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Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Associate Professor Anna Södergren, Umeå University, Sweden
- Second opponent: Professor Sella Aarrestad Provan, Inland Norway University of Applied Sciences
- Third member and chair of the evaluation committee: Professor II Theis Tønnessen, University of Oslo
Chair of the Defence
Professor II Marte Lie Høivik, University of Oslo
Principal Supervisor
Professor Emeritus Stefan Agewall, University of Oslo
Summary
Inflammatory arthritis (IA) is linked to a higher risk of cardiovascular disease (CVD). Due to the impact of coronary artery disease on patient prognosis, early treatment and prevention is crucial. This thesis aims to explore biomarkers involved in the development of CVD in IA patients, and investigates how these indicators change following antirheumatic treatment with methotrexate or tumor necrosis factor inhibitor (TNFi). It focuses on Nt-proBNP and hsTnT, indicators of heart wall stretching or pressure overload and myocardial damage, which predict poor prognosis. The complement system, essential in CVD pathophysiology, may also contribute to accelerated atherogenesis in IA.
The findings highlight the association between systemic inflammation and complement activation (as indicated by plasma TCC), hsTnT and Nt-proBNP in individuals without manifest heart failure. Changes in Nt-proBNP and TCC after treatment correlated with reductions in CRP and ESR and several clinical markers of disease activity. Patients with active rheumatoid arthritis had elevated TCC, which rapidly and lastingly reduced following antirheumatic therapy. However, while inflammatory markers significantly improved, Nt-proBNP and hsTnT did not change during the 6-month follow-up period. This is likely due to the low prevalence of cardiac dysfunction and myocardial injury in our cohort. Contrary to some previous studies suggesting the cardioprotective benefits of antirheumatic treatments, our results do not support the idea that these specific therapies protect against heart failure and myocardial injury in IA patients. Additionally, our findings do not indicate that TNFi treatment negatively impacts cardiac function in IA patients who do not have concurrent heart failure.
These findings enhance understanding of the pathogenesis of IA and its associated accelerated CVD. They underscore a need for improved screening and monitoring, leading to early intervention and prevention of CVD in IA patients.
Additional information
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