B61-18 Non-dipping Blood Pressure Pattern Exhibits Pro-inflammatory and Cardiometabolic Proteomic Alterations in Pediatric Obstructive Sleep Apnea

Introduction

Obstructive sleep apnea (OSA) in children has been increasingly associated with early cardiovascular (CV) alterations. Among these, the non-dipping blood pressure pattern (NDP) has emerged as a potential marker of increased CV risk. Objective: In this study, we investigated the CV risk associated with the NDP in pediatric patients with OSA through a comprehensive proteomic analysis, aiming to identify molecular pathways and protein signatures linked to early CV dysfunction.

Methods

This study is a sub-analysis of the nonrandomized clinical trial Kids Trial study (NCT03696654). A total of 27 children with moderate-to-severe OSA (obstructive apnea-hypopnea index [OAHI] ≥ 5 events/h) and NDP were included. NDP was defined as a nighttime decline of < 10% in mean blood pressure (BP) compared with daytime values. Proteomic profiling and characterization were performed using the Olink® platform, assessing targeted inflammation and cardiometabolic panels. Spearman correlation analysis was performed to evaluate the associations between individual protein levels and ambulatory blood pressure monitoring (ABPM) variables.

Results

Nighttime ABPM variables demonstrated widespread and strong positive correlations (Figure 1): nighttime mean arterial pressure was associated with FABP4 (r = 0.88), LEP (r = 0.85) and CA5A (r = 0.87); nighttime diastolic BP was correlated with CX3CL1 (r = 0.88) and CDCP1 (r = 0.83); and nighttime systolic BP was associated with PLC (r = 0.87) and Notch3 (r = 0.79).

Conclusion

In children with moderate-to-severe OSA, the NDP was associated with a pro-inflammatory and dysregulated cardiometabolic proteomic profile. These findings may suggest that loss of nighttime dipping may reflect early molecular pathways linked to endothelial dysfunction, vascular remodeling, and increased CV risk in pediatric OSA. Proteomic profiling may therefore provide valuable insights for early risk stratification and targeted prevention strategies in this population.

This abstract is funded by: This work was funded by the Instituto de Salud Carlos III (ISCIII: PI18/00565, PI22/01653 and IT24/00032) and co-funded by the European Regional Development Fund (ERDF)/“A way to make Europe”, the Spanish Respiratory Society (Sociedad Española de Neumología y Cirugía Torácica- SEPAR) (535-2018, 1073-2020 and 1425-2023), and an unconditional research grant from Menarini Laboratories, INNOCAM and Sociedad Madrileña de Neumología y Cirugía Torácica (NEUMOMADRID).