Hemodynamic and Inflammatory Markers of Sleep Apnea-Hypopnea Syndrome and Nocturnal Hypoxemia: Effects of Treatment With Nasal Continuous Positive Airway Pressure

Objective In this study, we assessed factors associated with cardiovascular risk in patients with sleep apnea-hypopnea syndrome (SAHS) through analysis of plasma concentrations of N-terminal prohormone brain natriuretic peptide (NTproBNP) and high-sensitivity C-reactive protein (hsCRP). In addition, we analyzed the effect of nasal continuous positive airway pressure (nCPAP) on these markers. Patients and Methods Forty-two patients with SAHS (mild to moderate in 15 cases and severe in 27) were compared with 14 individuals without SAHS. The participants were not receiving drug treatment and they did not have diabetes, hypertension, marked dyslipidemia, or cardiovascular disease, which was ruled out both clinically and by echocardiography and 99m Tc-tetrofosmin scintigraphy at rest and during exercise. The effects of nCPAP in patients with severe SAHS were analyzed after 6 months of treatment. Results Following adjustment for age, body mass index, and smoking habit, the mean concentrations of markers were not significantly higher in patients with severe SAHS than in those with mild-to-moderate SAHS or in control subjects. Nevertheless, in patients with SAHS the main factor influencing NTproBNP concentrations was the percentage of time with a nocturnal arterial oxygen saturation of less then 90% ( r =0.37, P =.017). No variables predictive of hsCRP concentration were identified. The concentrations of the markers were reduced by nCPAP, but the differences were not statistically significant. Conclusions While nocturnal hypoxemia in SAHS is responsible for variations in the plasma concentration of NTproBNP (as a result of cardiovascular changes), SAHS appears not to be associated with the inflammatory marker hsCRP when patients with heart disease, cardiovascular risk factors, or those receiving pharmacologic treatment are excluded.