C76-01 Persistent Oxygen Desaturation Despite Well-controlled OSA: A Case of PFO-associated Migraines Identified by Smartwatch

Abstract Introduction Persistent nocturnal oxygen desaturation despite optimized obstructive sleep apnea (OSA) management presents a diagnostic challenge. Patent foramen ovale (PFO) is present in 25% of adults1 and has been reported in 43-69% in patients with OSA. 2-4 PFO has been associated with increased nocturnal desaturation in moderate to severe OSA, though the impact of closure remains variable.3,5,6 We present a case of a smartwatch-detected nocturnal desaturations that led to the diagnosis and closure of a PFO, resulting in dramatic migraine improvement. Case A 38-year-old woman with obesity (BMI 40) was diagnosed with mild OSA, with an Apnea-Hypopnea Index (AHI) 13.5 events/hour, Rapid Eye Movement Apnea-Hypopnea Index (REM AHI) 64.2 events/hour, nadir oxygenation saturation 73.2%. She had significant chronic bilateral nasal obstruction due to prior trauma, requiring septoplasty and bilateral turbinate reduction. Post-operatively, her CPAP adherence significantly improved (not sure what word you had planned here) with a residual AHI of 0.6 and an average nightly use of 8.5 hours. Despite these improvements, she began to report nocturnal desaturation alerts on her smartwatch. She also had a longstanding history of refractory migraines and previously trialed multiple preventative and abortive therapies. Additional work up with a transesophageal echocardiogram revealed an interatrial shunt consistent with a PFO. She underwent percutaneous PFO closure and reported dramatic improvement in her migraines within one week. Discussion Our case underscores the diagnostic and therapeutic uncertainty in managing persistent nocturnal oxygen desaturation in patients with well-controlled OSA. Prior studies have demonstrated an association between PFO and worsened nocturnal hypoxemia in patients with untreated or severe OSA.4,7 However, closure has not consistently improved oxygenation metrics, even in those with large right-to-left shunts.3,5 Additionally, the presence of a PFO may function as a pressure-relief compensatory mechanism rather than pathologic shunt in some patients, particularly in the absence of overt pulmonary hypertension. A broader diagnostic framework and physiological nuance is needed in approaching these complex presentations. Finally, the dissociation between oxygenation and headache improvement observed in this case is consistent with prior evidence that PFO closure can restore neurovascular homeostasis.8,9 Notably, this patient had failed multiple preventative and abortive therapies, highlighting the potential role of PFO closure in refractory migraine cases where symptom burden remains high despite pharmacologic optimization. This abstract is funded by: None