There is increasing evidence that inflammation plays an important role in the development of cardiovascular complications in patients with obstructive sleep apnoea (OSA). No previous works have studied levels of soluble tumour necrosis factor-alpha receptor (sTNFR)-1 in patients with OSA. The aims of the present study were to examine serum levels of sTNFR-1 and the effect of nasal continuous positive airway pressure (CPAP) in patients with OSA. A prospective, randomised, placebo-controlled crossover study was performed. In total, 30 consecutive newly diagnosed OSA patients (apnoea/hypopnoea index 43.8+/-27.0 events x h(-1)) and 15 healthy obese patients were selected. Urinary levels of norepinephrine and epinephrine, as well as plasma sTNFR-1, tumour necrosis factor (TNF)-alpha, interleukin (IL)-6 and leukotriene (LT)B(4) levels were obtained at baseline and after 3 months of CPAP or sham CPAP. Nocturnal urinary levels of norepinephrine, epinephrine and sTNFR-1 (1,053+/-269 versus 820+/-166 pg x mL(-1)) were significantly higher in OSA patients. There were no significant differences in plasma levels of IL-6, LTB(4), or TNF-alpha between the two study groups. There were no significant differences in blood pressure, urinary catecholamine levels, or plasma IL-6, LTB(4) and TNF-alpha levels after both treatment modalities. However, after 3 months of effective CPAP usage, sTNFR-1 levels were significantly reduced (1,053+/-269 versus 899+/-254 pg x mL(-1)). Obstructive sleep apnoea patients have higher levels of soluble tumour necrosis factor-alpha receptor 1 than individuals without OSA; soluble tumour necrosis factor-alpha receptor 1 levels are lowered by continuous positive airway pressure therapy. These findings further corroborate a potential role of inflammation in the natural history of obstructive sleep apnoea.
"Interestingly, even one night of CPAP treatment was able to affect HRV with a reduction of sympathetic modulation and an improvement of baroreflex control (Bonsignore et al., 2006; Kufoy et al., 2012). Longer CPAP treatments revealed positive effects on hemodynamic and metabolic variables, such as an improvement of arterial stiffness, a reduction of inflammatory response (Arias et al., 2008; Dorkova et al., 2008) and a decrease of platelet aggregation (Shimizu et al., 2002). However, the effects of longer CPAP treatments showed contrasting results and conclusive results on its consequences on HRV are still lacking. "
[Show abstract][Hide abstract] ABSTRACT: Sleep is a physiological process involving different biological systems, from molecular to organ level; its integrity is essential for maintaining health and homeostasis in human beings. Although in the past sleep has been considered a state of quiet, experimental and clinical evidences suggest a noteworthy activation of different biological systems during sleep. A key role is played by the autonomic nervous system (ANS), whose modulation regulates cardiovascular functions during sleep onset and different sleep stages. Therefore, an interest on the evaluation of autonomic cardiovascular control in health and disease is growing by means of linear and non-linear heart rate variability (HRV) analyses. The application of classical tools for ANS analysis, such as HRV during physiological sleep, showed that the rapid eye movement (REM) stage is characterized by a likely sympathetic predominance associated with a vagal withdrawal, while the opposite trend is observed during non-REM sleep. More recently, the use of non-linear tools, such as entropy-derived indices, have provided new insight on the cardiac autonomic regulation, revealing for instance changes in the cardiovascular complexity during REM sleep, supporting the hypothesis of a reduced capability of the cardiovascular system to deal with stress challenges. Interestingly, different HRV tools have been applied to characterize autonomic cardiac control in different pathological conditions, from neurological sleep disorders to sleep disordered breathing (SDB). In summary, linear and non-linear analysis of HRV are reliable approaches to assess changes of autonomic cardiac modulation during sleep both in health and diseases. The use of these tools could provide important information of clinical and prognostic relevance.
