Obesity hypoventilation syndrome (OHS) is associated with increased cardiovascular morbidity-mortality. Little is known on what daytime moderate chronic hypoventilation adds to obesity on systemic inflammation, adipokine production and endothelial dysfunction. Aim: To compare inflammatory status and endothelial function in OHS versus “uncomplicated obese” patients (UO), matched for BMI, age and sex.
Diurnal blood gazes, respiratory function, CO2 ventilatory response, polysomnography and endothelial function, measured by reactive hyperemia peripheral arterial tonometry (RH-PAT), were assessed. Inflammatory (Leptin, RANTES, MCP1, IL6, IL8, TNFα, Resistin) and anti-inflammatory (adiponectin, IL1-RA) cytokines were measured by commercially available multiplex beads immunoassays.
14 OHS (BMI: 41 ± 5.2 kgm-2, PaCO2: 6.5 ± 0.4 kPa, age: 57 ± 10 years) and 39 UO patients (BMI: 40.9 ± 5.1 kgm-2, PaCO2: 5.3 ± 0.4 kPa, 56 ± 10 years) were included. PaCO2 was significantly higher in OHS (p < 0.0001) whereas PaO2, vital capacity and CO2 chemoresponsiveness were lowered (p < 0.02). Serum RANTES levels were significantly increased in OHS (55.9 ± 55.3 vs 23.3 ± 15.8 ng/ml p = 0.003) and correlated with daytime PaCO2 (r=0.53 p = 0.0001). Serum adiponectin was reduced in OHS (7.6 ± 2.9 vs 13.7 ± 7.8μg/ml p = 0.004). Endothelial function was more impaired in OHS (p = 0.006) compared to UO and negatively correlated with PaCO2 (r=−0.37 p = 0.009) and positively with PaO2 (r=0.36 p = 0.01).
Compared to UO, OHS is associated with a specific increase in the proatherosclerotic RANTES chemokine, a decrease in the antinflammatory adipokine adiponectin and impaired endothelial function. These three conditions are known to be strongly associated with an increased cardiovascular risk.
This study may explain why excess in cardiovascular morbidity is observed during OHS.
Jean-Louis Pepin, No Financial Disclosure Information; No Product/Research Disclosure Information