IntroductionThere is greater cardiovascular risk (CV) in those having chronic inflammatory diseases such as rheumatoid arthritis (RA) or spondyloarthropathies (SpA) than in the general population. This risk is not only explained by the association of the traditional risk factors of arterial hypertension (AHT), dyslipidemia, diabetes mellitus (DM) and smoking [1]. In this sense, early endothelial dysfunction and accelerated atherosclerotic process [2] have been described in these diseases and may be related to the same inflammatory process and be mediated by the tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) [3]. Sleep apnea-hypopnea syndrome (SAHS) has a 3-4% [4] prevalence in Western countries and is also associated to the metabolic syndrome and other CV risk factors [5]. SAHS per se constitutes an independent CV risk factor in male subjects and young subjects with this disease [6].Sleep abnormalities are common in RA [7,8] and SAHS has been attributed as being a factor that contributes to CV mortality in patients with RA [9]. There seems to be a systemic inflammatory component in the etiopathogeny of SAHS, although the mechanism is little known. The repeated episodes of hypoxia and reoxygenation cause oxidative stress that may play an important role in the associated systemic inflammatory process [10]. This would entail an increase in the expression of TNF-α.Association of inflammatory pathophysiology and an evolution occurring with more CV complications observed in RA as well as SpA and SAHS acquire greater conceptual support when we observe the response to the treatment. Thus, when SAHS is treated with continuing positive air pressure, a reduction is observed in blood pressure, triglycerides and glycated hemoglobin [11]. Furthermore, it has been stated that treatment with anti-TNF-α in patients with RA and sleep disorders improves sleep quality [12]. However, at present, there are still few studies that evaluate the severity of SAHS in patients with RA or SpA, the increase of CV risk that this association implies and the possible modulation of the nighttime anoxia-hypoxia episodes with treatment with anti TNF-α drugs. This study has aimed to evaluate the severity of SAHS in patients with RA or SpA and to verify the behavior of the apnea-hypopnea index (AHI) in patients with and without anti-TNF-α treatment.
AbstractObjective: To evaluate severity of the sleep apnea-hypopnea syndrome (SAHS) in patients with rheumatoid arthritis (RA) and spondyloarthropathies (SpA). To study the behavior of the apnea-hypopnea index (AHI) in patients treated with anti-TNF-α.
Materials and methods:An observational, retrospective study was conducted in patients with RA and SpA (study group) and with osteoarthritis (control group) who have SAHS symptoms. AHI (expressed in median and 25-75 percentiles), mean oxygen saturation (SaO 2 ) and information on associated cardiovascular risk factors (CVRF) were collected. This information was also collected in the anti-TNF-α treated study group.
Results:The study group (75 ...