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dc.contributor.authorEvans, Nicholas Richard
dc.date.accessioned2018-05-18T14:41:01Z
dc.date.available2018-05-18T14:41:01Z
dc.date.issued2018-03-07
dc.date.submitted2017-10-12
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/275947
dc.description.abstractA carotid atherosclerotic plaque represents a nidus of inflammation mere centimetres below the blood-brain barrier. This inflammation, along with associated regions of microcalcification, are histopathological features of atheroma at risk of rupture (so-called “vulnerable plaques”) that trigger thromboembolic stroke. While conventional clinical imaging simply measures the degree of vessel stenosis, it is a crude measure that reveals little of the metabolic processes affecting plaque vulnerability. Our research demonstrates the utility of positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) and 18F-sodium fluoride (NaF), measuring inflammation and microcalcification respectively, to identify culprit carotid atheroma in vivo, and establish how these processes influence plaque vulnerability. Furthermore, for stroke care it is the downstream thromboembolic effects upon the brain that are key. While proinflammatory conditions may increase the risk of stroke, the relationship between atheroma inflammation and the peri-infarct inflammatory response following a stroke remains poorly defined. Our work demonstrates how inflammatory activity in symptomatic carotid atheroma, measured using PET, influences both chronic small vessel disease and the evolution of lesion volume in the post-stroke period. Using metabolic imaging we can both identify vulnerable atheroma in vivo and demonstrate how these processes affect infarct evolution. We show that whilst inflammation is a generalised process, microcalcification is a focal process that may represent a point of maximum vulnerability. These results also reveal the complexity of the atheroma-brain interaction that may simultaneously trigger events while also influencing stroke evolution in the early recovery period. This has important implications for understanding pathophysiology of both atherosclerosis and stroke evolution, advancing drug-discovery, and potential clinical applications to minimise the impact from this devastating disease.
dc.description.sponsorshipThe Dunhill Medical Trust [RTF44/0114]
dc.language.isoen
dc.rightsAll rights reserved
dc.rightsAll Rights Reserveden
dc.rights.urihttps://www.rioxx.net/licenses/all-rights-reserved/en
dc.subjectStroke
dc.subjectCarotid artery
dc.subjectAtherosclerosis
dc.titleMultimodal Imaging of Inflammation at the Neurovascular Interface in Cerebrovascular Disease
dc.typeThesis
dc.type.qualificationlevelDoctoral
dc.type.qualificationnameDoctor of Philosophy (PhD)
dc.publisher.institutionUniversity of Cambridge
dc.publisher.departmentDepartment of Clinical Neurosciences
dc.date.updated2018-05-18T11:36:25Z
dc.identifier.doi10.17863/CAM.23228
dc.contributor.orcidEvans, Nicholas Richard [0000-0002-7640-4701]
dc.publisher.collegeGonville and Caius
dc.type.qualificationtitlePhD in Clinical Neurosciences
cam.supervisorWarburton, Elizabeth
cam.supervisorRudd, James
cam.supervisor.orcidRudd, James [0000-0003-2243-3117]
cam.thesis.fundingfalse
rioxxterms.freetoread.startdate2019-05-18


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