Cand.med. Birgit Småbrekke disputerer for ph.d.-graden i helsevitenskap og vil offentlig forsvare avhandlingen:
Shared risk factors for arterial cardiovascular diseases and venous thromboembolism
Kort sammendrag av avhandlingen:
Extensive evidence support an association between arterial cardiovascular diseases (CVD, i.e. myocardial infarction [MI] and ischemic stroke), and subsequent venous thromboembolism (VTE, i.e. deep vein thrombosis [DVT]) and pulmonary emboli [PE]). However, the mechanism behind the associations remains unclear. The aim of this thesis was to investigate the impact of ischemic stroke on VTE and to investigate potential shared risk factors for arterial CVD and VTE.
The study populations for Paper I, II and III were recruited from the fourth, fifth and sixth survey of the Tromsø study. In Paper IV, we recruited a subgroup of participants with genetic information from the fourth survey of the Tromsø Study and from the second survey of the Nord-Trøndelag Health (HUNT) Study.
Ischemic stroke was associated with a transient increased risk of VTE, and provoked VTE in particular, indicating that the stroke itself increased the VTE risk. We found no association between formation, presence or progression of atherosclerosis and VTE in time-varying analyses, indicating that atherosclerosis does not represent the missing link for the association between arterial CVD and VTE. Except for body mass index, none of the traditional cardiovascular risk factors increased the risk of VTE. Lastly, we showed that the association between a family history of MI and VTE is not explained by prothrombotic genotypes.
Our findings imply a strong and transient increased risk of VTE after ischemic stroke and that the association between arterial CVD and VTE cannot be explained by atherosclerosis. Of the well-known cardiovascular risk factors, only age, obesity and FHMI are associated with VTE. The association between arterial CVD and subsequent VTE is only partly explained by shared risk factors. The remaining association is likely mediated by risk factors following the arterial event, such as immobilization and infection, and direct effects of the arterial event, such as activation of the coagulation system.
Professor John-Bjarne Hansen, hovedveileder
Professor Sigrid K. Brækkan, bi-veileder
Professor Paolo Prandoni MD, Ph.D., Department of Cardiothoracic and Vascular Sciences, University of Padova, Italy - 1. opponent
Group leader Bob Siegerink Ph.D., Center for Stroke research Berlin, Charité Universitätsmedizin Berlin, Tyskland - 2. opponent
Professor Sameline Grimsgaard, Institutt for samfunnsmedisin, Det helsevitenskapelige fakultet, UiT Norges arktiske universitet - Leder av komite
Professor II Stig Norderval, Institutt for klinisk medisin, Det helsevitenskapelige fakultet, UiT Norges arktiske universitet
Prøveforelesning over oppgitt emne holdes kl. 10:15, samme sted: “Overweight, obesity and the risk of venous and arterial thrombosis. The obesity paradox”