Why the study?
The epidemiological and pathogenic relationships between obstructive sleep apnea and pulmonary embolism remain limited, despite potential overlapping pathophysiological mechanisms.
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Design
Review
Should not change PE or OSA management; novel Level 5 finding leaves mechanistic links hypothesis-generating.
Pulmonary embolism (PE) and obstructive sleep apnea (OSA) remain a major health issue worldwide with potential overlapping pathophysiological mechanisms. PE, the most severe form of venous thromboembolism, is associated with high morbidity and mortality, presenting challenges in management and prevention, especially in high-risk populations. OSA is a prevalent condition characterized by repeated episodes of upper airway closure resulting in intermittent hypoxia and sleep fragmentation. Although the understanding of epidemiological and pathogenic relationships between OSA and PE is still limited, current data suggest that interactions between these two conditions appear to be relevant. OSA is emerging as a novel risk factor for PE, potentially affecting all components of Virchow's triad: hypercoagulability, endothelial dysfunction, and venous stasis. Epidemiological studies indicate a high prevalence of undiagnosed OSA in acute PE patients. Moderate-to-severe OSA has been linked to worse clinical presentations and outcomes. Furthermore, OSA has been associated with increased risks of PE recurrence and mortality. Future research directions should include clarifying the bidirectional relationship between these conditions and evaluating the effectiveness and safety of continuous positive airway pressure therapy in improving outcomes in patients with concurrent acute PE and OSA.
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García‐Ortega et al. (2025) studied this question.
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