Introduction Prior studies of patients with obstructive sleep apnea (OSA) show racial differences in clinical presentation. When compared with White patients, Black patients present with more severe OSA and greater sleepiness. Racial differences in upper airway collapsibility could explain these differences. Here, we investigated whether mean positive airway pressure (PAP) levels, a clinically accessible measure of upper airway collapsibility, differed by race in a cohort of patients adherent to PAP. Methods We conducted a retrospective analysis of White and Black adults with OSA who were prescribed auto-adjusting PAP (aPAP) therapy at a single academic center between January 2018 and January 2020. The analysis included adherent patients (usage on >70% of nights for ≥4 hours per night) with well-controlled OSA (defined as ≥50% reduction in apnea-hypopnea index [AHI] on aPAP and residual AHI< 10). Mean PAP level was compared between White and Black patients using linear regression controlled for age, gender, body mass index (BMI), AHI, O2 nadir, and mask type (full face, nasal, or unknown). Results Overall, 148 Black (56% women) and 230 White (36% women) patients were included. On average, Black patients were younger (50.7±14.6 vs. 53.8±12.7 years; p=0.037) with higher BMI (40.4±9.5 vs. 34.9±7.6 kg/m2; p< 0.0001). Black patients had less severe OSA on average, but this difference was not statistically significant (AHI of 33.9±25.5 vs 38.6±24.9 events/hour; p=0.077). After adjusting for covariates, Black patients had a 0.62 cm H2O (95% CI: 0.21 to 1.03) higher mean PAP level than White patients (p=0.003). There was a larger racial difference in mean PAP level among men (0.76 [0.16, 1.35] cm H2O; p=0.013) compared to a non-significant difference among women (0.34 [-0.23, 0.91] cm H2O; p=0.242). While statistically significant, differences were < 1 cm H2O and, thus, not clinically meaningful. Conclusion Black patients with OSA had a statistically significant but clinically insignificant difference in mean PAP level when compared with White patients. There was evidence of stronger differences in men than women. Further studies are needed to explore other potential mechanisms, including craniofacial anatomy, which may underlie racial differences in OSA presentation and outcomes. Support (if any) National Institutes of Health R01 1R01HL144859 (PIs: Schwartz, Dedhia)
Introduction Obstructive sleep apnea (OSA) is characterized by repetitive episodes of pharyngeal obstruction at one or more collapse sites. Multilevel collapse is a negative predictive factor for PAP-alternative surgical treatments. Pharyngeal manometry during drug-induced sleep endoscopy (DISE) permits an objective evaluation of anatomical obstruction sites and mechanisms, and may play a role in patient selection for PAP alternative therapies. We hypothesized that patients with multilevel collapse would have primary velopharyngeal collapse and secondary, downstream sites. Methods This prospective cohort of twenty consecutive patients with diagnosed OSA underwent DISE with nasal airflow monitoring and pharyngeal manometry. Two pressure catheters were placed at the (1) distal margin of the soft palate (Pus) and (2) retroepiglottic space (Pds). We sought to delineate site(s) of collapse by evaluating dissociations in airflow and air pressure during inspiratory flow limitation and/or complete obstruction. The primary site of collapse was defined by the initial segment at which inspiratory airflow and pressure dissociated (the critical pressure, Pcrit). Secondary site(s) were defined as the pressure at which the Pus and/or Pds signals subsequently dissociated (beyond the initial point of maximal flow). Results Twenty-one patients were evaluated of which signal quality and catheter placement in twenty were sufficient for analysis. Participants were elderly (58.3±14.3yrs, mean±SD), overweight (BMI 28.7±2. kg/m2), and had moderate-severe OSA (AHI 28.2±14.2 events/hour). Six patients had a single site of collapse, of which one was naso-palatal (Pcrit -2.6cmH2O) and five were infra-palatal (mean Pcrit -1.3cmH2O). In the patients with multilevel collapse (N=14), all had primary naso-palatal collapse (mean Pcrit 0.17±2.0cmH2O) and secondary infra-palatal sites of collapse (mean Pcrit -11.7±5.8cmH2O). Pcrit differed between the primary and secondary site by 11.9±6.5cmH2O (p< 0.01). Conclusion These findings suggest that single-site pharyngeal collapse is usually infra-palatal. In contrast, multilevel collapse is primarily due to velopharyngeal collapse with varying degrees of instability in downstream pharyngeal segments. When secondary infra-palatal sites readily collapse with minimal additional respiratory effort, laxity of the tongue and/or lateral walls may be strongly implicated in the pathogenesis of pharyngeal obstruction. Future studies can utilize pharyngomanometry to further target specific pharyngeal structures for OSA therapy. Support (if any) National Institutes of Health 1R01HL144859 (PIs: Schwartz, Dedhia)
Introduction Obstructive sleep apnea (OSA) is linked to cardiovascular disease, particularly when left untreated. Hypoglossal nerve stimulation (HGNS) is a novel and promising PAP alternative as it is well-tolerated and reduces OSA severity; however, its effect on mitigating cardiovascular risk secondary to OSA is unknown. The aim of this study is to evaluate the effect of HGNS on sympathetic and vascular function. Our hypothesis is mean 24-hour systolic blood pressures (SBP) will be improved at “active” levels of HGNS. Methods This study is a double-blinded, sham-controlled, randomized controlled therapy crossover trial. Subjects are randomized for four weeks in each arm to either “active” HGNS or “sham” HGNS, with “sham” HGNS being defined as the lowest voltage at which HGNS was sensed by the patient and/or visualized by the principal investigator. Included patients had already been implanted with the Inspire® device. Patients were excluded for active PAP therapy use, recent automobile accidents, a minimum difference (<30%) between “active” and “sham” voltages, and pregnancy. Results 53 patients met all inclusion criteria. Overall, the study cohort was older (mean [SD] age 66.8 [10.2]), overweight (BMI 28.8 [4.36]), 60% male, and predominantly of white race. There was no significant difference in mean 24-hour SBP between “active” and “sham” HGNS (122.4 mmHg [12.2] vs. 122.4 mmHg [11.2], respectively). Further, there was no significant difference in mean SBP during sleep between “active” and “sham” HGNS (115.0 mmHg [15.2] vs. 115.2 mmHg [14.4], respectively). Conclusion This is a randomized controlled trial evaluating cardiovascular outcomes in patients with OSA using HGNS therapy. The HGNS system permits a unique investigation of the therapy “on/off” effect on measures of the sympathetic nervous system and vascular health. “Active” HGNS levels, compared to “sham” HGNS levels, do not appear to reduce mean systolic blood pressure during wake or sleep periods. Support (If Any) Raj C. Dedhia, MD, MSCR is supported by the American Heart Association and the American Sleep Medicine Foundation.
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