Show simple item record

dc.contributor.authorHuang, Yuanen
dc.contributor.authorTeng, Zhongzhaoen
dc.contributor.authorSadat, Umaren
dc.contributor.authorHe, Jingen
dc.contributor.authorGraves, Martinen
dc.contributor.authorGillard, Jonathanen
dc.date.accessioned2013-05-10T23:09:41Z
dc.date.available2013-05-10T23:09:41Z
dc.date.issued2013-04-23en
dc.identifier.issn1475-925X
dc.identifier.urihttp://www.dspace.cam.ac.uk/handle/1810/244586
dc.description.abstractAbstract Background Atherosclerotic plaque is subjected to a repetitive deformation due to arterial pulsatility during each cardiac cycle and damage may be accumulated over a time period causing fibrous cap (FC) fatigue, which may ultimately lead to rupture. In this study, we investigate the fatigue process in human carotid plaques using in vivo carotid magnetic resonance (MR) imaging. Method Twenty seven patients with atherosclerotic carotid artery disease were included in this study. Multi-sequence, high-resolution MR imaging was performed to depict the plaque structure. Twenty patients were found with ruptured FC or ulceration and 7 without. Modified Paris law was used to govern crack propagation and the propagation direction was perpendicular to the maximum principal stress at the element node located at the vulnerable site. Results The predicted crack initiations from 20 patients with FC defect all matched with the locations of the in vivo observed FC defect. Crack length increased rapidly with numerical steps. The natural logarithm of fatigue life decreased linearly with the local FC thickness (R2 = 0.67). Plaques (n=7) without FC defect had a longer fatigue life compared with those with FC defect (p = 0.03). Conclusion Fatigue process seems to explain the development of cracks in FC, which ultimately lead to plaque rupture.
dc.languageEnglishen
dc.language.isoen
dc.titleIn vivo MRI-based simulation of fatigue process: a possible trigger for human carotid atherosclerotic plaque ruptureen
dc.typeArticle
dc.date.updated2013-05-10T23:09:42Z
dc.description.versionRIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are.en
dc.rights.holderYuan Huang et al.; licensee BioMed Central Ltd.
prism.publicationDate2013en
dcterms.dateAccepted2013-04-15en
rioxxterms.versionofrecord10.1186/1475-925X-12-36en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2013-04-23en
dc.contributor.orcidTeng, Zhongzhao [0000-0003-3973-6157]
dc.contributor.orcidGraves, Martin [0000-0003-4327-3052]
dc.contributor.orcidGillard, Jonathan [0000-0003-4787-8091]
dc.identifier.eissn1475-925X
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idBritish Heart Foundation (PG/11/74/29100)


Files in this item

Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record