Frontiers in Physiology 10/2013; 4:294. DOI:10.3389/fphys.2013.00294 · 3.53 Impact Factor
"Moreover, inflammation is common in OSA patients, including elevated levels of proinflammatory cytokines. Tumor necrosis factor-í µí»¼ (TNF-í µí»¼) and IL-6 levels are elevated in OSA independent of obesity  . However, the initial trigger driving the elevation of proinflammatory cytokines in OSA patients has not been completely elucidated . "
[Show abstract][Hide abstract] ABSTRACT: Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive interruption of ventilation during sleep caused by recurrent upper airway collapse, which leads to intermittent hypoxia. The disorder is commonly undiagnosed despite its relationship with substantial cardiovascular morbidity and mortality. Moreover, the effects of the disorder appear to be particularly dangerous in young subjects. In the last decade, substantial clinical evidence has identified OSA as independent risk factor for both bradyarrhythmias and tachyarrhythmias. To date the mechanisms leading to such arrhythmias have not been completely understood. However, recent data from animal models and new molecular analyses have increased our knowledge of the field, which might lead to future improvement in current therapeutic strategies mainly based on continuous positive airway pressure. This paper aims at providing readers a brief and specific revision of current knowledge about the mechanisms underlying atrial arrhythmias in OSA and their clinical and therapeutic implications.
Pulmonary Medicine 04/2013; 2013:426758. DOI:10.1155/2013/426758
[Show abstract][Hide abstract] ABSTRACT: BACKGROUND: Obstructive sleep apnea (OSA) is associated with coronary artery disease (CAD). Intermittent hypoxia associated with OSA increases sympathetic activity and may cause systemic inflammation, which may contribute to CAD in patients with OSA. Treatment with continuous positive airway pressure (CPAP) has been shown to change levels of inflammatory markers. We analyzed data from published studies by a systematic meta-analysis. OBJECTIVE: To asses if treatment for sleep apnea by CPAP will affect levels of inflammatory markers.Data resources: PubMed, Embase and Cochrane library. METHODS: Study eligibility criteria full text English studies of adult, human subjects, addressing values of at least one of the inflammatory markers before and after CPAP treatment. We used the definition of OSA as an apnea-hypopnea index (AHI) of >= 5/h, reported values in mean and standard deviation or median with range.Participants: Adult, humanInterventions: CPAP treatment for OSAStudy appraisal and synthesis method: A total of 3835 studies were reviewed for inclusion, while 23 studies pooled for analysis. A total of 14 studies with 771 patients were pooled for C-reactive protein (CRP); 9 studies with 209 patients were pooled for tumor necrosis factor-alpha (TNF-alpha); and 8 studies with 165 patients were pooled for interleukin-6 (IL-6).Endpoint definitions: The following inflammatory markers were chosen: CRP, TNF-alpha, and IL-6. RESULTS: C-reactive protein: Study level means ranged from 0.18 to 0.85 mg/dl before CPAP treatment and 0.10 to 0.72 mg/dl after CPAP treatment. Mean differences, at a study level, ranged from -0.05 to 0.50. The pooled mean difference was 0.14 [95% confidence interval 0.08 to 0.20, p < 0.00001]. There was heterogeneity in this endpoint (df = 13, p < 0.00001, I2 = 95%).Tumor necrosis factor-alpha: Study level means ranged from 1.40 to 50.24 pg/ml before CPAP treatment and 1.80 to 28.63 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from -1.23 to 21.61. The pooled mean difference was 1.14 [95% confidence interval 0.12 to 2.15, p = 0.03]. There was heterogeneity in this endpoint (df = 8, p < 0.00001, I2 = 89%).Interleukin-6: Study level means ranged from 1.2 to 131.66 pg/ml before CPAP treatment and 0.45 to 66.04 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from -0.40 to 65.62. The pooled mean difference was 1.01 [95% confidence interval -0.00 to 2.03, p = 0.05]. There was heterogeneity in this endpoint (df = 7, p < 0.00001, I2 = 95%)Limitations: Only published data. Studies pooled were mainly small, non-randomized trials. CONCLUSION: Sleep apnea treatment with CPAP improves levels of inflammatory markers.
Journal of Inflammation 03/2013; 10(1):13. DOI:10.1186/1476-9255-10-13 · 2.02 Impact Factor
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