Effect of 5-year continuous positive airway pressure treatment on the lipid profile of patients with obstructive sleep apnea: A pilot study.

Continuous positive airway pressure (CPAP) provides a well-documented symptomatic relief for most patients with obstructive sleep apnea (OSA); however, its effect on dyslipidaemia remains contradictory. The aim of this longitudinal pilot study was to investigate the effect of long-term CPAP treatment on the lipid profile of patients with severe OSA. Fasting serum levels of total cholesterol (TC), low- and high-density lipoprotein cholesterol (LDL-C and HDL-C) and triglyceride (TG) were longitudinally measured in 33 OSA patients with an apnea-hypopnea index (AHI) of ≥30 events/hr, at the time of diagnosis (baseline) and at control visits following fixed-pressure CPAP treatment. Compared to baseline values, even as short as a 2-month CPAP therapy resulted in a significant decrease of both TC and LDL-C levels (TC, 5.62 ± 0.22 vs. 5.18 ± 0.21 mmol/L; LDL-C, 3.52 ± 0.19 vs. 3.19 ± 0.2 mmol/L; p < 0.05 for each). These lipid fractions exhibited similar improvements at 6 months and after 5 years of CPAP treatment (TC, 5.1 ± 0.17 mmol/L; LDL-C, 2.86 ± 0.16 mmol/L; p < 0.01 for each). The reduction in lipid levels was greater in younger patients and/or in those who had higher body mass index (BMI) (p < 0.05). There were no significant correlations between AHI and lipid levels (p > 0.05); BMI showed a weak negative association with HDL-C fraction (BMI, r = -0.263, p < 0.05). CPAP therapy had neither short- nor long-term effects on TG and HDL-C levels (p > 0.05). CPAP therapy has a rapid and long-lasting beneficial effect on the lipid profile of patients with severe OSA.

Effect of 5-year continuous positive airway pressure treatment on MMPs and TIMPs: implications for OSA comorbidities.

Continuous positive airway pressure (CPAP) treatment results in nearly complete remission of symptoms of obstructive sleep apnoea (OSA); however, its effect on OSA comorbidities including cardiovascular diseases remains contradictory. Here we investigated the short- and long-term effect of CPAP treatment on matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in patients with severe OSA. Serum levels of 7 MMPs and 3 TIMPs were followed in OSA patients (n = 28) with an apnoea-hypopnoea index of ≥30 events/h at the time of diagnosis and at control visits (2 months, 6 months and 5 years) after initiation of fixed-pressure CPAP treatment. The first few months of CPAP therapy resulted in significant decrease of MMP-8 and MMP-9 levels (MMP-8: 146 (79-237) vs. 287 (170-560) pg/mL; MMP-9: 10.1 (7.1-14.1) vs. 12.7 (10.4-15.6) ng/mL, p < 0.05 for each at 2 months), while the rest of the panel remained unchanged as compared to baseline values. In contrast, at 5 years, despite of uninterrupted CPAP treatment and excellent adherence the levels of MMP-8, MMP-9 and TIMPs significantly increased (p < 0.05). Our data suggest that initiation of CPAP therapy leads to a decrease in the level of key MMPs in the short-term; however, this effect is not sustained over the long-term.