Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.

Coronary artery thrombosis is the major risk associated with Kawasaki disease (KD). Long-term management of KD patients with persistent aneurysms requires a thrombotic risk assessment and clinical decisions regarding the administration of anticoagulation therapy. Computational fluid dynamics has dem...

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Autores principales:	Noelia Grande Gutiérrez, Mark Alber, Andrew M Kahn, Jane C Burns, Mathew Mathew, Brian W McCrindle, Alison L Marsden
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/533ba75e53ac4e98b8c71b3b43537203
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spelling	oai:doaj.org-article:533ba75e53ac4e98b8c71b3b435372032021-12-02T19:57:50ZComputational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.1553-734X1553-735810.1371/journal.pcbi.1009331https://doaj.org/article/533ba75e53ac4e98b8c71b3b435372032021-09-01T00:00:00Zhttps://doi.org/10.1371/journal.pcbi.1009331https://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358Coronary artery thrombosis is the major risk associated with Kawasaki disease (KD). Long-term management of KD patients with persistent aneurysms requires a thrombotic risk assessment and clinical decisions regarding the administration of anticoagulation therapy. Computational fluid dynamics has demonstrated that abnormal KD coronary artery hemodynamics can be associated with thrombosis. However, the underlying mechanisms of clot formation are not yet fully understood. Here we present a new model incorporating data from patient-specific simulated velocity fields to track platelet activation and accumulation. We use a system of Reaction-Advection-Diffusion equations solved with a stabilized finite element method to describe the evolution of non-activated platelets and activated platelet concentrations [AP], local concentrations of adenosine diphosphate (ADP) and poly-phosphate (PolyP). The activation of platelets is modeled as a function of shear-rate exposure and local concentration of agonists. We compared the distribution of activated platelets in a healthy coronary case and six cases with coronary artery aneurysms caused by KD, including three with confirmed thrombosis. Results show spatial correlation between regions of higher concentration of activated platelets and the reported location of the clot, suggesting predictive capabilities of this model towards identifying regions at high risk for thrombosis. Also, the concentration levels of ADP and PolyP in cases with confirmed thrombosis are higher than the reported critical values associated with platelet aggregation (ADP) and activation of the intrinsic coagulation pathway (PolyP). These findings suggest the potential initiation of a coagulation pathway even in the absence of an extrinsic factor. Finally, computational simulations show that in regions of flow stagnation, biochemical activation, as a result of local agonist concentration, is dominant. Identifying the leading factors to a pro-coagulant environment in each case-mechanical or biochemical-could help define improved strategies for thrombosis prevention tailored for each patient.Noelia Grande GutiérrezMark AlberAndrew M KahnJane C BurnsMathew MathewBrian W McCrindleAlison L MarsdenPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 17, Iss 9, p e1009331 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Noelia Grande Gutiérrez Mark Alber Andrew M Kahn Jane C Burns Mathew Mathew Brian W McCrindle Alison L Marsden Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.
description	Coronary artery thrombosis is the major risk associated with Kawasaki disease (KD). Long-term management of KD patients with persistent aneurysms requires a thrombotic risk assessment and clinical decisions regarding the administration of anticoagulation therapy. Computational fluid dynamics has demonstrated that abnormal KD coronary artery hemodynamics can be associated with thrombosis. However, the underlying mechanisms of clot formation are not yet fully understood. Here we present a new model incorporating data from patient-specific simulated velocity fields to track platelet activation and accumulation. We use a system of Reaction-Advection-Diffusion equations solved with a stabilized finite element method to describe the evolution of non-activated platelets and activated platelet concentrations [AP], local concentrations of adenosine diphosphate (ADP) and poly-phosphate (PolyP). The activation of platelets is modeled as a function of shear-rate exposure and local concentration of agonists. We compared the distribution of activated platelets in a healthy coronary case and six cases with coronary artery aneurysms caused by KD, including three with confirmed thrombosis. Results show spatial correlation between regions of higher concentration of activated platelets and the reported location of the clot, suggesting predictive capabilities of this model towards identifying regions at high risk for thrombosis. Also, the concentration levels of ADP and PolyP in cases with confirmed thrombosis are higher than the reported critical values associated with platelet aggregation (ADP) and activation of the intrinsic coagulation pathway (PolyP). These findings suggest the potential initiation of a coagulation pathway even in the absence of an extrinsic factor. Finally, computational simulations show that in regions of flow stagnation, biochemical activation, as a result of local agonist concentration, is dominant. Identifying the leading factors to a pro-coagulant environment in each case-mechanical or biochemical-could help define improved strategies for thrombosis prevention tailored for each patient.
format	article
author	Noelia Grande Gutiérrez Mark Alber Andrew M Kahn Jane C Burns Mathew Mathew Brian W McCrindle Alison L Marsden
author_facet	Noelia Grande Gutiérrez Mark Alber Andrew M Kahn Jane C Burns Mathew Mathew Brian W McCrindle Alison L Marsden
author_sort	Noelia Grande Gutiérrez
title	Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.
title_short	Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.
title_full	Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.
title_fullStr	Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.
title_full_unstemmed	Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.
title_sort	computational modeling of blood component transport related to coronary artery thrombosis in kawasaki disease.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/533ba75e53ac4e98b8c71b3b43537203
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Computational modeling of blood component transport related to coronary artery thrombosis in Kawasaki disease.

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