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 Raffaele De Caterina, University of Pisa, Italy
- Second opponent: Head of Department Ellen Elisabeth Brodin, Akershus University Hospital, Norway
- Third member and chair of the evaluation committee: Professor II Pål Andre Holme, University of Oslo
Chair of the Defence
Professor II Magnus Nakrem Lyngbakken, University of Oslo
Principal Supervisor
Senior Cardiologist Ragnhild Helseth, Oslo University Hospital
Summary
Inflammation is central in coronary artery disease (CAD), but which pathways are activated, and how they relate to each other is still incompletely understood.
The aims of the thesis were to investigate the association between activation of the complement system and neutrophil extracellular traps (NETs), as well as their relation to activation of the coagulation system and clinical endpoints. This was done by measuring markers of complement activation NETs and coagulation in two cohorts - chronic CAD and ST-elevation myocardial infarction (STEMI).
Complement and NET markers were weakly associated in both chronic CAD and STEMI, and complement activation was associated with coagulation in both cohorts. Complement activation was associated with risk of acute myocardial infarction in chronic CAD and risk of death during follow-up in STEMI.
Furthermore, when examining the combined effect of complement activation and NETs in STEMI, combining markers of complement and NETs did not add to the prognostic value compared to NET markers alone. Moreover, when combining complement and coagulation markers, we did not find any synergistic associations on the risk of myocardial injury or dysfunction beyond purely additive effects.
Overall, this thesis adds to a growing understanding of the complex pathways involved in CAD, and contributes to future identification of useful targets for novel therapies targeting inflammation.
Additional information
Contact the research support staff.