Abstract
Intermittent hypoxia (IH), particularly in obstructive sleep apnea (OSA), has a complex role in cardiovascular health, acting both as a risk factor for disease and, under specific circumstances, as a therapeutic tool. This narrative review aims to explore the molecular mechanisms by which IH contributes to cardiovascular diseases, including hypertension, heart failure, arrhythmias, and atherosclerosis. Key processes such as oxidative stress, sympathetic hyperactivity, and hypoxia-inducible factor 1-alpha (HIF-1α)-mediated inflammation are discussed in relation to vascular and myocardial remodeling. Clinical and experimental data highlight the significant association between IH and increased cardiovascular morbidity and mortality, especially in high-risk populations. This review also evaluates the effectiveness of treatments like continuous positive airway pressure (CPAP), mandibular advancement devices, weight reduction, pharmacotherapy, and intermittent hypoxic conditioning (IHC). It emphasizes the importance of early screening and personalized treatment strategies for better patient outcomes. Emerging research on IH-based cardioprotection and biomarker discovery suggests promising avenues for future therapies. Ultimately, IH has both detrimental and potentially beneficial effects on cardiovascular health, depending on its context and management.