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The Effect of Nocturnal Oxygen Desaturations on Plasma Levels of Nf-κB-Controlled Gene Products in Patients with Obstructive Sleep Apnea
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A2433 - The Effect of Nocturnal Oxygen Desaturations on Plasma Levels of Nf-κB-Controlled Gene Products in Patients with Obstructive Sleep Apnea
Author Block: A. P. Noriega Aldave1, K. A. Oursler2, T. Pelleg3, D. C. Smith4, R. D. Mantilla5, M. Thomas2, M. Macrea6; 1Pulmonary and Critical Care Medicine, Pulmonary Critical Care Medicine, Roanoke, VA, United States, 2Salem VA Hospital, Salem, VA, United States, 3Carilion Clinic, Roanoke, VA, United States, 4Pulmonary and Critical Care, Roanoke, VA, United States, 5Pulmonary/Critical Care, Carilion Clinic, Roanoke, VA, United States, 6Salem VAMC, Salem, VA, United States.
Introduction Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (CIH) with reoxygenation, a phenomenon that induces oxidative stress and activates the oxidant-sensitive transcription factor nuclear factor κB (NF-κB), a known contributor to inflammation-induced atherogenesis. Although recent studies have shown that patients with OSA have increased plasma levels of NF-κB-controlled gene products soluble E (sE)-selectin and soluble vascular cell adhesion molecule-1 (sVCAM-1), the responsible mechanisms have not been fully identified. Thus, we analyzed the effect of nocturnal oxygen desaturations (NOD) on (sE)-selectin and sVCAM-1 in patients with OSA before continuous positive airway pressure (CPAP) therapy. Methods Five patients who were diagnosed with OSA by diagnostic polysomnogram (PSG) at the Salem VAMC were recruited into a cross-sectional study. Demographic, clinical, pharmacological and comorbidity data were extracted from the Electronic Medical Record (EMR). Plasma levels (sE)-selectin and sVCAM-1 Fasting were measured the morning after PSG. The severity of NOD was expressed as lowest oxygen saturation (LO2sat), and percentage of time (PercO2sat) and longest time interval spent (TimeO2sat) at an oxygen saturation less than 88%. Correlations between severity of NOD and plasma (sE)-selectin and sVCAM-1 and were analyzed using Spearman correlations. Results Mean patients’ age (years) and BMI (kg/m2) was 65 and 35, respectively. Plasma (sE)-selectin and sVCAM-1 levels (ng/ml, mean ± SD) were 42±15 and 767±154, respectively. The LO2sat, PercO2sat and TimeO2sat (%, mean ± SD) were as follows: 82.2±3, 37.6±11 and 109±41. Plasma SVCAM-1 levels correlated with LO2 sat (p= 0.04, ro= -0.89) and PercO2sat (p= 0.01, ro= 0.94). Conclusion Severity of NOD in OSA correlates with plasma levels of sVCAM-1, a NF-κB-controlled gene product. This may reveal an important pathway linking hypoxia-activated NF-κB activation to systemic inflammation and atherogenesis in patients with OSA.
Author Block: A. P. Noriega Aldave1, K. A. Oursler2, T. Pelleg3, D. C. Smith4, R. D. Mantilla5, M. Thomas2, M. Macrea6; 1Pulmonary and Critical Care Medicine, Pulmonary Critical Care Medicine, Roanoke, VA, United States, 2Salem VA Hospital, Salem, VA, United States, 3Carilion Clinic, Roanoke, VA, United States, 4Pulmonary and Critical Care, Roanoke, VA, United States, 5Pulmonary/Critical Care, Carilion Clinic, Roanoke, VA, United States, 6Salem VAMC, Salem, VA, United States.
Introduction Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (CIH) with reoxygenation, a phenomenon that induces oxidative stress and activates the oxidant-sensitive transcription factor nuclear factor κB (NF-κB), a known contributor to inflammation-induced atherogenesis. Although recent studies have shown that patients with OSA have increased plasma levels of NF-κB-controlled gene products soluble E (sE)-selectin and soluble vascular cell adhesion molecule-1 (sVCAM-1), the responsible mechanisms have not been fully identified. Thus, we analyzed the effect of nocturnal oxygen desaturations (NOD) on (sE)-selectin and sVCAM-1 in patients with OSA before continuous positive airway pressure (CPAP) therapy. Methods Five patients who were diagnosed with OSA by diagnostic polysomnogram (PSG) at the Salem VAMC were recruited into a cross-sectional study. Demographic, clinical, pharmacological and comorbidity data were extracted from the Electronic Medical Record (EMR). Plasma levels (sE)-selectin and sVCAM-1 Fasting were measured the morning after PSG. The severity of NOD was expressed as lowest oxygen saturation (LO2sat), and percentage of time (PercO2sat) and longest time interval spent (TimeO2sat) at an oxygen saturation less than 88%. Correlations between severity of NOD and plasma (sE)-selectin and sVCAM-1 and were analyzed using Spearman correlations. Results Mean patients’ age (years) and BMI (kg/m2) was 65 and 35, respectively. Plasma (sE)-selectin and sVCAM-1 levels (ng/ml, mean ± SD) were 42±15 and 767±154, respectively. The LO2sat, PercO2sat and TimeO2sat (%, mean ± SD) were as follows: 82.2±3, 37.6±11 and 109±41. Plasma SVCAM-1 levels correlated with LO2 sat (p= 0.04, ro= -0.89) and PercO2sat (p= 0.01, ro= 0.94). Conclusion Severity of NOD in OSA correlates with plasma levels of sVCAM-1, a NF-κB-controlled gene product. This may reveal an important pathway linking hypoxia-activated NF-κB activation to systemic inflammation and atherogenesis in patients with OSA.
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