0489 Event-Related Airflow Obstruction in Obstructive Sleep Apnea is Associated with Hypertension in the Hispanic Community Health Study (HCHS/SOL)

Introduction Obstructive sleep apnea (OSA) is a well-established risk factor for hypertension, but not all individuals with OSA have the same risk. We investigated whether specific features of respiratory events—magnitude of ventilation reduction or airflow obstruction—can identify individuals at greatest risk for hypertension. Methods Nasal pressure from baseline in-home sleep apnea tests of Hispanic Community Health Study/Study of Latinos (HCHS/SOL) were used to derive two respiratory-event-related ventilation measures. Ventilation was estimated from square-root–transformed, integrated nasal pressure signal (tidal volume × respiratory rate) and was scaled 0–100% (0% = apnea, 100% = normal). Peak reduction in ventilation during respiratory events relative to baseline was then calculated using ensemble averaging. Additionally, airflow-shape analysis (100% = open airway, 0% = fully obstructed) was used to quantify changes in airflow obstruction during respiratory events relative to baseline. Logistic regression assessed associations of ventilation measures with hypertension defined by NHANES criteria at both a) baseline and b) follow-up (adjusting for baseline hypertension). Models were adjusted for age, sex, body mass index (BMI), Hispanic background, site, sampling weights, apnea-hypopnea index (AHI), and total sleep time. Results Sample included 12,073 participants (Age:47.4±13.2 years, BMI:29.9±5.9 kg/m2, AHI:21.5±15.6 events/hr; follow-up: 6.04±0.79 years); 23.1% had hypertension at baseline and 30% at follow-up. At baseline, greater event-related reduction in ventilation was associated with prevalent hypertension (OR [95%CI]: 1.37[1.15–1.63] per 2 SD). Greater airflow obstruction showed an overall trend toward higher odds of hypertension (1.15[0.99–1.33], p=0.05) and was significant in participants with mild-to-no OSA (AHI< 15 events/hr; 1.56[1.17–2.10]; p-interaction=0.018). In contrast, greater event-related reduction in ventilation was not associated with hypertension at follow-up, whereas greater airflow obstruction was (1.24[1.06–1.46]); there was a trend toward higher odds in mild-to-no OSA (1.35[0.99–1.38], p=0.05). Additional adjustment for hypoxic burden modestly attenuated associations (< 13% coefficient change at baseline; < 2% at follow-up). Conclusion The magnitude of increase in airflow obstruction during respiratory events is associated with prevalent hypertension and the development of hypertension at follow-up. The degree of obstruction per se, beyond its downstream impact on ventilation and hypoxia, may be an important determinant of OSA-related hypertension risk. Support (if any)