Intermittent Hypoxia and Its Impact on Right Ventricular Remodeling: Pathophysiological Mechanisms and Clinical Implications

Intermittent hypoxia (IH) is a recurrent phenomenon observed in various pathological conditions, most notably in obstructive sleep apnea (OSA), chronic thromboembolic pulmonary hypertension (CTEPH), and high-altitude diseases. This cyclic pattern of oxygen deprivation and reoxygenation induces significant structural and functional alterations in the right ventricle (RV), leading to maladaptive remodeling. The RV is highly susceptible to increased afterload, particularly due to pulmonary vascular changes driven by hypoxia-induced endothelial dysfunction, oxidative stress, and inflammatory cascades. These factors contribute to myocardial fibrosis, increased RV wall stress, and ultimately right ventricular failure. This review aims to provide a comprehensive analysis of the molecular and cellular mechanisms by which IH influences RV remodeling, focusing on mitochondrial dysfunction, reactive oxygen species (ROS) production, autonomic dysregulation, and hypoxia-inducible factor-1α (HIF-1α)-mediated pathways. Furthermore, we discuss the potential role of biomarkers, imaging modalities, and emerging therapeutic strategies to mitigate the adverse effects of IH on the RV. Given the rising clinical burden of conditions associated with IH, understanding these mechanisms is critical for developing targeted interventions to prevent or reverse RV dysfunction.