Increased circulating endothelial microparticles and carotid atherosclerosis in obstructive sleep apnea.

BACKGROUND AND PURPOSE

Endothelial impairment is a linking mechanism between obstructive sleep apnea (OSA) and cardiovascular diseases. Profiles of endothelial microparticles (EMPs) and endothelial progenitor cells (EPCs) reflect the degree of endothelial impairment. The aims of this study were to measure the levels of EMPs and progenitor cells in OSA, determine the correlations between these factors and OSA severity and the degree of atherosclerosis, and document any changes in these factors after therapy.

METHODS

Subjects with (n=82) and without (n=22) OSA were recruited prospectively. We measured the number of colony-forming units (CFU) in cell culture as the endothelial progenitor cell index, and the number of EMPs using flow cytometry with CD31 [platelet endothelial cell adhesion molecule (PECAM)], CD42 (platelet glycoprotein), annexin V, and CD62E (E-selectin) antibodies at baseline and after 4-6 weeks of continuous positive airway pressure (CPAP) therapy. Carotid intima-media thickness (IMT) was regarded as a marker of atherosclerosis.

RESULTS

The levels of PECAM(+)CD42(-) (p<0.001), PECAM(+)annexin V(+) (p<0.001), and E-selectin(+) microparticles (p=0.001) were higher in OSA subjects than in non-OSA subjects. The number of CFU did not differ between the two groups. OSA severity independently predicted the levels of PECAM(+)CD42(-) (p=0.02) and PECAM(+)annexin V(+) (p=0.004). Carotid IMT was correlated with OSA severity (p<0.001), PECAM(+)CD42(-) (p=0.03), and PECAM(+)annexin V(+) (p=0.01). Neither OSA severity nor carotid IMT was correlated with either the number of CFU or E-selectin(+). CPAP therapy decreased the occurrence of E-selectin(+) (p<0.001) in 21 of the OSA subjects, but had no effect on the other microparticles of the number of CFU.

CONCLUSIONS

OSA led to the overproduction of EMPs, which moderately correlated with OSA severity and the degree of atherosclerosis, and partly responded to therapy. The endothelial impairment might contribute to future cardiovascular events.