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dc.contributor.authorBrown, Adamen
dc.contributor.authorTeng, Zhongzhaoen
dc.contributor.authorCalvert, Patrick Aen
dc.contributor.authorRajani, Nikil Ken
dc.contributor.authorHennessy, Orlaen
dc.contributor.authorNerlekar, Niteshen
dc.contributor.authorObaid, Daniel Ren
dc.contributor.authorCostopoulos, Charisen
dc.contributor.authorHuang, Yuanen
dc.contributor.authorHoole, Stephen Pen
dc.contributor.authorGoddard, Martinen
dc.contributor.authorWest, Nick EJen
dc.contributor.authorGillard, Jonathanen
dc.contributor.authorBennett, Martinen
dc.date.accessioned2016-06-09T11:22:55Z
dc.date.available2016-06-09T11:22:55Z
dc.date.issued2016-06-15en
dc.identifier.issn1941-9651
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/256225
dc.description.abstractBackground—Although plaque rupture is responsible for most myocardial infarctions, few high-risk plaques identified by intracoronary imaging actually result in future major adverse cardiovascular events (MACE). Nonimaging markers of individual plaque behavior are therefore required. Rupture occurs when plaque structural stress (PSS) exceeds material strength. We therefore assessed whether PSS could predict future MACE in high-risk nonculprit lesions identified on virtual-histology intravascular ultrasound. Methods and Results—Baseline nonculprit lesion features associated with MACE during long-term follow-up (median: 1115 days) were determined in 170 patients undergoing 3-vessel virtual-histology intravascular ultrasound. MACE was associated with plaque burden ≥70% (hazard ratio: 8.6; 95% confidence interval, 2.5–30.6; P<0.001) and minimal luminal area ≤4 mm2 (hazard ratio: 6.6; 95% confidence interval, 2.1–20.1; P=0.036), although absolute event rates for high-risk lesions remained <10%. PSS derived from virtual-histology intravascular ultrasound was subsequently estimated in nonculprit lesions responsible for MACE (n=22) versus matched control lesions (n=22). PSS showed marked heterogeneity across and between similar lesions but was significantly increased in MACE lesions at high-risk regions, including plaque burden ≥70% (13.9±11.5 versus 10.2±4.7; P<0.001) and thin-cap fibroatheroma (14.0±8.9 versus 11.6±4.5; P=0.02). Furthermore, PSS improved the ability of virtual-histology intravascular ultrasound to predict MACE in plaques with plaque burden ≥70% (adjusted log-rank, P=0.003) and minimal luminal area ≤4 mm2 (P=0.002). Plaques responsible for MACE had larger superficial calcium inclusions, which acted to increase PSS (P<0.05). Conclusions—Baseline PSS is increased in plaques responsible for MACE and improves the ability of intracoronary imaging to predict events. Biomechanical modeling may complement plaque imaging for risk stratification of coronary nonculprit lesions.
dc.description.sponsorshipBritish Heart Foundation (Grant ID: FS/13/33/30168)
dc.languageEnglishen
dc.language.isoenen
dc.publisherWolters Kluwer
dc.subjectarteriosclerosisen
dc.subjectcoronary diseaseen
dc.subjectintravascular ultrasounden
dc.subjectimagingen
dc.titlePlaque Structural Stress Estimations Improve Prediction of Future Major Adverse Cardiovascular Events After Intracoronary Imagingen
dc.typeArticle
dc.description.versionThis is the author accepted manuscript. The final version is available from Wolters Kluwer via https://doi.org/10.1161/CIRCIMAGING.115.004172en
prism.numbere004172en
prism.publicationDate2016en
prism.publicationNameCirculation Cardiovascular Imagingen
prism.volume9en
dc.identifier.doi10.17863/CAM.167
dcterms.dateAccepted2016-05-09en
rioxxterms.versionofrecord10.1161/CIRCIMAGING.115.004172en
rioxxterms.versionAMen
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2016-06-15en
dc.contributor.orcidTeng, Zhongzhao [0000-0003-3973-6157]
dc.contributor.orcidGillard, Jonathan [0000-0003-4787-8091]
dc.contributor.orcidBennett, Martin [0000-0002-2565-1825]
dc.identifier.eissn1942-0080
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idTCC (NIHR/CS/009/011)
pubs.funder-project-idBritish Heart Foundation (PG/11/74/29100)
pubs.funder-project-idBritish Heart Foundation (RG/10/007/28300)
pubs.funder-project-idEC FP7 CP (224297)
pubs.funder-project-idBritish Heart Foundation (CH/2000003)
pubs.funder-project-idMRC (MC_PC_14116 v2)
pubs.funder-project-idBritish Heart Foundation (FS/15/26/31441)
pubs.funder-project-idBritish Heart Foundation (FS/13/33/30168)
pubs.funder-project-idBritish Heart Foundation (RG/13/14/30314)


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