Table 3.

Beneficial effects of different therapies for CSA on AF outcomes.

Therapy	Beneficial Effect	Outcomes
CPAP	Diminish frequency of periodic arousals seen with apneic episodes resulting in: •Improved nocturnal oxygenation •Improved sympathetic overactivity •Down-regulation of RAAS •Diminished catecholamine levels •Early detection of AF induced CSA in patients requiring a CPAP for previously diagnosed OSA due to long-term patient monitoring All the above thought to be involved in the pathophysiology of AF induced by CSA	•Significantly ↓ the recurrence of AF •≥ 50% ↓ in AHI •Improved LVEF •No mortality benefit
Supplemental Oxygen	•Decreases hypoxic drive and thus weakens the hyperventilatory response according to change in PaCO2 •Overall very well tolerated Diminishing hypoxic episodes may prevent electrical and structural cardiac remodeling that potentially predisposes patients to AF	•≥50% ↓in AHI •No mortality benefit, yet shows improvement in quality of life
Bi-PAP	•Good alternative therapy for patients with hypoventilation CSA and no response to CPAP or oxygen supplementation. •Normalize AHI by increasing ventilation through tidal volume augmentation As mentioned with CPAP therapy, improvement in nocturnal oxygenation by normalizing AHI can diminish the risk of AF	•When used with a high IPAP-to-EPAP difference, may worsen CSA by lowering the PaCO2
ASV	•May be beneficial in patients with hyperventilation-related CSA (especially those with CSB-CSA) and HF with preserved EF. •The acute use of ASV is effective on CSA by increasing oxygen saturation and reducing heart rate and heart rate variability •ASV combined with OMT has demonstrated a reduction in arrhythmias, including AF when compared to OMT alone. •Better tolerated by patients compared to PAP as the continuous pressure of the machine can be highly irritating for some patients. •The delivery of inspiratory pressure over expiratory pressure allows for substantial improvement of AHI ultimately reducing the risk for arrhythmias such as AF Caution: ASV in HFrEF associated with moderate-severe CSA has been linked to increased risk of all-cause and cardiac mortality	•Decreased AHI •Decreased hypoxia •Increase in all-cause and cardiovascular mortality in patients with HFrEF
Respiratory Stimulants	•May be beneficial in patients with hyperventilation-related CSA intolerant to PAP machines or supplemental oxygen •Stimulates respiration and decreases frequency of central apnea by provoking metabolic acidosis Improved nocturnal oxygenation by decreasing the number of central apnea and hypopnea episodes can result in less arrhythmias by mechanisms shown in Fig. 1	•Approximate 40–70% ↓ in AHI •↓ Daytime sleepiness and fatigue •Limited benefits on cardiac function and sleeping architecture
Phrenic nerve stimulation	•May be an option for patients with symptomatic CSA who fail or are intolerant to CPAP and/or other therapies. •Attain diaphragmatic contraction similar to normal breathing by delivering transvenous stimulation to the phrenic nerve Improves quality of life and sleep in patients with CSA and AF regardless of heart failure status	•>50% Reduction in AHI •Long-term safety under investigation (Safety and efficacy through 36 months has been published)Decreased daytime sleepiness •Improved Quality of Life •Decreased arousals and improved REM sleep

CSA = Central sleep apnea; AF = Atrial fibrillation; CPAP = Continuous positive airway pressure; RAAS = Renin angiotensin aldosterone system; OSA = Obstructive sleep apnea; Bi-PAP = Bilevel positive airway pressure; AHI = apnea-hypopnea index; ASV = Adaptive sero-ventilation; PNS = Phrenic Nerve stimulation