Children with any obstructive sleep apnea had nearly double the odds of morning hypertension versus non-OSA peers (adjusted OR 1.87; 95% CI 1.30-2.70; p=0.001).
Observational (n=806)
No
Does obstructive sleep apnea increase the risk of morning hypertension in a pediatric population?
Severe obstructive sleep apnea in children independently doubles the odds of morning hypertension, highlighting the importance of early detection and management.
Effect estimate: adjusted OR 1.87 (95% CI 1.30-2.70)
p-value: p=0.001
Abstract Introduction Obstructive sleep apnea (OSA) is becoming increasingly recognized as a cause of pediatric hypertension through various mechanisms. Our aim of this study is to evaluate the impact of OSA on nocturnal blood pressure (BP) in children with OSA. Methods This study was a single-center retrospective analysis of children under 18 years old who underwent polysomnography (PSG) and had their blood pressure recorded before and after sleep studies. OSA severity was categorized by obstructive apnea-hypopnea index (OAHI) as normal ( 1 event/hr), mild (1–4.9 events/h), moderate (5–9.9 events/h), and severe (≥ 10 events/h). BP was categorized as normal, elevated, or stage 1 or 2 hypertension (HTN) according to AAP 2017 guidelines. Results Eight hundred and six children who underwent PSG with recorded and pre- and post-PSG BP were analyzed. Primary snoring (group A), mild (group B), moderate (group C), and severe OSA (group D) were 39.5%, 25.4%, 12.8%, and 22.3%, respectively. BP categories were normal (50%, 44.9%, 36.9%, and 30.6%), elevated (16%, 15.6%, 18.5%, and 23.9%), stage I HTN (27.7%, 27.3%, 31.1%, and 33.9%), and stage 2 HTN (6.3%, 12.2%, 13.6%, and 11.7%) in each group. A significant dose-response relationship was observed between OSA severity and morning hypertension. Each 1-event/hour increase in AHI was associated with a 2% increase in the odds of hypertension (OR 1.02, 95% CI 1.01–1.03, p 0.001), consistent across all adjusted models. Children with any OSA had nearly double the odds of morning hypertension versus non-OSA peers (adjusted OR 1.87, 95% CI 1.30–2.70, p = 0.001). When stratified by severity, mild OSA showed a nonsignificant trend (OR 1.25, 95% CI 0.84–1.86, p = 0.27), moderate OSA demonstrated attenuation after BMI adjustment, and severe OSA independently doubled hypertension risk across all models (fully adjusted OR 2.35, 95% CI 1.57–3.52, p 0.001). The impact of BMI was the most significant confounding variable, especially diminishing correlations in moderate OSA. Conclusion Severe pediatric OSA independently doubles the odds of morning hypertension, demonstrating a clear dose-response gradient with apnea severity. These findings emphasize the clinical importance of early OSA detection and its management in children. Support (if any) No Financial Disclosures
Bellary et al. (Fri,) conducted a observational in Obstructive sleep apnea (n=806). Obstructive sleep apnea vs. Non-OSA peers (primary snoring) was evaluated on Morning hypertension (adjusted OR 1.87, 95% CI 1.30-2.70, p=0.001). Children with any obstructive sleep apnea had nearly double the odds of morning hypertension versus non-OSA peers (adjusted OR 1.87; 95% CI 1.30-2.70; p=0.001).