Occupational Stress as a Modifiable Risk Factor for Atherosclerotic Coronary Artery Disease: Evidence, Mechanisms, and Interventions

Cardiovascular diseases, particularly atherosclerotic coronary artery disease (CAD), remain among the leading causes of mortality worldwide. Although traditional risk factors—such as arterial hypertension, dyslipidemia, diabetes mellitus, obesity, smoking, and physical inactivity—are well established, accumulating evidence highlights the significant role of psychosocial factors in modulating cardiovascular risk. Among these, occupational stress—conceptualized through models such as job strain (high job demands combined with low control) and effort–reward imbalance—has been consistently associated with an increased risk of coronary events. The interaction between occupational stress and classical cardiovascular risk factors remains insufficiently elucidated and challenging to quantify. This review examines the current scientific evidence regarding the relationship between occupational stress and CAD, synthesizing findings from major epidemiological studies and relevant meta-analyses. Chronic exposure to work-related stress activates neuroendocrine pathways, including the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system, promotes a state of low-grade systemic inflammation, and facilitates the adoption of unhealthy behaviors such as smoking, poor dietary habits, physical inactivity, and excessive alcohol consumption. These mechanisms contribute to endothelial dysfunction, hypercoagulability, and acceleration of the atherosclerotic process. Landmark investigations, including the INTERHEART study, meta-analyses conducted by Kivimäki and colleagues, and prospective studies by Chandola on the metabolic syndrome, support both the cumulative and independent impact of occupational stress on cardiovascular risk. Although the proportion of risk attributable to occupational stress is lower than that associated with traditional risk factors, its modifiable nature underscores a substantial potential for targeted preventive interventions. Strategies aimed at reducing occupational stress encompass individual-level approaches (stress management programs, lifestyle modification, psychological support), organizational interventions (optimizing the balance between job demands and employee control, enhancing social support in the workplace), and public health policies (occupational health promotion programs, regulatory measures addressing work-related stress, and screening for occupational stress). Recognizing occupational stress as a modifiable risk factor for CAD has important implications for both clinical practice and public health. Future research should focus on large-scale longitudinal studies, the identification of stress-related biomarkers, and the cost-effectiveness of stress-reduction interventions in the prevention and management of coronary artery disease.