0632 Retrospective Cohort Analysis of Diagnostic Polysomnography to Predict Treatment Response to Hypoglossal Nerve Stimulation in Obstructive Sleep Apnea
Abstract Introduction Hypoglossal nerve stimulators (HGNS) are used in patients with moderate-to-severe obstructive sleep apnea (OSA) who are unable to tolerate or do not respond to continuous positive airway pressure (CPAP) therapy. However, a subgroup of patients fail to achieve resolution of OSA with HGNS alone. Previous studies have shown that lower BMI, lower nadir oxygenation, decreased sleep latency, and higher VOTE score on drug-induced sleep endoscopy (DISE) predict better treatment outcome. We hypothesize that baseline diagnostic polysomnography (PSG) may further predict which patients will achieve successful therapeutic outcome with HGNS therapy. Methods We conducted a retrospective analysis of all adult patients who underwent HGNS implantation at Mayo Clinic Arizona between 2019-2025 and had a pre-implantation diagnostic PSG available for review. Treatment success was defined by Sher Criteria: >50% reduction in post-treatment apnea hypopnea index (AHI) to a final AHI of < 20/hr. Responders met Sher criteria and non-responders did not meet Sher criteria. Demographics, sleep questionnaire results, PSG variables, and VOTE score on DISE were collected and analyzed using Spearman’s rank correlation of reduction in AHI. Results Twenty-three patients (11M/12F, median age: 69[IQR:64,75] years) met inclusion criteria. Median baseline AHI was 24[IQR:19,37]/hr. Median post-implant AHI was 8 [IQR:3, 14]/hr. Responders (n=15, 65%) and non-responders (n=8, 35%) demonstrated median post-implant AHI of 4.5[IQR:2.3,7.3]/hr and 15.7[IQR:12.3,28.5]/hr, respectively. Treatment response was associated with less time with SpO2 < 88% (T88%) (21min [IQR:3,64] vs. 73[IQR:36,105mins]; p=0.023) and higher central apnea index (CAI) (1[IQR:0.1,3] vs. 0[IQR:0,1], p=0.03) on pre-implantation PSG. Conclusion In this small cohort of OSA patients, less nocturnal hypoxemia as defined by T88% and higher baseline central apnea index were predictors of better treatment response to HGNS therapy as measured by Sher criteria. We hypothesize that greater nocturnal hypoxemia likely reflects more severe airway obstruction during sleep. Our analysis also showed that responders had higher baseline CAI than non-responders, however we believe this association is not clinically significant and likely driven by one outlier (CAI 13/hr). Further analysis in a larger HGNS cohort is needed to confirm these findings. Data enrichment efforts and more sophisticated analyses are underway. Support (if any)
Effects of Acute Hypocapnia on Postural Standing Balance Measured by Sharpened Romberg Testing (SRT) in Healthy Subjects
Introduction The sharpened Romberg test (SRT) is a physical maneuver that has been used to identify ataxia in individuals in resource-limited settings. Previous research has suggested that performance on balance testing may be affected by hypocapnia. In this study, we sought to determine whether acute hyperventilation-induced hypocapnia affects performance on the SRT at 501 meters above sea level. Methods We recruited 22 healthy subjects. Each subject performed a baseline SRT. Subjects were then asked to hyperventilate to the point of hypocapnia, confirmed by measurement with a capnometer. Subjects were then asked to re-perform SRT. The primary endpoint was time to loss of balance, measured as time-to-stepout. Results Time-to-stepout (TTS) on SRT at baseline had a mean ± standard deviation of 101 ± 117 s. In the hypocapnic condition, TTS was reduced to 48 ± 68 s. TTS normalized to 121 ± 132 s after recovery to normal capnic levels. Time-to-stepout was found to be significantly shorter in the hypocapnic measurement compared to the baseline measurement ( P = .0128). Statistical analysis was conducted using one-tailed, paired sample T-tests using a P-value of < .05. Conclusions Our study found a statistically and clinically significant reduction in performance on a balance test (SRT) when exposed to acute hyperventilation-induced hypocapnia compared to a eucapnic control. Our results suggest that acute hypocapnia may contribute to neurological dysfunction independently of hypobaric hypoxia.