Background: Obstructive sleep apnoea (OSA) is associated with high cardiovascular morbidity and mortality and is an independent risk factor for hypertension. Novel circulating cardiovascular risk markers enabling a more accurate prediction of cardiovascular risk have been identified. Examination of these markers may clarify the increased risk in OSA and contribute to an analysis of the benefits of treatment. Methods: Plasma levels of total cholesterol and triglyceride and activated coagulation factors XIIa and VIIa, factors VII, VIII, XII, fibrinogen, thrombin-antithrombin (TAT), von Willebrand factor antigen (vWFAg), soluble P-selectin (sP-sel), and homocysteine were measured before and after treatment for 1 month with therapeutic or subtherapeutic (control) continuous positive airways pressure (CPAP) in 220 patients with OSA. Results: Levels of activated coagulation factors XIIa, VIIa, TAT and sP-sel were higher in OSA patients at baseline than in unmatched controls, but did not fall with 1 month of therapeutic CPAP treatment. The raised sP-sel levels correlated only with body mass index (p = 0.002). There was a trend towards a significant fall in total cholesterol with therapeutic CPAP (p = 0.06) compared with the control group. In the therapeutic group there was a clinically significant mean fall in total cholesterol of 0.28 mmol/l (95% confidence interval 0.11 to 0.45, p = 0.001) which may reduce cardiovascular risk by about 15%. Conclusion: A number of activated coagulation factors are increased in untreated OSA patients, potentially contributing to vascular risk, but they do not fall with 1 month of CPAP treatment. Nasal CPAP may produce a clinically relevant fall in total cholesterol level, potentially reducing cardiovascular risk, but this needs to be verified in a larger prospective study.
Obstructive sleep apnoea (OSA) is associated with high cardiovascular morbidity and mortality. Several randomised controlled trials have shown that continuous positive airway pressure (CPAP) treatment of OSA reduces blood pressure (BP). This randomised, sham-placebo controlled crossover trial assesses whether CPAP produces a similar clinically significant fall in BP in hypertensive OSA patients, but without hypersomnolence.Thirty-five, nonsleepy, hypertensive patients with OSA were treated with CPAP for 1 month, randomised first to either therapeutic or sham-placebo (subtherapeutic CPAP, about 1 cmH 2 O pressure). The second months' alternative treatment followed a 2-week washout period. BP was measured over 24 h, before and at the end of the two treatment periods: mean 24-h BP was the primary outcome variable.There was no overall significant difference in mean 24-h BP: the change in mean 24-h BP on therapeutic CPAP was -2.1 mmHg (SD 8.1), and -1.1 mmHg (SD 8.1) on subtherapeutic CPAP, with a difference of 0.7 mmHg (95% confidence interval (CI) +2.9--4.4). There was a small significant fall in Epworth Sleepiness Score, therapeutic (-1.4) versus sham (-0.3), and difference -1.2 (95% CI -2.0--0.4), but no change in objective sleepiness.In nonhypersomnolent hypertensive patients with obstructive sleep apnoea, there is no significant fall in mean 24-h blood pressure with continuous positive airway pressure, in contrast to the fall seen in hypersomnolent patients with obstructive sleep apnoea.
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Background: Obstructive sleep apnoea (OSA) is associated with high cardiovascular morbidity and mortality. Randomised controlled trials have shown that, on average, treatment of OSA with continuous positive airway pressure (CPAP) reduces blood pressure (BP) by 3-5 mm Hg, although with considerable variation between individuals. No predictors of the change in BP with CPAP have been convincingly identified. This prospective study aimed to determine predictors of BP change, which might provide an insight into the aetiology of the raised BP seen in untreated OSA. Methods: Eighty-six patients with daytime hypersomnolence warranting treatment with CPAP were recruited. 24 h mean BP (24 hMBP), subjective sleepiness, fasting venous blood samples and anthropometric measurements were assessed at baseline and after 6 months of CPAP treatment. Results: The mean (SD) 24 hMBP fell at 6 months from 101.0 (10.3) mm Hg to 96.1 (9.1) mm Hg (change 24.92 mm Hg (95% CI 22.8 to 27.1)). The Epworth Sleepiness Score (ESS) fell from a median of 16 (IQR 12-18) to 4 (2-7) with a mean fall of 9.7 (95% CI 8.6 to 10.8). Several factors correlated with the fall in 24 hMBP but, after allowing for the baseline 24 hMBP, only the fall in ESS and the body mass index (BMI) remained significant independent predictors (p = 0.006 and 0.007, respectively). There was also a correlation between the fall in 24 hMBP and the fall in pulse rate (r = 0.44, p,0.001). Baseline severity of OSA, overnight hypoxia, caffeine intake or being on antihypertensive drugs were not independent predictors of a fall in 24 hMBP. Conclusion: Improvement in hypersomnolence and the BMI are independent correlates of the fall in 24 hMBP following CPAP therapy. Markers of initial OSA severity did not predict the fall in 24 hMBP. This suggests that sleep fragmentation and its effects may be more important than hypoxia in the pathogenesis of the hypertension associated with human sleep apnoea.Obstructive sleep apnoea syndrome (OSAS) is a common problem 1 2 and randomised controlled trials have shown improvement of daytime sleepiness with continuous positive airway pressure (CPAP).3-5 Recurrent upper airway collapse leads to transient asphyxia and hypoxia which cause sleep fragmentation and daytime hypersomnolence. A raised blood pressure (BP) is seen in epidemiological 6 and hospital-based studies 7 of OSA; it is independent of obesity (the most common cause of OSA) and the other common risk factors for hypertension which are also frequently present in this patient population.Recent randomised controlled trials have shown that CPAP treatment of severe symptomatic OSA reduces 24 h BP at 4 weeks. [8][9][10][11][12][13] In the Oxford randomised parallel controlled trial, 8 there was a small fall in 24 h mean ambulatory BP of 3.3 mm Hg (95% confidence interval (CI) 25.3 to 21.3) with CPAP treatment relative to control subjects in whom there was no such reduction. Patients with more severe disease (characterised either from the sleep study or by degree of sleepiness) had greater...
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