Xuan-Lan Nguyen

Impact of Mandibular Advancement Therapy on Endothelial Function in Severe Obstructive Sleep Apnea

Rationale: Endothelial dysfunction, a major predictor of late cardiovascular events, is linked to the severity of obstructive sleep apnea (OSA). Objectives: To determine whether treatment with mandibular advancement device, the main alternative to continuous positive airway pressure, improves endothelial function in patients with severe OSA. Methods: In this trial, we randomized patients with severe OSA and no overt cardiovascular disease to receive 2 months of treatment with either effective mandibular advancement device or a sham device. The primary outcome, change in reactive hyperemia index, a validated measurement of endothelial function, was assessed on an intention‐to‐treat basis. An embedded microsensor objectively measured treatment compliance. Measurements and Main Results: A total of 150 patients (86% males; mean [SD] age, 54 [10] yr; median [interquartile range] apnea‐hypopnea index, 41 [35‐53]; mean [SD] Epworth sleepiness scale, 9.3 [4.2]) were randomized to effective mandibular advancement device (n = 75) or sham device (n = 75). On intention‐to‐treat analysis, effective mandibular advancement device therapy was not associated with improvement of endothelial function compared with the sham device. Office and ambulatory blood pressure outcomes did not differ between the two groups. Effective mandibular advancement device therapy was associated with significant improvements in apnea‐hypopnea index (P < 0.001); microarousal index (P = 0.008); and symptoms of snoring, fatigue, and sleepiness (P < 0.001). Mean (SD) objective compliance was 6.6 (1.4) h/night with the effective mandibular advancement device versus 5.6 (2.3) h/night with the sham device (P = 0.006). Conclusions: In moderately sleepy patients with severe OSA, mandibular advancement therapy reduced OSA severity and related symptoms but had no effect on endothelial function and blood pressure despite high treatment compliance. Clinical trial registered with www.clinicaltrials.gov (NCT 01426607).

Left ventricular diastolic dysfunction in obstructive sleep apnoea syndrome by an echocardiographic standardized approach: An observational study

BACKGROUND The association between obstructive sleep apnoea syndrome (OSAS), left ventricular (LV) diastolic dysfunction and LV geometry remains controversial because of coexisting disorders. AIMS To evaluate LV diastolic dysfunction and its independent predictors in a real-life cohort of OSAS patients, by a standardized approach. METHODS We consecutively included 188 OSAS patients after an overnight polysomnography to undergo clinical evaluation, ambulatory blood pressure measurement and complete echocardiography, combining M-mode, two-dimensional Doppler and tissue Doppler imaging modes. Correlations between OSAS severity and clinical and echocardiographical variables were assessed, and logistic regression models were used to identify possible determining factors of LV diastolic dysfunction. RESULTS Most patients were hypertensive (n=148, 78.7%) and already receiving treatment by continuous positive airway pressure (n=158, 84.5%). The prevalence of LV hypertrophy, defined by LV mass index (LVMi) normalized by height (2.7), was 12.4%, with a significant correlation with hypertension (P=0.004). The apnoea-hypopnoea index was correlated with body mass index (P<0.0001), 24-hour systolic blood pressure (P=0.01) and LVMi normalized by height (2.7) (P=0.03). Diastolic function assessed by a global approach was impaired for 70 patients (37.2%) and none of the OSAS severity variables was a determining factor after multivariable analysis with adjustment for age and sex. CONCLUSION Diastolic dysfunction assessed by a standardized approach is common in OSAS and should be routinely evaluated; it is independently predicted by none of the respiratory severity variables.

Impact of mandibular advancement therapy on endothelial function in severe obstructive sleep apnoea

This study aimed to determine whether treatment with mandibular advancement device, the main alternative to continuous positive airway pressure, improves endothelial function in patients with severe OSA. We randomized patients with severe OSA and no medical history of cardiovascular disease to receive 2 months of treatment with either effective mandibular advancement device or a sham device. The primary outcome, change in reactive hyperemia index, a validated measurement of endothelial function, was assessed on intention-to-treat bases. An embedded micro sensor objectively measured treatment compliance. 150 patients [86% males; mean (SD) age, 54 (10); median [IQR] apnea-hypopnoea index, 41 [35-53]; mean Epworth sleepiness scale, 9.3 (4.2)] were randomized to effective mandibular advancement device (n=75) or sham device (n=75). In the intention-to-treat analysis, effective mandibular advancement device therapy was not associated with an improvement in endothelial function when compared to sham device. Office and ambulatory blood pressure outcomes did not differ between the 2 groups. Effective mandibular advancement device therapy was associated with significant improvements in apnea-hypopnea index (p vs 5.6 (2.3) h/night with sham device (p=0.006). Conclusion In moderately sleepy patients with severe OSA, mandibular advancement therapy reduced OSA severity and related symptoms with no effect on endothelial function and blood pressure despite high treatment compliance.