Source: [ctgov](https://clinicaltrials.gov/study/NCT07409649)
Authors: Poitiers University Hospital
Venue: NOT_YET_RECRUITING · 2026-05-27
Abstract
Sleep apnoea-hypopnoea syndrome (SAHOS), which causes numerous comorbidities, particularly cardiovascular ones, is widespread worldwide today and incurs significant healthcare costs.
Current research in this field focuses on identifying different phenotypes in affected patients in order to provide more personalised treatment.
One of these phenotypes appears to be linked to instability in ventilatory control due to an increase in loop gain (LG) in these subjects.
However, the pathophysiology of this ventilatory control instability due to increased LG is not fully understood. It is still difficult to determine whether subjects have an intrinsically high LG or if exposure to intermittent hypoxia during OSA promotes an increase in LG.
It has also been demonstrated that OSA causes vascular hyperreactivity by increasing oxidative stress through elevated ROS production. This leads to endothelial dysfunction in response to intermittent hypoxia associated with apnoea. Extracellular vesicles
AI relevance (4/5): Sleep apnea pathophysiology study exploring ventilatory control mechanisms and hypoxia effects; directly aligns with corpus focus on sleep apnea biology.
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