Public Defence - Vibeke Nordmo Ritschel - The Heart
MD. Vibeke Nordmo Ritschel at Institute of Clinical Medicine will be defending the thesis Markers of inflammation and haemostatis: Associations with myocardial injury, adverse remodelling, and future clinical events in patients with ST-elevation myocardial infarction for the degree of PhD.
Trial Lecture - time and place
See Trial Lecture.
- 1. opponent: Professor Jan Kristian Damås, The Norwegian University of Science and Technology
- 2. opponent: Professor Lars Gullestad, University of Oslo
- 3. member of the adjudication committee: Professor Kirsten Bjørklund Holven, University of Oslo
Chair of the Defence
Professor Finn Olav Levy, University of Oslo
Geir Øystein Andersen, Oslo University Hospital
Cardiovascular disease including acute myocardial infarction is still a major cause of death despite better treatment and improved prognosis during the last decades. In the thesis “Markers of inflammation and haemostasis: Associations with myocardial injury, adverse remodelling and future clinical events in patients with ST-elevation myocardial infarction” we examined patients with acute ST-elevation myocardial infarction (STEMI) and their relation to different circulating markers reflecting activation of the inflammatory system, haemostatic variables and a marker associated with ischemia/reperfusion injury and cardiac fibrosis. The aims of the thesis were to improve our understanding of the complex mechanism involved in the interaction between inflammation, thrombosis and infarct healing, remodelling and future prognosis. We found that a novel inflammatory marker, soluble IL-6 receptor (sIL-6R) measured in patients with STEMI was associated with increased risk of future cardiovascular events including new myocardial infarction, readmission for heart failure, stroke or all-cause mortality. Activation of some inflammatory markers and markers of the coagulation system were associated with larger infarcts and reduced left ventricular function. The marker associated with ischemia-reperfusion injury, and remodelling, was not related with either infarct size, left ventricular function or increased risk of new adverse events. In conclusion, higher levels of sIL-6R are associated with adverse prognosis and inhibition of the IL-6 receptor may be a therapeutic approach.
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