of LDL mass accumulation and inti- mal thickeness, which may well be considered instantaneous compared to the usual periods involved in the lesion formation. This allows the use of simple quasi-steady solution in future computational implementations of more realistic applications involving 3D arterial geometries with wall remodelling, that will significantly reduce the computational effort.
publishDate 2012
dc.date.none.fl_str_mv 2012-04
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/195454
Gessaghi, Valeria Cristina; Tanoni, Debora; Perazzo, Carlos Alberto; Larreteguy, Axel Eduardo; A simple model for cholesterol accumulation on the artery wall near stagnation points; Planta Piloto de Ingeniería Química; Latin American Applied Research; 42; 4-2012; 1-9
0327-0793
1851-8796
CONICET Digital
CONICET
url http://hdl.handle.net/11336/195454
identifier_str_mv Gessaghi, Valeria Cristina; Tanoni, Debora; Perazzo, Carlos Alberto; Larreteguy, Axel Eduardo; A simple model for cholesterol accumulation on the artery wall near stagnation points; Planta Piloto de Ingeniería Química; Latin American Applied Research; 42; 4-2012; 1-9
0327-0793
1851-8796
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.scielo.org.ar/scielo.php?script=sci_arttext&pid=S0327-07932012000100001
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Planta Piloto de Ingeniería Química
publisher.none.fl_str_mv Planta Piloto de Ingeniería Química
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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