CPAP may promote an endothelial inflammatory milieu in sleep apnoea after coronary revascularization

Figures

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  Fig. 1. Flow diagram and study protocol.

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  Fig. 2. Circulating levels of angiopoietin-2 are associated with median CPAP pressure in patients with obstructive sleep apnoea after coronary revascularization (linear regression slope 0.30, 95% CI 0.03, 0.57, p = 0.039). The shaded area represents 95% confidence band. CPAP, continuous positive airway pressure.

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  Fig. 3. The association of the composite cardiovascular outcome with CPAP pressure. Cox regression analysis for the composite cardiovascular outcome stratified by the CPAP pressure below vs. above the median pressure, adjusted for age, sex, BMI and baseline AHI (HR 2.81; 95% CI 1.22, 6.44, p = 0.021). The shaded areas represent 95% confidence bands. CPAP, continuous positive airway pressure.

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  Fig. 4. CPAP therapy alters the pattern of plasma biomarker expression after coronary revascularization in patients with obstructive sleep apnoea (OSA) in a direction that favors inflammatory over angiogenic processes. While CPAP therapy reduces OSA-associated hypoxemia, with expected beneficial effects on endothelial function and inflammation, increased lung volumes during CPAP therapy may promote persistent increase in circulating levels of a pro-inflammatory factor angiopoietin-2 while elimination of intermittent hypoxia reduces levels of a proangiogenic factor VEGF-A. The reduction in VEGF-A in the setting of persistent elevation in angiopoietin-2 observed after CPAP therapy is hypothesized to increase the risk of recurrent events after coronary revascularization. Greater levels of angiopoietin-2 and sRAGE, a marker of lung epithelial injury, after 12 months of CPAP therapy were associated with significantly greater mortality and an increased incidence of cardiovascular events in patients with OSA. CPAP, continuous positive airway pressure; VEGF-A, vascular endothelial growth factor; sRAGE, soluble receptor of advanced glycation end-products.