Endothelial dysfunction and specific inflammation in obesity hypoventilation syndrome
Jean-Christian Borel1, Pascale Roux-Lombard, Renaud Tamisier
1INSERM ERI17, Laboratoire HP2, Université Joseph Fourier, Faculté de Médecine, Grenoble, France.
Plos One
|August 25, 2009
Summary
Obesity hypoventilation syndrome (OHS) significantly worsens systemic inflammation and endothelial dysfunction compared to simple obesity. This is linked to increased RANTES, decreased adiponectin, and impaired blood vessel function, raising cardiovascular risk.
Area of Science:
- Cardiology
- Pulmonology
- Metabolic Disorders
Background:
- Obesity hypoventilation syndrome (OHS) is linked to higher cardiovascular morbidity.
- The specific impact of chronic hypoventilation in obesity on systemic inflammation and endothelial dysfunction is not well understood.
Purpose of the Study:
- To compare inflammatory markers and endothelial function in patients with OHS versus obese patients without hypoventilation (eucapnic).
Main Methods:
- Compared 14 OHS patients with 39 eucapnic obese patients matched for BMI and age.
- Assessed diurnal blood gases, polysomnography, and endothelial function using reactive hyperemia peripheral arterial tonometry (RH-PAT).
- Measured inflammatory and anti-inflammatory cytokines including RANTES and adiponectin.
Main Results:
- OHS patients had higher PaCO2, lower forced vital capacity, and increased levels of hs-CRP, RANTES, and HbA1c.
- Serum adiponectin levels were significantly lower in OHS patients.
- Endothelial function, measured by RH-PAT index, was markedly impaired in OHS patients.
Conclusions:
- OHS is associated with elevated pro-atherosclerotic RANTES and reduced anti-inflammatory adiponectin.
- Impaired endothelial function is a key finding in OHS compared to eucapnic obesity.
- These factors collectively contribute to the increased cardiovascular risk observed in OHS.
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