Shear-mediated dilation of the internal carotid artery in patients with obstructive sleep apnea

Background: Obstructive sleep apnea (OSA) is a common sleep disorder with multiple unfavorable health outcomes including an increase in the risk of cerebrovascular disease. The complex mechanisms by which OSA increases the risk of cerebrovascular disease are not fully understood, but cerebrovascular endothelial dysfunction may play a role. However, a direct assessment of cerebrovascular endothelial function has not been performed in humans. It is well known that peripheral vascular endothelial function is impaired in OSA patients, but this impairment can be alleviated by continuous positive airway pressure (CPAP) treatment. Peripheral endothelial dysfunction is partly caused by increased oxidative stress and enhanced sympathetic nerve activity. Since these changes are also detrimental to cerebral vasculature, cerebral endothelial function is assumed to be attenuated in OSA patients. Purpose: This study aimed to evaluate whether the cerebrovascular endothelial function is impaired in OSA patients undergoing CPAP treatment compared to their age-matched counterparts. Methods: This study included seven middle-aged to elderly individuals diagnosed with OSA (63 ± 8 years; BMI 26 ± 7 kg/m 2 ; Apnea-hypopnea index 30 ± 10 events/hour, mean ± SD) and seven age-matched control subjects without OSA (64 ± 4 years; BMI 22 ± 7 kg/m 2 ). All patients were undergoing treatment with CPAP. Cerebrovascular endothelial function was evaluated using shear-mediated dilation of the internal carotid artery (ICA), which was induced by 30 seconds of hypercapnia (target end-tidal partial pressure of carbon dioxide +10 mmHg above baseline). ICA blood velocity and diameter were measured using a duplex ultrasound. Shear-mediated dilation was calculated as the percentage change in diameter compared with the baseline value. SR was calculated as 4 x blood velocity/diameter. The SR area under the curve (SR AUC ) above the baseline level was quantified as the incremental area under the curve from the onset of hypercapnia to peak ICA dilation. Results: No differences in baseline ICA diameter and SR AUC were found between the OSA and control groups. Shear-mediated dilation of the ICA was lower in OSA patients (3.6 ± 2.0%) compared to controls (6.2 ± 2.4%, P = 0.04). However, when shear-mediated dilation was adjusted using baseline diameter and SR AUC , no significant differences were observed between the OSA and control groups (3.8 ± 1.9% vs. 5.9 ± 1.9%, P = 0.08). Conclusion: Our findings suggest that cerebrovascular endothelial function in OSA patients undergoing CPAP treatment does not significantly differ from that in age-matched individuals. The current results imply that CPAP treatment may also have protective effects on cerebrovascular endothelial function. This study was supported by JSPS KAKENHI #21K11170. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.