Effective Handling of Health Care Transition for Young People Living With HIV: A Consensus of Experts in Thailand Using Modified Delphi Method.

Obstructive sleep apnea (OSA) is associated with long-term cardiovascular and metabolic morbidity, impaired cognitive function, and increased mortality [–]. Importantly, apnea–hypopnea index (AHI) and oxygen desaturation index (ODI) do not fully capture disease burden. Growing evidence suggests that cumulative hypoxic burden (depth and duration of desaturations), reduced N3 sleep, REM-predominant OSA, sleep fragmentation from recurrent arousals, and nocturnal autonomic dysregulation independently contribute to adverse cardiovascular and neurocognitive outcomes [–]. Sleep is a fundamental physiologic process in humans and is regulated by coupled circadian and homeostatic processes. The circadian process modulates sleep propensity throughout the 24 h, whereas sleep homeostasis (SH) is a process where sleep pressure accumulates during prior wakefulness and dissipates during subsequent sleep []. SH is typically quantified by the power in delta activity or slow wave activity (SWA; 0.5–4 Hz) during non-rapid eye movement (NREM) sleep, in electroencephalogram (EEG) or local field potentials (LFPs) [, ]. Although preceding sleep–wake history is considered a key determinant of sleep amount and intensity, the circadian process also plays an important role []. According to synaptic homeostasis hypothesis, sleep pressure reflects the strength of the synapses which increase with wakefulness and downscales during sleep. Thus, sleep pressure and synaptic potentiation are consequences of wakefulness, and sleep homeostasis serves to downscale synapses and reduce sleep pressure []. In addition, SH serves to maintain energy balance [, ] and cognition [, ] and supports immune function []. Experimentally, SH is assessed mainly by measuring an increase in SWA in humans and animals after sleep deprivation []. A second SH measure is the overnight dynamics of SWA, where it is highest at the beginning of the night, gradually dissipating in successive NREM episodes across the night []. Other measures include amplitude, frequency, and slopes of the slow waves which are all higher at the beginning of the night and lower in the end of the night [, ]. Since SWA homeostatically increases with time awake, increase in SWA with wake after sleep onset (WASO) time is also expected. This was previously demonstrated in rodents as well as humans [, ] and hence is another measure of SH.