<p><b>BACKGROUND</b>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 plasmainterleukin-18 (IL-18) levels, carotid IMT and the severity of OSAHS.</p><p><b>METHODS</b>Based on the apnea hypopnea index (AHI) during sleep monitored by polysomnography, 52 malepatients 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 OSAHSpatients, 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. PlasmaIL-18 levels were measured by ELISA.</p><p><b>RESULTS</b>Compared with the plasmaIL-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 plasmaIL-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, plasmaIL-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, plasmaIL-18 levels were significantly declined but carotid IMT was not changed significantly.</p><p><b>CONCLUSIONS</b>In untreated OSAHSpatients carotid IMT and plasmaIL-18 were positively correlated and were significantly higher than in normal controls; the elevation of plasmaIL-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, miniSaO(2), and reducing plasmaIL-18 levels, CPAP treatment may slow down or prevent the development of AS in OSAHSpatients.</p>