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Identification of the haemodynamic environment permissive for plaque erosion

Lookup NU author(s): Dr Stephen WhiteORCiD

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

© 2021, The Author(s). Endothelial erosion of atherosclerotic plaques is the underlying cause of approximately 30% of acute coronary syndromes (ACS). As the vascular endothelium is profoundly affected by the haemodynamic environment to which it is exposed, we employed computational fluid dynamic (CFD) analysis of the luminal geometry from 17 patients with optical coherence tomography (OCT)-defined plaque erosion, to determine the flow environment permissive for plaque erosion. Our results demonstrate that 15 of the 17 cases analysed occurred on stenotic plaques with median 31% diameter stenosis (interquartile range 28–52%), where all but one of the adherent thrombi located proximal to, or within the region of maximum stenosis. Consequently, all flow metrics related to elevated flow were significantly increased (time averaged wall shear stress, maximum wall shear stress, time averaged wall shear stress gradient) with a reduction in relative residence time, compared to a non-diseased reference segment. We also identified two cases that did not exhibit an elevation of flow, but occurred in a region exposed to elevated oscillatory flow. Our study demonstrates that the majority of OCT-defined erosions occur where the endothelium is exposed to elevated flow, a haemodynamic environment known to evoke a distinctive phenotypic response in endothelial cells.


Publication metadata

Author(s): McElroy M, Kim Y, Niccoli G, Vergallo R, Langford-Smith A, Crea F, Gijsen F, Johnson T, Keshmiri A, White SJ

Publication type: Article

Publication status: Published

Journal: Scientific Reports

Year: 2021

Volume: 11

Online publication date: 31/03/2021

Acceptance date: 11/03/2021

Date deposited: 08/11/2023

ISSN (electronic): 2045-2322

Publisher: Springer Nature

URL: https://doi.org/10.1038/s41598-021-86501-x

DOI: 10.1038/s41598-021-86501-x

PubMed id: 33790317


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Funding

Funder referenceFunder name
CH95/001
British Heart Foundation
FS/12/77/29887
Manchester Metropolitan University
PG/17/67/33218
PG/11/44/28972

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