0490 Loop Gain and Arousal Threshold Association with Nocturnal Blood Pressure Dysregulation in OSA

Abstract Introduction Unstable ventilatory control from high loop gain and low arousal threshold are non-anatomical traits that predispose to sleep disordered breathing. In OSA, sympathetic response from respiratory events lead to blood pressure (BP) surges, nocturnal hypertension, and further BP dysregulation. We examined the association of loop gain and arousal threshold with average nocturnal BP during sleep, non-dipping BP, and respiratory event induced BP surge. Methods Data was collected from 60 adults with newly diagnosed moderate to severe OSA, of which data on 22 participants have been analyzed. Participants completed polysomnography with nocturnal beat to beat BP monitoring. Subsequently, loop gain, arousal threshold, average nocturnal BP, BP dipping, and BP surge in response to respiratory events were quantified. Age, sex, body mass index (BMI), and number of antihypertensives were recorded as covariates. The study was approved by the institutional review board (IRB). STATA v19.5 was used for data analysis. Results The mean age was 46.5±9.5 years, average BMI 36.4±6.9 kg/m2, 12/22 were men, and 12/22 were on antihypertensive therapy. The apnea hypopnea index was in the severe OSA range (AHI3% 41.4±36.9/hour, average hypoxia burden was 91.4±112%). Higher loop gain was associated with non-dipping mean arterial BP (MAP, t-statistic=-2.72, p=0.01) and higher respiratory event induced MAP surge (t-statistic=3.35, p=0.004) but was not associated with average MAP during sleep. Higher arousal threshold was associated with higher average MAP during sleep (t-statistic=2.43, p=0.02), non-dipping MAP (t-statistic=-2.39, p=0.03), and respiratory event induced MAP surge (t-statistic=2.80, p = 0.01). Conclusion This preliminary analysis demonstrates that key pathophysiological traits of high loop gain (increased chemosensitivity and downstream sympathetic activation) and high arousal threshold (possibly through longer, more severe respiratory events) are associated with nocturnal BP dysregulation in OSA. We plan to analyze the full dataset of 60 participants to confirm these findings and compare the association of nocturnal BP dysregulation to pathophysiological traits vs. AHI and hypoxia burden. These findings will provide novel mechanistic insights and potential biomarkers for OSA-induced hypertension. Support (if any) NIH Grant number NHLBI R56HL157182