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Trial Lecture – time and place
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Adjudication committee
- First opponent: Associate Professor Nina Kupper, Tilburg University, The Netherlands
- Second opponent: Professor Stefan Johansson, University of Bergen, Norway
- Third member and chair of the evaluation committee: Associate professor Kjersti Narud, Faculty of Medicine, University of Oslo
Chair of the Defence
Professor emeritus Pål Zeiner, University of Oslo
Principal Supervisor
Professor II Toril Dammen, University of Oslo
Summary
The aim of this thesis was to gain new knowledge about the relationship between personality traits and cardiovascular risk factors and prognosis in patients with established coronary artery disease (CAD) and assess the common genetic background of neuroticism, and depression and CAD risk. First, we investigated the associations between Type D personality and the risk of recurrent major adverse cardiovascular events (MACE) as well as Type D and cardiovascular disease (CVD) risk factors in 1068 patients with established CAD. Second, we explored the shared genetic architecture of neuroticism and risk factors for CAD and CAD. Third, we explored the genetic associations between depression and CVD risk factors and CAD, respectively. We used large international databases (UK Biobank, 23andMe, Inc. and others) and advanced statistical methods to estimate the total amount of shared genetic overlap and to identify specific shared loci.
We found an association between the Type D personality trait negative affectivity and increased risk for recurrent cardiovascular events, but not after controlling for symptoms of anxiety and depression. We also found associations between Type D personality and low adherence to statins and smoking as well as higher levels of symptoms of depression and anxiety.
We found polygenic overlap between neuroticism and risk of CAD, with positive effect directions for CAD, higher waist- hip ratio and blood pressure. There was an opposite or mixed pattern of effect direction for the other CVD risk factors. Several genetic loci were associated with neuroticism and multiple CVD risk factors.
There was substantial part of the genetic underpinning for depression that also influenced body mass index and systolic blood pressure. We identified specific genetic loci associated with depression and CAD or CVD risk factors, mainly with blood pressure and lipids and the inflammation marker c-reactive protein with positive effect directions, while there was a mixed pattern of effect direction for other CVD risk factors.
The results suggest that negative affectivity is the Type D trait most strongly associated with CAD prognosis, but the association was not significant after controlling for symptoms of depression and anxiety. Type D personality was associated with not taking statins and smoking as well as higher scores of anxiety and depression. There is genetic overlap for neuroticism, depression and CAD and CVD risk factors indicating that those with a genetic susceptibility for neuroticism or depression may also have an increased risk of CAD. The discovery of shared loci with mixed effect directions for several CVD risk factors and neuroticism and depression indicates variation in genetic susceptibility to CVD across subgroups of patients with neuroticism and depression.
These findings emphasize the importance of a biopsychosocial approach to CAD patients focusing on biological aspects, lifestyle and behavior as well as psychological factors, and suggest that shared genetic factors may link psychological and CVD risk factors.
Additional information
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