B80-3-11 Effect of Cpap Treatment on Vascular Biomarkers in Coronary Artery Disease With Obstructive Sleep Apnea: The Riccadsa Randomized Controlled Trial

Rationale

Obstructive sleep apnea (OSA) is associated with increased cardiovascular risk, potentially mediated by endothelial activation and impaired fibrinolytic balance. The impact of continuous positive airway pressure (CPAP) therapy on these pathways in patients with coronary artery disease (CAD) remains unclear. We aimed to investigate the effect of CPAP treatment on endothelial adhesion molecules (intercellular adhesion molecule-1 [ICAM-1] and vascular cell adhesion molecule-1[VCAM-1]) and fibrinolytic balance assessed by plasminogen activator inhibitor-1 (PAI-1) in patients with CAD and OSA.

Methods

A total of 210 revascularized CAD patients with nonsleepy (Epworth Sleepiness Scale score<10) OSA (apnea-hypopnea-index ≥ 15/h) from the RICCADSA cohort randomized to CPAP (n = 104) or no-CPAP (n = 106) with available blood samples at baseline and after 12 months were included in the current study. Circulating levels of ICAM-1, VCAM-1, and PAI-1 were measured. Linear mixed-effects models were used to assess time-by-treatment interactions, adjusted for clinically relevant cardiometabolic covariates.

Results

For ICAM-1, no significant time-by-treatment interaction was observed. For PAI-1, a borderline time-by-treatment interaction suggested a numerically smaller increase in the CPAP group compared with no-CPAP (p = 0.09). CPAP treatment was associated with a significantly greater reduction in VCAM-1 over time compared with no-CPAP (time-by-treatment interaction p = 0.045 in adjusted models). Conclusions In revascularized CAD patients with OSA, CPAP treatment was associated with differential effects on vascular biomarkers, suggesting pathway-specific vascular modulation. The attenuation of endothelial activation, reflected by reduced VCAM-1 levels, and the partial mitigation of worsening fibrinolytic balance support a potential role for CPAP targeting residual vascular risk in this high-risk population.

This abstract is funded by: Swedish Research Council, Swedish Heart-Lung Foundation, ResMed Foundation