Background Epidermic studies have suggested a pathophysiological link between obstructive sleep apnea hypopnea syndrome (OSAHS) and atherosclerosis (AS); for which carotid intima-media thickness (IMT) has been considered as an early marker. The pathogenesis by which OSAHS can induce AS has not been elucidated. This study was conducted to investigate the association among plasma interleukin-18 (IL-18) levels, carotid IMT and the severity of OSAHS.Methods Based on the apnea hypopnea index (AHI) during sleep monitored by polysomnography, 52 male patients with OSAHS were recruited as the OSAHS group which was further divided into mild OSAHS (n=16), moderate OSAHS (n=18), and severe OSAHS (n=18) subgroups. Eighteen healthy subjects were selected as the control group. Of all OSAHS patients, 20 with moderate-to-severe OSAHS underwent continuous positive airway pressure (CPAP) treatment for 90 days. HDL5000 color Doppler ultrasonography was used to measure carotid IMT. Plasma IL-18 levels were measured by ELISA. Results Compared with the plasma lL-18 levels in the control group ((250.27±76.48) pg/ml), there was a significant increase in the mild OSAHS subgroup ((352.08±76.32) pg/ml), the moderate subgroup((600.17±83.91) pg/ml), and the severe OSAHS subgroup ((9797.64±109.83) pg/ml) (all P<0.01). Moreover, there was a significant difference in plasma IL-18 levels among the three OSAHS subgroups (P<0.01). Carotid IMT was significantly greater in the severe OSAHS subgroup than in the mild OSAHS subgroup (P<0.01). Before CPAP treatment, plasma IL-18 levels were positively correlated with carotid IMT (r=0.486, P <0.001) and with AHI (r=0.865, P<0.001). On day 90 of CPAP treatment, plasma IL-18 levels were significantly declined but carotid IMT was not changed significantly. Conclusions In untreated OSAHS patients carotid IMT and plasma IL-18 were positively correlated and were significantly higher than in normal controls; the elevation of plasma IL-18 levels was correlated with the severity of OSAHS. Inflammatory response associated with OSAHS may be related to the development of AS. By improving AHI, miniSaO2, and reducing plasma IL-18 levels, CPAP treatment may slow down or prevent the development of AS in OSAHS patients.