Treatment of Central Sleep Apnea in Heart Failure Patients

Background Central sleep apnea (CSA) is a neurological breathing disorder, resulting from intermittent disruptions in the neural drive to breath. CSA differs substantially from the more prevalent Obstructive Sleep Apnea (OSA), which occurs as a result of muscles relaxing in the upper airway and preventing the passage of airflow. Sleep apnea is classified as "central" when over 50% of the apnea-hypopnea index (AHI) is driven by central events. CSA is a common and serious comorbidity in patients with heart failure (HF), with a prevalence of 30-50% in patients with a reduced left ventricular ejection fraction LVEF 45%. Patients with HF and untreated CSA suffer from poor outcomes, including increased morbidity and mortality as well as increased hospitalizations. Historically, CSA patients have received the same treatment options as patients suffering from OSA, including positive airway pressure (PAP) devices, nocturnal oxygen, and pharmacological treatments. However, recently published data has highlighted safety and mortality concerns with some forms of PAP therapy on patients with HF, CSA and reduced LVEF. A new FDA-approved implantable device therapy, phrenic nerve stimulation (PNS), has been designed specifically to treat CSA. Unlike positive airway pressure devices that use pressure to overcome obstructions and inflate the lungs, PNS activates the diaphragm to create negative pressure in the chest - mimicking the physiologic mechanism of natural breathing. In our institution we have developed a care pathway with a nurse practitioner designated as care coordinator responsible for initial screening, coordination of testing, and facilitation of treatment plan, whether that be with a sleep physician PAP device or electrophysiologist for implantable treatment. Objectives Describe a methodology and pathway to identify and treat HF patients with CSA. Methodology Guideline directed therapy for patients with HF now recommends sleep testing due to the deleterious effects of untreated sleep disordered breathing. With no clear patient characteristic that is predictive of CSA in patients with HF, clinicians should consider broadly testing patients with HF using polysomnography (PSG) or a home sleep apnea test (HSAT) with the ability to differentiate CSA from OSA. Results Clinical patient information from sleep (e.g. AHI) and cardiology (e.g. LVEF) should be used when determining a treatment plan. Implantable treatment options for CSA necessitate a robust pathway that requires communication across specialties (Figure 1). PNS requires collaboration among three clinical specialties: heart failure, sleep, and electrophysiology. Typically, heart failure identifies patients, sleep diagnoses, and electrophysiology implants the device. Providers also need to make a decision on how to best manage the CSA patient following the implant procedure for therapy titration and long-term patient follow-up. Regardless of which specialty manages the patientu0027s CSA therapy long-term, success in treating patients with heart failure and CSA depends on collaboration and communication among the clinicians. Conclusions Given newly available treatment options for CSA and the risks associated with some forms of PAP therapy for HF patients with reduced LVEF, providers should design a robust treatment pathway across sleep, heart failure, and EP to manage treatment of patients with CSA and HF.