Study objectives: It has been suggested that obstructive sleep apnea (OSA)-induced hypoxic stress might contribute to cardiovascular disorders by promoting expression of soluble adhesion molecules. The reported increase of circulating adhesion molecules in patients with OSA remains controversial because confounders such as cardiovascular risk factors and left ventricular function have not been adequately controlled for. We hypothesized that soluble intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, L-selectin, and E-selectin levels are correlated with OSA independent of coexisting coronary artery disease (CAD).
Settings: University-affiliated teaching hospitals.
Design and participants: A prospective study of 61 consecutive subjects with angiographically proven CAD deemed to have stable angina.
Interventions: Fifteen patients (mean +/- SD) 61.2 +/- 1.9 years old with moderate-to-severe OSA (apnea-hypopnea index [AHI] > or = 20/h) were matched to a control group (AHI < or = 5/h) for age, gender, body mass index, and severity of CAD. Venous blood samples were collected the morning of the sleep study and assayed for human ICAM-1, VCAM-1, L-selectin, and E-selectin with commercially available enzyme-linked immunosorbent assay kits.
Results: All but L-selectin were significantly increased in the OSA group compared to the control subjects (ICAM-1, 367.4 +/- 85.2 ng/mL vs 252.8 +/- 68.4 ng/mL, p = 0.008; VCAM-1, 961.5 +/- 281.7 ng/mL vs 639.1 +/- 294.4 ng/mL, p = 0.004; E-selectin, 81.0 +/- 30.4 ng/mL vs 58.1 +/- 23.2 ng/mL, p = 0.03, respectively). The increased levels of adhesion molecules correlated with the AHI and the oxygen desaturation index but not with the severity of hypoxemia or the frequency of arousals.
Conclusions: These findings suggest that OSA modulates the expression of proinflammatory mediators. Further studies should evaluate the influence of adhesion molecules on cardiovascular outcome in CAD patients with OSA.