Sleep Medicine

Slow-wave homeostasis is impaired in idiopathic hypersomnia, especially in long-sleepers

In a 32-hour ad libitum PSG protocol, 208 idiopathic hypersomnia (IH) patients and 25 controls were studied without circadian cues. Slow-wave activity persisted during extended sleep in all IH participants, indicating incomplete dissipation of sleep pressure. Wakefulness produced greater SWA rebound only in IH with long sleep time, suggesting faster sleep-pressure accumulation in this subgroup. Modeling showed sleep pressure failed to dissipate even after nine hours of sleep and accumulated more rapidly in early wake in IH-long sleepers. 1

Acetazolamide modestly improves REM-predominant OSA via upper-airway mechanics

This randomized, double-blind, crossover trial enrolled 11 patients with REM-predominant OSA to acetazolamide 500 mg or placebo for three nights. Acetazolamide reduced AHI by 35.5% and hypoxic burden by 35.9% versus placebo, meeting co-primary endpoints. Contrary to expectations, acetazolamide did not mitigate REM-related dips in ventilatory drive compared with placebo. Instead, it reduced pharyngeal collapsibility and increased genioglossus responsiveness, improving ventilation at eupneic drive and ventilation–drive slopes. 2

OSA increases post-ACS events mainly when lipoprotein(a) is elevated

This OSA-ACS sub-analysis followed 1137 acute coronary syndrome patients, 53.5% with OSA defined as AHI ≥15 events per hour. Over a median 3.6 years, OSA increased MACCE risk only among patients with lipoprotein(a) above the cohort median. In that higher Lp(a) group, OSA was associated with a MACCE hazard ratio of 1.59, with confidence intervals excluding 1. Rising Lp(a) levels showed progressively higher MACCE risk in the OSA group and more high-risk and low-attenuation plaques on coronary CTA. 3

Mechanistic review: how sleep-disordered breathing drives cardiometabolic disease

This review summarizes mechanistic links between sleep-disordered breathing and cardiometabolic disease using human and experimental data. Key upstream factors include intermittent hypoxia, autonomic imbalance, intrathoracic pressure swings, systemic inflammation, sleep fragmentation, and oxidative stress. These perturbations influence molecular pathways such as hypoxia-inducible factors, microRNAs, and the gut microbiome. Downstream, they promote vascular and myocardial dysfunction, hypertension, insulin resistance, dyslipidemia, and weight gain. 4