Shift Work and Acute Coronary Syndrome: Mechanisms, Modifying Factors, and Clinical Prevention
Luling Wang, Kumar Ganesan, Xing Liu, Lili Yu, Qiu ChenBackground/Objectives: Shift work causes recurrent circadian misalignment. This review synthesizes evidence linking shift work to acute coronary syndrome (ACS) and proposes a framework for prevention, return-to-work decisions, and future research. Methods: We conducted a narrative review using targeted searches of PubMed and major guideline repositories through July 2026. Search terms included shift work, night work, acute coronary syndrome, myocardial infarction, coronary heart disease, circadian misalignment, sleep, thrombosis, and cardiovascular risk. Revision-stage verification also examined atherosclerosis, coronary plaque, plaque vulnerability, and ischemia. Priority was given to prospective cohorts, systematic reviews, meta-analyses, controlled human studies, consensus statements, and major guidelines. Results: Night and rotating shift work are associated with a modestly increased risk of coronary heart disease (relative risk ~1.2–1.3), with duration-response gradients. Direct ACS-specific evidence is more limited but consistent with increased incidence and recurrence. Mechanistically, circadian misalignment and sleep deficiency promote autonomic dysregulation, hypertension, insulin resistance, dyslipidemia, inflammation, endothelial dysfunction, and atherosclerosis. Acute autonomic, hemodynamic, and prothrombotic changes may trigger plaque disruption or supply-demand ischemia. Risk modifiers include schedule intensity, cumulative exposure, chronotype, age, sex, comorbidities, sleep disorders, occupation, and health behaviors. Pregnancy is a specific evidence gap. Conclusions: Night and rotating shift work are probable contributory risk factors for ACS in susceptible workers. Clinical practice should integrate work schedule and sleep health into cardiovascular assessment, especially after ACS. Roster redesign offers the most defensible preventive strategy. Evidence that circadian interventions prevent ACS remains insufficient. More prospective ACS-specific studies are needed.