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-α 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·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)-α, interleukin (IL)-6 and leukotriene (LT)B₄levels were obtained at baseline and after 3 months of CPAP or sham CPAP.Nocturnal urinary levels of norepinephrine, epinephrine and sTNFR-1 (1,053±269versus820±166 pg·mL⁻¹) were significantly higher in OSA patients. There were no significant differences in plasma levels of IL-6, LTB₄, or TNF-α between the two study groups. There were no significant differences in blood pressure, urinary catecholamine levels, or plasma IL-6, LTB₄and TNF-α levels after both treatment modalities. However, after 3 months of effective CPAP usage, sTNFR-1 levels were significantly reduced (1,053±269versus899±254 pg·mL⁻¹).Obstructive sleep apnoea patients have higher levels of soluble tumour necrosis factor-α receptor 1 than individuals without OSA; soluble tumour necrosis factor-α 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.

Atrial fibrillation is associated with substantial morbidity and mortality and both its incidence and prevalence are high. Nevertheless, comprehensive data on this condition in Spain are lacking. The aim of this study was to estimate the prevalence of atrial fibrillation in Spain. A cross-sectional study was conducted in the general Spanish population older than 40 years. Two-stage random sampling was used, in which first-stage units were primary care physicians randomly selected in every Spanish province and second-stage units were 20 randomly selected persons drawn from each participating physician's assigned population. The reported prevalence was standardized for the age and sex distribution of the Spanish population. The electrocardiogram recordings were read centrally. Overall, 8343 individuals were evaluated. The mean age was 59.2 years (95% confidence interval, 58.6-59.8 years), and 52.4% of the participants were female. The overall age-adjusted prevalence of atrial fibrillation was 4.4% (95% confidence interval, 3.8-5.1). Prevalence was similar in both sexes, men 4.4% (3.6-5.2) and women 4.5% (3.6-5.3), rising with increasing age older than 60 years. In patients older than 80 years, the prevalence was 17.7% (14.1-21.3). In 10% of patients an unknown atrial fibrillation was diagnosed. The prevalence of atrial fibrillation in the general Spanish population older than 40 years is high, at 4.4%. The prevalence is similar in both sexes and rises steeply above 60 years of age. It is estimated that there are over 1 million patients with atrial fibrillation in the Spanish population, of whom over 90,000 are undiagnosed.

Coronary atherosclerosis still represents the major cause of mortality in western societies. Initiation of atherosclerosis occurs within the intima, where major histological and molecular changes are produced during pathogenesis. So far, proteomic analysis of the atherome plaque has been mainly tackled by the analysis of the entire tissue, which may be a challenging approach because of the great complexity of this sample in terms of layers and cell type composition. Based on this, we aimed to study the intimal proteome from the human atherosclerotic coronary artery. For this purpose, we analyzed the intimal layer from human atherosclerotic coronaries, which were isolated by laser microdissection, and compared with those from preatherosclerotic coronary and radial arteries, using a two-dimensional Differential-In-Gel-Electrophoresis (DIGE) approach. Results have pointed out 13 proteins to be altered (seven up-regulated and six down-regulated), which are implicated in the migrative capacity of vascular smooth muscle cells, extracellular matrix composition, coagulation, apoptosis, heat shock response, and intraplaque hemorrhage deposition. Among these, three proteins (annexin 4, myosin regulatory light 2, smooth muscle isoform, and ferritin light chain) constitute novel atherosclerotic coronary intima proteins, because they were not previously identified at this human coronary layer. For this reason, these novel proteins were validated by immunohistochemistry, together with hemoglobin and vimentin, in an independent cohort of arteries.