1173 Unmasking Severe OSA After Transvenous Phrenic Nerve Stimulation for Central Sleep Apnea

Abstract Introduction In the absence of reversible etiology, central sleep apnea (CSA) may be treated with positive airway pressure (CPAP or BPAP), adaptive servo-ventilation, or supplemental oxygen. In 2017, a transvenous phrenic nerve stimulator (PNS), the remedē System™, was FDA-approved for moderate-to-severe CSA. Five-year outcomes data confirmed the device’s sustained efficacy, with improvements in symptoms, apnea-hypopnea index(AHI), and central apnea index(CAI). While the device effectively treats CSA, unrecognized upper airway obstruction may hinder clinical success. This case report describes a patient whose polysomnography (PSG) suggested candidacy for PNS; however, his airway collapsibility led to severe obstructive sleep apnea(OSA), unmasked after PNS implantation. Report of case(s) Our patient is a 74-year-old with longstanding severe CSA and chronic insomnia. He has a history of spasmodic dysphonia status post recurrent laryngeal nerve ablation. His unilateral vocal fold paralysis was followed by injection medialization for voice augmentation. He is also an asymptomatic carrier of myotonic dystrophy(MD), identified after his grandchild was diagnosed with MD. He presented to our institution for daytime sleepiness, disrupted sleep and snoring with complaints of PAP intolerance. PSG revealed an AHI4% of 49.1 events/hour with 0 obstructive apneas, 89 central apneas, and 53 unclassified hypopneas. Transthoracic echocardiogram was unremarkable. Pulmonary function tests were normal without evidence of neuromuscular weakness or extrathoracic obstruction. He underwent PNS implantation. Postoperatively, the patient continued endorsing unrefreshed sleep. His PNS titration study demonstrated prolonged flow limitation and an AHI4% of 35.2 events/hour with frequent obstructive events. He is now using a mandibular advancement device (MAD) with the PNS. Conclusion This case highlights the impact of upper airway collapsibility on PNS treatment response. Although our patient’s history may have indicated greater susceptibility to airway collapse, preoperative PSG did not reveal unequivocal OSA. However, frequent obstructive hypopneas were unmasked after PNS implantation. This patient’s upper airway collapse was underrepresented on PSG, and increased negative intrathoracic pressure during the PNS titration may have worsened the severity. Since differentiating central from obstructive hypopneas can be challenging, PNS may not be ideal for CSA patients with increased hypopnea burdens. If OSA emerges postoperatively, adjuncts like MAD, CPAP, or hypoglossal nerve stimulation may stabilize the upper airway. Support (if any)