Abstract 3627: Increased Low-Grade Inflammation and Plasminogen-Activator Inhibitor-1 Level in Non-Dippers with Sleep Apnea Syndrome in Relation to Activation of Renin-Angiotensin System
Objective: Sleep apnea syndrome (SAS) is often associated with various neurohumoral activations and multiple risk factors. SAS patients have increased risk of sleep-onset cardiovascular events and frequently exhibits non-dipper pattern (blunted nocturnal decline of systolic blood pressure (BP) <10%), which predicts poor cardiovascular outcome. We investigated SAS-associated neurohumoral activation and risk factors in relation to nocturnal BP dipping pattern.
Methods: We conducted sleep plysomonography and ambulatory BP monitoring, and measured cardiovascular risk factors including high-sensitivity C-reactive protein (hsCRP) and tissue-type plasminogen activator inhibitor-1 (PAI-1; a marker of hypofibrinolytic activity), and neurohumoral factors in 121 SAS-suspected outpatients.
Results: Non-dippers with SAS had significantly higher serum hsCRP level than non-dippers without SAS (geometric mean: 1.64 vs. 0.36 mg/L, P<0.001) and than dippers with SAS (0.80mg/L, P=0.036). Non-dippers with SAS had significantly higher PAI-1 (41.5 ± 18.1 ng/ml vs. 26.7 ± 12.2 ng/ml, P=0.007) and aldosterone (108.5 ± 51.0 pg/ml vs. 74.7 ± 31.1 pg/ml, P=0.009) than non-dippers without SAS, while there were no significant differences in these factors between non-dippers with SAS and dippers with SAS. Even after adjustment for confounding factors such as age, sex, and BMI, non-dippers with SAS had significantly higher serum hsCRP level than non-dippers without SAS (geometric mean 1.40 vs. 0.41 mg/L, P<0.001). There were positive correlations of aldosterone level with hsCRP (r=0.180, P=0.048) and PAI-1 (r=0.168, P=0.065).
Conclusion: Non-dippers and SAS additively increased levels of hsCRP. Increased PAI-1 in relation to increased aldosterone level in non-dippers with SAS than non-dippers without SAS, indicating that SAS per se associated with impaired fibrinolysis in relation to activation of renin-angiotensin-aldosteron system. However, non-dippers without SAS is not associated with these risk factors.