Trial lecture - time and place
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Adjudication committee
- First opponent: Professor Stefan James, Department of Medical Sciences, Uppsala University, Sweden
- Second opponent: Professor Stein Ørn, Faculty of Health Sciences, University of Stavanger
- Third member and chair of the evaluation committee: Associate Professor Aud Høieggen, Institute of Clinical Medicine, University of Oslo
Chair of defence
Professor Lars Gullestad, Institute of Clinical Medicine, University of Oslo
Principal supervisor
Overlege Geir Øystein Andersen, Department of Cardiology, Oslo University Hospital, Ullevål
Summary
Despite great advances in the treatment of ST-elevation myocardial infarction (STEMI) during the last decades, including acute reperfusion therapy, many patients still develop large myocardial infarctions (MI). Reperfusion of ischaemic myocardium can itself paradoxically result in further injury, a process termed ischaemia-reperfusion injury. After the acute phase, one of the most important consequences of MI is ventricular remodelling with subsequent risk of heart failure development. Inflammation plays a key role in all stages of an MI. However, there is emerging evidence that excessive inflammation following MI can have detrimental effects on myocardial injury and subsequent ventricular remodelling.
The aim of this thesis was to explore specific inflammatory pathways activated during an acute STEMI suspected to play an important role in ischaemia-reperfusion injury and left ventricular remodelling.
The main finding of the thesis was that high levels of interleukin-8, measured both in the acute phase and during follow-up, were strongly associated with large infarct size and adverse clinical outcome.
Additional information
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