Objective: To synthesize contemporary evidence on how obstructive sleep apnea (OSA) relates to the epidemiology and pathophysiology of coronary artery disease (CAD).
Methods: Narrative review of society statements, randomized trials, individual-participant meta-analyses, and mechanistic studies indexed in PubMed/Medline through October 12, 2025. We prioritized high-quality evidence addressing OSA prevalence in CAD/acute coronary syndrome (ACS), cardiovascular outcomes with continuous positive airway pressure (CPAP), and biological pathways linking OSA-related sleep disruption with atherothrombosis.
Results: OSA is highly prevalent in CAD/ACS cohorts (commonly 30–60%). Large randomized trials in mostly non-sleepy patients (SAVE, RICCADSA, ISAACC) did not show overall reductions in major adverse cardiovascular events (MACE) with routine CPAP, whereas adherence ≥4 h/night was associated with lower recurrence of events in individual-level pooled analyses. Mechanisms connecting OSA to atherothrombosis include intermittent hypoxia, sleep fragmentation, and circadian disruption driving sympathetic activation, endothelial dysfunction, oxidative stress, inflammation, platelet activation, and prothrombotic signaling.
Conclusion: OSA is an important, potentially modifiable contributor within the broader framework of cardiovascular prevention. Although routine CPAP solely for secondary prevention in non-sleepy CAD populations has not reduced events, targeted screening of high-risk OSA phenotypes, structured adherence support, and integrated “sleep–cardiology” care remain biologically and clinically justified.