Stressful life events in adulthood predict cardiovascular disease: the mediating role of behavioral and depressive pathways
S Wu, L H Zheng, Y M Yang, S Q Lyu, Y M Wang, Y ChenAbstract
Background
Stressful life events (SLEs) in adulthood are suspected risk factors for cardiovascular disease (CVD), yet the evidence is inconclusive. This study investigated the association between adulthood SLEs and incident CVD and explored the mediating roles of depression, physical activity, and smoking.
Methods
We analyzed harmonized data from two prospective, nationally representative aging cohorts: the US Health and Retirement Study and the English Longitudinal Study of Ageing. Adulthood SLE exposure was assessed at baseline. Incident CVD, a composite of myocardial infarction, angina, heart failure, other heart diseases, and stroke, was ascertained through physician diagnoses. Multivariable Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs). Population-attributable fractions (PAFs) quantified the contribution of SLEs to CVD burden, and mediation analyses assessed the pathways linking SLEs to CVD.
Results
The analysis included 18,898 participants (mean age 64.5 years) free of prevalent CVD at baseline. Over a median follow-up of 90 months, 2,782 incident CVD cases occurred. Compared to no SLE exposure, any exposure was associated with a significantly higher risk of CVD (HR 1.19; 95% CI: 1.10-1.28), heart disease (HR 1.15; 95% CI: 1.06-1.25), and stroke (HR 1.24; 95% CI: 1.07-1.43). A dose-dependent relationship was observed; each additional SLE was associated with a 10% increased risk of CVD and stroke, and a 9% increased risk of heart disease. PAF estimates indicated that 5.9%-9.4% of incident CVD cases were attributable to adulthood SLE exposure. Mediation analyses revealed that depression, physical activity, and smoking explained 11.9%, 4.3%, and 8.3% of the SLE-CVD association, respectively.
Conclusions
Adulthood SLE exposure is independently associated with a higher risk of incident CVD in a dose-dependent manner, with depressive symptoms and health behaviors partially mediating this relationship. These findings underscore the potential of public health strategies focused on stress reduction and resilience to mitigate the CVD burden attributable to psychosocial stressors.Table 1Table 2