Compared to other forms of PAP therapy, ASV offers significant benefits for the treatment of central SDB*– including improvement of apnoea hypopnoea index (AHI), reduction of respiratory events and alleviation of daytime sleepiness. This has been demonstrated in multiple clinical trials across various patient types.
In an intention-to-treat analysis, success (apnoeahypopnoea index [AHI] < 10) at 90 days of therapy was achieved in 89.7% of patients treated with ASV versus 64.5% of participants treated with CPAP.1
[N =66, prospective randomised trial]
After 30 days of APAP treatment, ASV provided a further reduction (compared to baseline) of 12.9% in AHI, 48.5% in central sleep apnoea index (CSAI), 26.1% in micro-arousal index (MAI), and 37.9% in Epworth Sleepiness Scale (ESS) score at similar mean pressure.2
[N = 42, sequential study].
In opioid-induced CSA, ASV therapy reduced AHI by 84.7%, central apnoea index (CAI) by 95.7%, apnoea index (AI) by 96.4%, and respiratory arousal index (RAI) by 77.1% when compared to bi-level ST. Respiratory parameters were normalised in 83.3% of patients on ASVAuto but only 33.3% of patientson bi-level ST.3
[N = 18, prospective, randomised crossover polysomnography study]
ASV therapy improved outcomes for post-acute ischemic stroke patients with CSA, reducing AHI by 81.8% and ESS by 35.6%.4
[N = 15, single centre retrospective analysis]
Prospective randomised and observational heart failure studies (already presented and shortly to be published) have suggested that ASV may be beneficial in HF patients with preserved ejection fraction and in those who have CSA with coexisting obstructive sleep apnoea (OSA).5,6 Currently there is no evidence that these patients would be at any risk of harm from ASV therapy.
* ASV therapy is contraindicated in patients with chronic, symptomatic heart failure (NYHA 2-4) with reduced left ventricular ejection fraction (LVEF ≤ 45%) and moderate to severe predominant central sleep apnoea.