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Management Committee of EU COST ACTION B26. Sleep apnea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities

Università degli Studi di Palermo, Palermo, Sicily, Italy
European Respiratory Journal (Impact Factor: 7.13). 02/2007; 29(1):156-78. DOI: 10.1183/09031936.00027406
Source: PubMed

ABSTRACT Considerable evidence is available in support of an independent association between obstructive sleep apnoea syndrome (OSAS) and cardiovascular disease, which is particularly strong for systemic arterial hypertension and growing for ischaemic heart disease, stroke, heart failure, atrial fibrillation and cardiac sudden death. The pathogenesis of cardiovascular disease in OSAS is not completely understood but likely to be multifactorial, involving a diverse range of mechanisms including sympathetic nervous system overactivity, selective activation of inflammatory molecular pathways, endothelial dysfunction, abnormal coagulation and metabolic dysregulation, the latter particularly involving insulin resistance and disordered lipid metabolism. The present report, which arose out of a European Union Cooperation in the field of Scientific and Technical Research (COST) action on OSAS (COST B26), reviews the current evidence for an independent association and proposes research priorities to identify the underlying mechanisms involved, with a view to identifying novel therapeutic strategies. Large-scale collaborative studies of carefully defined patient populations with obstructive sleep apnoea syndrome, adequately controlled for potential confounders, are needed. Such studies carry the prospect of evaluating potential interactions between different basic mechanisms operating in obstructive sleep apnoea syndrome and cardiovascular disease, and interactions with other related disorders, such as obesity, diabetes and dyslipidaemia. Furthermore, translational studies involving cell culture and animal models linked to studies of obstructive sleep apnoea syndrome patients are necessary to integrate basic mechanisms with the clinical disorder.

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    • "OSA is known to be associated with significant atrial structural remodeling, including atrial enlargement and significant conduction abnormalities [7] [8] [9]. It is thought that the electrical substrate for AF resulting from OSA is due to these structural changes, which result in increased sympathetic tone, systemic and pulmonary hypertension, intermittent hypoxia, and inflammation [10] [11] [12] [13] [14] [15] [16] [17]. "
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    ABSTRACT: Background: Obstructive Sleep Apnea (OSA) results in intermittent hypoxia leading to atrial remodeling, which, among other things, facilitates development of atrial fibrillation. While much data exists on the macrostructural changes in cardiac physiology induced by OSA, there is a lack of studies looking for histologic changes in human atrial tissue induced by OSA which might lead to the observed macrostructural changes. Methods: A case control study was performed. Patients undergoing coronary artery bypass grafting (CABG) were evaluated for OSA and categorized as high-risk or low-risk. The right atrial tissue samples were obtained during CABG and both microscopic histological analysis and Sirius Red staining were performed. Results: 18 patients undergoing CABG were included; 10 high-risk OSA and 8 low-risk OSA in evenly matched populations. No statistically significant difference between the two groups was observed in amount of myocytolysis ( p= 0.181), nuclear hypertrophy ( p= 0.671), myocardial inflammation ( p= n/a), amyloid deposition ( p= n/a), or presence of thrombi ( p= n/a), as measured through routine H&E staining. As well, no statistically significant difference in interstitial and epicardial collagen was observed, as measured by Sirius Red staining (for total tissue: p= 0.619: for myocardium: p= 0.776). Conclusions: In this pilot study there were no observable histological differences in human right atrial tissue from individuals at high- and low-risk for OSA. Further investigation would be required for more definitive results.
    03/2015; 6:71-75. DOI:10.1016/j.ijcha.2015.01.008
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    • "Obstructive sleep apnoea (OSA) is an independent risk factor for cardiovascular morbidity and mortality [1], due to increased production of reactive oxygen species and pro-inflammatory cytokines, resulting from chronic intermittent hypoxia–reoxygenation [2]. Oxidative stress and inflammation cause endothelial dysfunction leading to cardiovascular diseases [3]. "
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    ABSTRACT: To assess distal/alveolar inflammation in patients with suggestive symptoms of obstructive sleep apnoea (OSA) using exhaled nitric oxide (NO) measured by two-compartment model (2-CM) after correction for axial NO back-diffusion (trumpet model). Ninety five patients suspected for OSA prospectively underwent pulmonary function test, overnight polysomnography (PSG), and exhaled NO measurement. Patients with apnoea-hypopnoea index (AHI) <5/hour were included in non-OSA group. Exhaled NO was repeatedly measured after PSG in 21 OSA patients and 8 non-OSA subjects. Alveolar NO concentration (CANO) was significantly higher in OSA patients (n=71; 4.07±1.7ppb) as compared with non-OSA subjects (n=24; 2.24±1.06ppb; p<0.0001) whilst maximal bronchial NO flux (J'awNO) and fractional exhaled NO (FENO) did not differ between the two groups. CANO was strongly associated to AHI (r=0.701; p<0.0001) and to recording time with SaO2<90% (ST-90%; r=0.659; p<0.0001) in OSA patients but not in non-OSA persons. The area under ROC curve for screening patients with OSA and significant nocturnal oxygen desaturation (ST-90%>1%) was 0.865±0.036 (95% IC, 0.793-0.937; p<0.0001). CANO at 4.5 ppb could detect these patients with specificity of 94% and sensitivity of 46%. Increase of CANO measured after PSG was significantly related to oxygen desaturation index (ST-90%) in OSA patients. Increased alveolar NO concentration was related to the severity of nocturnal oxygen desaturation in patients with OSA, linking the distal airway inflammation to intermittent hypoxia. (250 words). Copyright © 2015. Published by Elsevier Inc.
    Nitric Oxide 01/2015; 45. DOI:10.1016/j.niox.2015.01.008 · 3.18 Impact Factor
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    • "The severity of OSAS is estimated by the number of apneahypopnea episodes per hour of sleep and is expressed as the apnea-hypopnea index (AHI) [2]. Although the underlying mechanisms and etiologies are not completely understood, OSAS can lead to significant cardiovascular complications [3], including heart failure, acute myocardial infarction, arrhythmias, hypertension, pulmonary hypertension, and stroke [4]. Increased platelet activation and aggregation are closely related to cardiovascular complications [5]. "
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    ABSTRACT: Obstructive sleep apnea syndrome (OSAS) is a common disorder that can lead to significant cardiovascular complications. Several studies have reported increased platelet activation and aggregation in patients with OSAS. In this study we aimed to show a correlation between mean platelet volume (MPV) and severity of OSAS in patients with OSAS without any overt cardiac disease or diabetes. The polysomnography recordings of 556 consecutive patients admitted to the sleep laboratory between January 2012 and July 2012 were retrospectively evaluated. The relationship between polysomnographic parameters and biochemical parameters was assessed. Polysomnographic results of 200 patients (154 males [77%]; mean age, 44.5 ± 11.4 years) were included. No correlation was observed between MPV and the average oxygen saturation index, the minimum desaturation index, or the oxygen desaturation index in the study population as well as in severe OSAS group (AHI > 30). The only correlation was found between MPV and AHI in the severe OSAS group (P = 0.010). MPV was not correlated with OSAS severity in patients without any overt cardiac disease or diabetes. These findings raise doubts about the suggestion that MPV might be a marker for OSAS severity, as recommended in earlier studies. Thus, further prospective data are needed.
    09/2014; 2014:754839. DOI:10.1155/2014/754839
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