Causal mechanisms of atrial fibrillation (AF) are still under investigation, with different studies presenting mixed results for possible associations between psychosocial distress or depression and occurrence of AF. This prospective study in four US communities aimed to explore the association of psychosocial measures (vital exhaustion, anger and social ties, use of anti-depressant medications) with the risk of atrial fibrillation (AF) in a cohort of ARIC (Atherosclerosis Risk in Communities) study.
Study population in the final analyses included 11,445 participants for whom baseline data (demographics, lifestyle measures, lipid profile, medication use, presence of diabetes or CVD) were available and without history of previous AF. The participants were evaluated at 1990–1992 with exposure data on psychosocial measures with follow-up until 2016. 10-item Spielberger Trait Anger scale, 21-item Vital Exhaustion Questionnaire (VEQ), Interpersonal Support Evaluation List (ISEL-SF) and Lubben Social Network Scale (LSNS) were all used to assess anger, vital exhaustion and social ties.
Over the follow-up period of 23.4 years, 19.4% of the study population developed AF with an incidence rate per 1,000 person-years of 9.8, 95% CI 9.5-10.2. After multi-variant adjustment for the baseline psychosocial factors and stratified analyses, only participants with VEQ scores in the 4th quartile, suggesting more depressive symptoms, and without anti-depressants use were associated with an increased risk of developing AF. On the contrary with previous studies, no significant associations were found between anti-depressant use, anger and poor social ties with the incidence of AF.
Even though the psychosocial factors were only assessed once using questionnaires and VEQ was not developed to measure specifically depression but mostly fatigue, this study adds to our knowledge that vital exhaustion (defined as excessive fatigue, feelings of demoralisation and increased irritability as well as symptoms of depression) is associated with an increased risk of developing AF, probably through an increase inflammation mechanism. However, clinical implications remain to be further explored through larger cohorts using more comprehensive validated tools.