Phrenic Nerve Stimulation in an LVAD Patient with Severe Sleep Apnea

Abstract

Introduction Central sleep apnea (CSA) occurs in approximately 35% of patients with heart failure, thought to be an acquired pattern of respiratory control instability related in part to elevated sympathetic nervous system activation. Studies show that CSA is an independent risk factor for morbidity and mortality in these patients. A newer approach to treatment involves implantation of a unilateral, transvenous phrenic nerve stimulator to restore a physiological breathing pattern during sleep. We present a case of a patient with heart failure and CSA who underwent placement of a phrenic nerve stimulator and subsequently a left ventricular assist device (LVAD). Case A 62 year-old male with NYHA III, ACC/AHA C heart failure (EF 15%), paroxysmal ventricular tachycardia with biventricular pacing and ICD placement who had polysomnography (PSG) that revealed severe CSA. He underwent placement of a transvenous phrenic nerve stimulation system. He subsequently reported improved symptoms, with less daytime sleeping and increased duration of daily exercise. His apnea hypopnea index decreased from 46.3 events/hour at baseline to 6.9 events/hour 18 months post-therapy, and his central apnea index decreased from 42.6 events/hour to 0.2 events/hour. Two years after device implant he underwent placement of an LVAD in the setting of worsening heart failure symptoms and refractory ventricular arrhythmias. Prior to surgery his device was placed in monitor mode. After successful LVAD implantation, despite normalization of cardiac output, he reported return of excessive daytime fatigue; PSG confirmed severe CSA. With device adjustment, the biventricular pacing leads, phrenic nerve stimulator system, and LVAD were able to run concurrently without artifact or interference. Subsequent PSG confirmed successful treatment of CSA along with improvement in symptoms. Discussion CSA is common in patients with heart failure, thought to be related to elevated sympathetic nervous system activation and hemodynamic perturbations. Medical treatment of heart failure has shown limited success in improving CSA, and small studies have shown that optimization of hemodynamics and end-organ function with LVAD implantation does not reverse CSA. We report the first case of a patient with successful implantation of both a transvenous phrenic nerve stimulator and an LVAD. Despite normalization of cardiac output after LVAD implantation, severe CSA persisted, consistent with prior case reports. Conclusion Phrenic nerve stimulation is an option for patients with heart failure and moderate to severe CSA, including LVAD patients.