Digital Public Defence: Kjartan Moe
MD Kjartan Moe at Institute of Clinical Medicine will be defending the thesis “Cardiovascular Risk markers after Preeclampsia and Gestational Hypertension” for the degree of PhD (Philosophiae Doctor).
Photo: Amalie Huth Hovland, Fotograflærling, Foto- og videotjenesten, Institutt for klinisk medisin, UiO/Oslo universitetssykehus, Rikshospitalet.
The University of Oslo is closed and the public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Digital Trial Lecture – time and place
- First opponent: Associate Professor Bas van Rijn, Erasmus MC University Medical Center Rotterdam, Rotterdam, The Netherlands
- Second opponent: Professor Eva Gerdts, University of Bergen and Haukeland University Hospital
- Third member and chair of the evaluation committee: Professor Kirsten Bjørklund Holven, Faculty of Medicine, University of Oslo
Chair of the Defence
Professor II Arnljot Tveit, Faculty of Medicine, University of Oslo
Professor Anne Cathrine Staff, Faculty of Medicine, University of Oslo
Hypertensive pregnancy complications (preeclampsia; PE and gestational hypertension; GH) confer 2-8 fold increased risks of long-term maternal cardiovascular disease (CVD). As women with PE/GH are young, primary prevention of CVD might prove especially beneficial in this group. The thesis aimed to examine if biomarkers at delivery or 1 year postpartum are applicable and valid for identifying this CVD risk, and consequently if they could be used to improve risk stratification.
When examining 235 women at delivery, uteroplacental acute atherosis (AcA), a histological foam cell lesion resembling early atherosclerosis, was associated with increased systolic blood pressure in early pregnancy. This was likely due to more women with PE in the group with AcA. AcA did not associate with other classical CVD risk factors in pregnancy. In the oldest age quartile, women with AcA had higher levels of Apolipoprotein B-containing lipoproteins which may be initiators of the atherosclerotic process. Although AcA associated with increased CVD risk in some women, our study does not support the general use of AcA as a CVD risk marker.
Three long-term CVD risk scores were assessed in 235 women 1 year postpartum, and did not reflect the epidemiologically increased CVD risks after PE/GH.
In 221 women 1 year postpartum several vascular function markers were assessed: reactive hyperemia index, pulse wave velocity (PWV), augmentation index, and carotid intima-media thickness. Preterm PE and term GH associated with elevated PWV levels (compared to controls), but after adjusting for classical CVD risk factors, there were no significant differences to controls for PWV or other vascular markers.
Although none of the investigated markers helped stratify CVD risk in the first years postpartum, PE/GH associated with adverse CVD risk profiles in all studies. Previous PE/GH should thus be considered as an easily accessible risk marker for targeted follow-up and preventive strategies for future CVD.
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