Plasma pentraxin3 and arterial stiffness in men with obstructive sleep apnea

Obstructive sleep apnea (OSA) induces inflammation and vascular damage that might contribute to an increased risk of cardiovascular disease (CVD). However, the mechanisms linking OSA and CVD are not fully understood. Pentraxin3 may play a significant role in vascular inflammation and damage. Currently, there is lack of data on pentraxin3 and its role in vascular damage associated with OSA.

We enrolled 50 males with OSA and 25 controls matched for age and body mass index (BMI). Patients with OSA were further divided into mild and moderate to severe groups. We measured plasma pentraxin3 and evaluated vascular damage using an arterial stiffness parameter--the cardio-ankle vascular index (CAVI)--in all subjects. In the moderate to severe OSA group, pentraxin3 and CAVI were repeatedly measured following continuous positive airway pressure (CPAP) therapy for 1 month.

Pentraxin3 levels in the moderate-to-severe OSA group were significantly higher than those in the mild OSA and control groups, with median levels (25th-75th percentile) of 2.36 (1.79-2.78), 1.63 (1.15-2.05), and 1.53 (1.14-2.04) ng/ml, respectively (P < 0.01). Pentraxin3 level was independently correlated with CAVI (coefficient, 0.34 P < 0.01). In the moderate-to-severe OSA group, pentraxin3 and CAVI levels were significantly reduced (P < 0.01 and P = 0.04, respectively) after 1 month of CPAP therapy.

Plasma pentraxin3 and arterial stiffness levels in the moderate-to-severe OSA group were greater than the corresponding levels in patients without OSA. However, pentraxin3 level can be managed by CPAP therapy for OSA.