What question did this study set out to answer?

To evaluate the effects of hypoglossal nerve stimulation on obstructive sleep apnea and central sleep apnea detection.

May 10, 2026

1316 Treatment of Severe Obstructive Sleep Apnea with Hypoglossal Nerve Stimulation Unmasks Underlying Central Sleep Apnea and Cardiac Conduction Block

Puntos clave

To evaluate the effects of hypoglossal nerve stimulation on obstructive sleep apnea and central sleep apnea detection.
Case report of an 84-year-old male with severe obstructive sleep apnea considered for HGNS due to PAP intolerance.
Home sleep apnea testing and in-lab polysomnogram were utilized for evaluations.
Follow-up included titration and adjustment of HGNS settings with subsequent cardiology evaluation.
Initial AHI was 58.9 with CAI of 1.2, showing severe OSA; central apneas predominated during HGNS titration.
Intermittent complete heart block was revealed, leading to pacemaker implantation after confirming CSA persists despite HGNS treatment.
Case emphasizes importance of in-lab PSG to detect CSA and the complexities in managing patients intolerant to PAP.

Resumen

Abstract Introduction Hypoglossal nerve stimulation (HGNS) is a safe and effective therapy for obstructive sleep apnea (OSA) in patients who are intolerant of positive airway pressure (PAP) therapy. HGNS does not address central sleep apnea (CSA), and patients with 25% central apneas are not considered HGNS candidates. Home sleep apnea testing (HSAT) is less reliable at diagnosing CSA, but there is no requirement to undergo in-lab polysomnogram (PSG) to determine candidacy for HGNS. We present a case of underlying CSA due to cardiac conduction block revealed during HGNS titration. Report of case(s) 84-year-old male with severe OSA presented for consideration of HGNS due to persistent daytime sleepiness and PAP intolerance despite excellent PAP adherence. PAP download revealed residual apnea-hypopnea index (AHI) 12.9 with central apnea index (CAI) 7.4 and 18% Cheyne-Stokes Respiration (CSR). PAP settings were adjusted to temporarily reduce AHI as he underwent workup for HGNS. Diagnostic HSAT showed severe OSA with AHI 58.9 (CAI 1.2). Drug Induced Sleep Endoscopy did not show complete concentric collapse of the soft palate. HGNS was implanted. Patient tolerated therapy well with good adherence and subjective benefit. During follow up PSG, central apneas predominated prior to initiation of HGNS and during HGNS titration, yet appeared to resolve at amplitude of 2.3V. The patient underwent additional programming of HGNS, including awake endoscopy and advanced fine-tuning PSG, which confirmed adequate reduction of obstructive events with HGNS but persistent CSA/CSR. Cardiology evaluation revealed intermittent complete heart block with junctional escape rhythm. Cardiac events occurred primarily at night. The patient ultimately underwent dual chamber pacemaker implantation. Conclusion Effective treatment of OSA with HGNS can reveal clinically significant CSA and underlying occult cardiac conduction disease. CSA is often underdiagnosed, and PAP downloads may provide clues of more complex sleep disordered breathing in OSA patients who have comorbid CSA. This is a cautionary tale of the limitations of HSAT in detection of CSA and the importance of in-lab diagnostic PSG to determine appropriateness for HGNS. The case also highlights the importance of a multidisciplinary approach to treatment of sleep disordered breathing particularly in PAP intolerant patients. Support (if any)

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