1188 Decreased Tolerance to Hypoglossal Nerve Stimulator After Cardioversion

Abstract Introduction Hypoglossal nerve stimulator (HNS) therapy is a treatment for moderate to severe obstructive sleep apnea (OSA) in patients who cannot tolerate positive airway pressure (PAP) therapy. HNS is an implanted device that stimulates tongue protrusion at the start of inspiration 1,2,3. OSA is associated with atrial fibrillation and increased risk of recurrence after cardioversion and catheter ablation 4. Currently, the presence of atrial fibrillation is not a contraindication to HNS implantation. However, there are accumulating reports that HNS patients requiring external cardioversion for atrial fibrillation have resulted in device dysfunction. 5 Report of case(s) An eighty-two-year-old female with past medical history of obstructive sleep apnea with respiratory event index (REI) of 27.8 and atrial fibrillation/flutter who was implanted with HNS on 3/11/22. She was activated with configuration +-+ and functional threshold of 2.0 volts and able to increase her amplitude comfortably to 2.5V. Two months after activation, she underwent cardioversion for persistent atrial fibrillation and immediately found her stimulation intolerable. She reduced her amplitude to 1.8V and was able to gradually escalate to 2.7V. Her device was checked with no apparent malfunction. She received a second cardioversion with similar results, and again reduced her amplitude and slowly increased to 2.5V. Her subsequent titration study determined that 2.6V was ideal. Following an ablation 2 months later, stimulation was intolerable once more. Therapy was paused for 2 weeks; her amplitude was reduced to 1.4V and eventually returned to 2.0V. Follow up home study showed REI of 10.5 on 2.0V. Conclusion This case report highlights a rare occurrence of HNS intolerance after cardioversion. There has been one other report of device intolerance related to neurapraxia after cardioversion. The neuropraxia was believed to have been a direct effect of nerve injury related to electrical current traveling along the lead body to the electrode-tissue interface 6. It is possible that the intolerance in our case is related to a similar mechanism. Clinicians should be aware of potential complications given the high incidence of atrial fibrillation in patients with OSA. This case may also serve as an example of how to re-introduce therapy in patients with HNS intolerance proceeding cardioversion. Support (if any)