Association between depressive symptoms and atherosclerotic cardiovascular disease: a Swedish population-based cohort study

Background: Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of morbidity and mortality globally. While traditional risk factors such as hypertension, smoking, and dyslipidemia are well established, the role of depressive symptoms in ASCVD development, particularly in premature cases, is less understood. This study aims to determine the association between depressive symptoms, including severity and anxious distress as specifiers, with ASCVD and premature ASCVD in a Swedish population-based cohort. Methods: We utilized data from the PART study (acronym in Swedish for: Psykisk hälsa, Arbete och RelaTioner: Mental Health, Work and Relationships), a longitudinal cohort study which include a total of 11,175 adults in Stockholm, Sweden. Depressive symptoms were assessed using the Major Depression Inventory across three waves from 1998 to 2010 Incident ASCVD cases were identified through the National Patient Register (NPR) until 2021. Premature ASCVD was defined as occurring before age 55 in men and 65 in women. Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs), adjusting for sociodemographic factors, lifestyle behaviors, and cardiometabolic conditions. Results: Participants with depressive symptoms had a 42% increased risk of ASCVD (HR 1.42, 95% CI 1.19–1.68), independent of traditional cardiovascular risk factors. When stratifying by ASCVD type, depressive symptoms were associated with ischemic heart disease (HR 1.39, CI 1.06–1.83) and stroke (HR 1.53, CI 1.15–2.05). The risk varied by severity, with mild depressive symptoms associated with ischemic heart disease (HR 1.62, CI 1.11–2.37) and moderate (HR 1.70, 95% CI 1.04–2.78) and severe depressive symptoms (HR 1.61, 95% CI 1.04–2.49) were associated with stroke. Furthermore, participants with combined depressive symptoms and anxious distress had an increased risk of stroke (HR 1.50, CI 1.09–2.07), whereas participants with depressive symptoms without anxious distress had an increased risk of ischemic heart disease (HR 1.88, CI 1.25–2.82). The risk of premature ASCVD was increased among individuals with depressive symptoms (HR = 1.52, 95% CI 1.12–2.05). When examined by level of severity, only among subjects with mild depressive symptoms, a statistically significant association with premature ASCVD (HR = 1.61, 95% CI 1.05–2.48) was found. Conclusions: This study provides evidence linking depressive symptoms to ASCVD and premature ASCVD in a Swedish population. The findings underscore the need to consider the effects of depressive symptoms as well as potential prevention strategies for depressive symptoms in regard to cardiovascular diseases. Future research should explore whether early identification and treatment of depressive symptoms can mitigate ASCVD risk and improve long-term cardiovascular outcomes.