Impact of mandibular advancement device therapy on cerebrovascular reactivity in patients with carotid atherosclerosis combined with OSAHS.

Abstract

Obstructive sleep apnea-hypopnea syndrome (OSAHS) may affect cerebrovascular reactivity (CVR), representing cerebrovascular endothelial function, through complex cerebral functional changes. This study aimed to evaluate the change of CVR after 1-month and 6-month mandibular advancement device (MAD) treatment of patients withcarotid atherosclerosis (CAS) combined with OSAHS. Patients with carotid atherosclerosis combined withOSAHS who voluntarily accepted Silensor-IL MAD therapy were prospectively enrolled. All patients underwent polysomnographic (PSG) examinations and CVR evaluation by breath-holding test using transcranial Doppler ultrasound at baseline (T0), 1month (T1), and 6months (T2) of MAD treatment. Of 46 patients(mean age 54.4± 12.4 years, mean body mass index [BMI] 27.5± 4.5 kg/m2), 41 patients (responsive group) responded to the 1-month and 6-month treatment of MAD, an effective treatment rate of 89%. The remaining 5 patients (non-responsive group) were younger (47.4 ± 13.5years) and had ahigher BMI (35.8 ± 1.8kg/m2). The responsive group had an improvement of apnea-hypopnea index (AHI) (events/h) from 33.0 ± 25.0 (T0) to 12.4 ± 10.4 (T1) and 8.7 ± 8.8 (T2), P < 0.001; minimum arterial oxygen saturation (minSpO2) (%) increasedfrom 79.8 ± 9.1 (T0) to 81.8 ± 9.4 (T1) and 85.2 ± 5.4 (T2), P < 0.01; longest apnea (LA) (s) decreasedfrom 46.5 ± 23.1 (T0) to 33.3 ± 22.7 (T1) and 29.4 ± 18.5 (T2), P < 0.001; T90 (%) decreasedfrom 10.3 ± 14.9 (T0) to 6.1 ± 11.8 (T1) and 3.3 ± 7.5 (T2), P < 0.05. Sleep architecture of these patients also improved significantly. The responsive group had a significant increase in left, right, and mean breath-holding index (BHI): left BHI(/s) from 0.52 ± 0.42 (T0) to 0.94 ± 0.56 (T1) and 1.04 ± 0.64 (T2), P < 0.01; right BHI(/s) from 0.60 ± 0.38 (T0) to 1.01 ± 0.58 (T1) and 1.11 ± 0.60 (T2), P < 0.01; mean BHI(/s) from 0.56 ± 0.38 (T0) to 0.97 ± 0.55 (T1) and 1.07 ± 0.59 (T2), P < 0.01), suggesting improved CVR. Effective MAD therapy is beneficial for restoring cerebrovascular endothelial function in patients with CAS and OSAHS in a short period (1month and 6months). Clinical trial registration number: NCT03665818. September 11, 2018.