Endothelial Dysfunction and Specific Inflammation in Obesity Hypoventilation Syndrome

Background: Obesity hypoventilation syndrome (OHS) is associated with increased cardiovascular morbidity. What moderate chronic hypoventilation adds to obesity on systemic inflammation and endothelial dysfunction remains unknown. Question: To compare inflammatory status and endothelial function in OHS versus eucapnic obese patients. Methodology: 14 OHS and 39 eucapnic obese patients matched for BMI and age were compared. Diurnal blood gazes, overnight polysomnography and endothelial function, measured by reactive hyperemia peripheral arterial tonometry (RHPAT), were assessed. Inflammatory (Leptin, RANTES, MCP-1, IL-6, IL-8, TNF alpha, Resistin) and anti-inflammatory (adiponectin, IL-1Ra) cytokines were measured by multiplex beads immunoassays. Principal Findings: OHS exhibited a higher PaCO2, a lower forced vital capacity (FVC) and tended to have a lower PaO2 than eucapnic obese patients. HS-CRP, RANTES levels and glycated haemoglobin (HbA1c) were significantly increased in OHS (respectively 11.1 +/- 10.9 vs. 5.7 +/- 5.5 mg.l(-1) for (HS)-CRP, 55.9 +/- 55.3 vs 23.3 +/- 15.8 ng/ml for RANTES and 7.3 +/- 4.3 vs 6.1 +/- 1.7 for HbA1c). Serum adiponectin was reduced in OHS (760662977 vs 1366067854 ng/ml). Endothelial function was significantly more impaired in OHS (RH-PAT index:0.22 +/- 0.06 vs 0.51 +/- 0.11). Conclusions: Compared to eucapnic obesity, OHS is associated with a specific increase in the pro- atherosclerotic RANTES chemokine, a decrease in the anti-inflammatory adipokine adiponectin and impaired endothelial function. These three conditions are known to be strongly associated with an increased cardiovascular risk.