The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
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Digital Trial Lecture - time and place
Adjudication committee
- First opponent: Professor Ulrike Waje-Andreassen, University of Bergen
- Second opponent: Professor Martin O'Connell, Mater Misericordiae University Hospital, Dublin, Ireland
- Third member and chair of the evaluation committee: Professor Jonny Hisdal, Institute of Clinical Medicine, University of Oslo
Chair of defence
Adjunct Professor Nils Einar Kløw, Institute of Clinical Medicine, University of Oslo
Principal Supervisor
Associate Professor Mona-Elisabeth Rootwelt-Revheim, Institute of Clinical Medicine, University of Oslo
Summary
Stroke leads to severe disability and death worldwide. An atherosclerotic plaque causing stenosis of the carotid artery is an important cause of ischemic stroke. Today’s treatment selection is mainly based on the degree of stenosis caused by the plaque. Increasing knowledge indicates that luminal stenosis alone may not be the best predictor of stroke risk.
Inflammation is one of the key processes causing atherosclerotic plaque progression, plaque rupture and increased risk of the development of an embolus causing a clinical ischemic cerebral event. Positron emission tomography (PET) with radiolabelled glucose (18F-FDG) can detect and quantify glucose hypermetabolism in inflammatory cells.
The aims of this thesis were to determine if 18F-FDG PET can be established as a reliable imaging modality for the detection of atherosclerotic plaques which have a high risk of causing thromboembolic events. Furthermore, to explore if any quantification methods were more suitable than others for implementing 18F-FDG PET assessments of atherosclerosis in multicenter studies and in clinical routine.
The study population consisted of symptomatic (minor stroke or transient ischemic attack within the past 30 days) and asymptomatic patients referred to surgical treatment for severe atherosclerotic carotid stenosis (≥70 %). Symptomatic patients had higher carotid plaque uptake of 18F-FDG than asymptomatic. The uptake of 18F-FDG correlated significantly with inflammation on histological assessment. Analysis of different quantification methods showed that all had a good correlation to inflammation on histology. Correction for background activity was not necessary and slightly lowered the inter-reader agreement.
The thesis confirms that 18F-FDG PET/CT can detect inflammation and clinical vulnerability in large carotid atherosclerotic plaques. Easy achievable and reproducible quantification measurements are feasible and necessary for the methods use in clinical practice.
Additional information
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