Obstructive sleep apnoea (OSA) is associated with cardiovascular and metabolic comorbidities, including hypertension, dyslipidaemia, insulin resistance and atherosclerosis. Strong evidence suggests that OSA is associated with an altered lipid profile including elevated levels of triglyceride-rich lipoproteins and decreased levels of high-density lipoprotein (HDL). Intermittent hypoxia; sleep fragmentation; and consequential surges in the sympathetic activity, enhanced oxidative stress and systemic inflammation are the postulated mechanisms leading to metabolic alterations in OSA. Although the exact mechanisms of OSA-associated dyslipidaemia have not been fully elucidated, three main points have been found to be impaired: activated lipolysis in the adipose tissue, decreased lipid clearance from the circulation and accelerated de novo lipid synthesis. This is further complicated by the oxidisation of atherogenic lipoproteins, adipose tissue dysfunction, hormonal changes, and the reduced function of HDL particles in OSA. In this comprehensive review, we summarise and critically evaluate the current evidence about the possible mechanisms involved in OSA-associated dyslipidaemia.

Obstructive sleep apnoea (OSA) is a common disease which is characterised by repetitive collapse of the upper airways during sleep resulting in chronic intermittent hypoxaemia and frequent microarousals, consequently leading to sympathetic overflow, enhanced oxidative stress, systemic inflammation, and metabolic disturbances. OSA is associated with increased risk for cardiovascular morbidity and mortality, and accelerated coagulation, platelet activation, and impaired fibrinolysis serve the link between OSA and cardiovascular disease. In this article we briefly describe physiological coagulation and fibrinolysis focusing on processes which could be altered in OSA. Then, we discuss how OSA-associated disturbances, such as hypoxaemia, sympathetic system activation, and systemic inflammation, affect these processes. Finally, we critically review the literature on OSA-related changes in markers of coagulation and fibrinolysis, discuss potential reasons for discrepancies, and comment on the clinical implications and future research needs.

Pulmonary vascular diseases (PVDs), defined as arterial or chronic thromboembolic pulmonary hypertension, are associated with autonomic cardiovascular dysregulation. Resting heart rate variability (HRV) is commonly used to assess autonomic function. Hypoxia is associated with sympathetic overactivation and patients with PVD might be particularly vulnerable to hypoxia-induced autonomic dysregulation. In a randomised crossover trial, 17 stable patients with PVD (resting PaO₂ ≥ 7.3 kPa) were exposed to ambient air (FiO₂ = 21%) and normobaric hypoxia (FiO₂ = 15%) in random order. Indices of resting HRV were derived from two nonoverlapping 5–10-min three-lead electrocardiography segments. We found a significant increase in all time- and frequency-domain HRV measures in response to normobaric hypoxia. There was a significant increase in root mean squared sum difference of RR intervals (RMSSD; 33.49 (27.14) vs. 20.76 (25.19) ms; p < 0.01) and RR50 count divided by the total number of all RR intervals (pRR50; 2.75 (7.81) vs. 2.24 (3.39) ms; p = 0.03) values in normobaric hypoxia compared to ambient air. Both high-frequency (HF; 431.40 (661.56) vs. 183.70 (251.25) ms²; p < 0.01) and low-frequency (LF; 558.60 (746.10) vs. 203.90 (425.63) ms²; p = 0.02) values were significantly higher in normobaric hypoxia compared to normoxia. These results suggest a parasympathetic dominance during acute exposure to normobaric hypoxia in PVD.

Background: Patients with COPD are vulnerable to hypoxia-induced autonomic dysregulation. Hypoxaemia is marked during sleep. In COPD, altitude exposure is associated with an increase in blood pressure (BP) and a decrease in baroreflex-sensitivity (BRS). Whether nocturnal oxygen therapy (NOT) mitigates these cardiovascular autonomic changes in COPD at altitude is unknown. Methods: In a randomised placebo-controlled cross-over trial, 32 patients with moderate-to-severe COPD living <800m were allocated to NOT or placebo during acute exposure to altitude. Measurements were done at low altitude at 490m and during two stays at 2048m on NOT (3 l/min) or placebo (ambient air) via nasal cannula. Allocation and intervention sequence were randomised. Outcomes of interest were BP, BRS, and heart rate. Results: 23 patients finished the trial per protocol (mean(SD) age 66(5)y, FEV1 62(14)%predicted). The others had altitude-related adverse health effects. NOT significantly decreased the altitude-induced increase in systolic BP compared to placebo (-10.6 [95%CI -20.1 to -1.0] mmHg, p=0.05) but not diastolic BP (-4.4 mmHg, 95%CI -11.4 to 2.6; p=0.29). BRS at altitude was significantly higher in NOT than in placebo (+1.5 [95%CI 0.01 to 2.95], p=0.02). Conclusions: NOT may protect from hypoxia-induced autonomic dysregulation upon altitude exposure in COPD. Oxygen supplementation may provide cardiovascular benefits in COPD during conditions of increased hypoxaemia.