Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Order a digital copy of the thesis here
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Pedro Castro, São João University Hospital, Portugal
- Second opponent: Professor Ellisiv Mathiesen, UiT - The Arctic University of Norway
- Third member and chair of the evaluation committee: Professor Ole Morten Rønning, University of Oslo
Chair of the Defence
Professor Øystein Jørstad, University of Oslo
Principal Supervisor
Mona Skjelland, University of Oslo
Summary
Carotid atherosclerosis is a major cause of ischemic stroke, yet patient selection for revascularization still relies largely on the degree of luminal stenosis. However, unstable plaques can cause stroke even at low-grade stenosis. Intraplaque neovascularization (IPN), the ingrowth of fragile, leaky microvessels, is a hallmark of unstable plaques, but conventional ultrasound cannot reliably detect it, and contrast-enhanced ultrasound (CEUS) requires intravenous contrast.
The aims of this thesis in vascular neurology and neurosonology were to evaluate superb microvascular imaging (SMI), an advanced ultrasound technique without contrast, for detecting IPN, and to explore whether circulating biomarkers reflect SMI-defined IPN. In a prospective study of 44 patients with ≥50% carotid stenosis, SMI was compared with CEUS and plaque histology, and plasma biomarkers were measured in 29 patients.
SMI visualized microvascular flow in two-thirds of plaques, agreed strongly with CEUS (r = 0.91) and showed substantial inter-observer agreement. SMI-derived neovessel grades and counts correlated with histological neovascularization, inflammation and granulation tissue.
Plasma fibroblast growth factor 23 (FGF‑23) was associated with SMI-defined IPN independently of renal function, and soluble Flt‑1 (sFlt‑1) correlated with neovessel burden on SMI and histology.
Overall, SMI is a feasible bedside method for visualizing IPN without contrast, and FGF‑23 and sFlt‑1 emerge as promising circulating markers of plaque neovascularization. These findings support a multimodal framework combining SMI with circulating biomarkers to capture complementary aspects of plaque biology and potentially refine risk stratification beyond stenosis. Larger longitudinal studies are needed to confirm these findings and their prognostic value.
Additional information
Contact the research support staff.