Objectives:Atrial fibrillation has been associated with obesity in epidemiological studies. Epicardial adipose tissue is an ectopic fat depot in the proximity of atria, with endocrine and inflammatory properties that is implicated in the pathophysiology of atrial fibrillation. Inflammation also has a role in atrial arrhythmogenesis. The aim of this study was to investigate the potential relations of epicardial adipose tissue to left atrial size and to adiponectin and the pro-inflammatory mediators, high-sensitivity C-reactive protein, and interleukin-6 in paroxysmal and permanent atrial fibrillation.Methods:This was a cross-sectional study of 103 atrial fibrillation patients, divided into two subgroups of paroxysmal and permanent atrial fibrillation, and 81 controls, in sinus rhythm. Echocardiography was used for estimation of epicardial adipose tissue and left atrial size and high-sensitivity C-reactive protein, interleukin-6 and adiponectin were measured in all subjects.Results:Atrial fibrillation patients had significantly larger epicardial adipose tissue compared with controls (0.43 ± 0.17 vs 0.34 ± 0.17 cm, p = 0.002). Atrial fibrillation presence was independently related to epicardial adipose tissue thickness (b = 0.09, p = 0.002). Opposite associations of epicardial adipose tissue with left atrial volume existed in atrial fibrillation subgroups; in the paroxysmal subgroup, epicardial adipose tissue was directly related to left atrial volume (R = 0.3, p = 0.03), but in the permanent one the relation was inverse (R = −0.7, p < 0.0001). Adiponectin, high-sensitivity C-reactive protein and interleukin-6 were elevated in both atrial fibrillation groups. Only interleukin-6 was related to epicardial adipose tissue size.Conclusion:Opposite associations of epicardial adipose tissue with left atrial size in paroxysmal and permanent Atrial fibrillation and elevated inflammatory markers, suggest a role of epicardial adipose tissue and inflammation in the fibrotic and remodeling process.
Aquatic macrophytes are one of the four biological quality elements (BQE) used for assessing the ecological status of inland waters according to the EU Water Framework Directive (WFD 2000/60). With this article, we present the methodological approach for the implementation of a WFD compliant macrophyte index to the riverine systems of Greece. In addition to the definition and harmonization of the ecological quality class boundaries, the results from the pilot application of the index and the ecological classification of the monitored river reaches are also presented. Aquatic plants and environmental parameters were sampled from 93 river reaches between 2012 and 2015. A multivariate analysis with optimal scaling (MVAOS) was conducted to define the main stressor gradient and to identify the least disturbed sites and the reference conditions that are required for the derivation of the ecological quality classes. The Macrophyte Biological Index IBMR for Greek rivers (IBMRGR) was calculated for all the sites and the boundaries for the five quality classes were derived according to the methodology proposed by the Mediterranean Geographic Intercalibration Group (MedGIG). The main findings showed that the hydromorphological modifications were the main environmental stressors that correlated strongly with the IBMRGR, whereas physicochemical stressors were of lesser importance. More specifically, the first principal component explained 51% of the total variance of the data, representing a moderately strong gradient of hydromorphological stress, whereas the second component explained 22.5%, representing a weaker gradient of physicochemical stress. In addition, the ecological assessment showed that almost 60% of the sites failed the WFD target of the “Good” ecological quality class, which agrees with classification assessments based on other BQEs for Greece and many Mediterranean countries. Overall, this work provides a first assessment of the ecological classification of Greek rivers with the BQE of aquatic macrophytes with significant implications for ecological monitoring and decision making within the frame of the WFD implementation.
cTnI and CRP can increase early after permanent pacemaker implantation, indicating mechanical myocardial injury and inflammation. The extent of these biomarkers elevation depends on the lead fixation type, and is not related to worse short-term prognosis.
Inspiratory resistive breathing (IRB), a hallmark of obstructive airway diseases, is associated with strenuous contractions of the inspiratory muscles and increased negative intrathoracic pressures that act as an injurious stimulus to the lung. We have shown that IRB induces pulmonary inflammation in healthy animals. p38 kinase is activated in the lung under stress. We hypothesized that p38 is activated during IRB and contributes to IRB-induced pulmonary inflammation. Anesthetized, tracheostomized rats breathed spontaneously through a two-way valve. Resistance was connected to the inspiratory port to provoke a peak tidal inspiratory pressure 50% of maximum. Following 3 and 6 h of IRB, respiratory system mechanics were measured and bronchoalveolar lavage (BAL) was performed. Phosphorylated p38, TNF-α, and MIP-2α were detected in lung tissue. Lung injury was estimated histologically. SB203580 (p38 inhibitor) was administered prior to IRB (1 mg kg). Six hours of IRB increased phosphorylated p38 in the lung, compared with quietly breathing controls (p = 0.001). Six hours of IRB increased the numbers of macrophages and neutrophils (p = 0.01 and p = 0.005) in BAL fluid. BAL protein levels and lung elasticity increased after both 3 and 6 h IRB. TNF-α and MIP-2α increased after 6 h of IRB (p = 0.01 and p < 0.001, respectively). Increased lung injury score was detected at 6 h IRB. SB203580 administration blocked the increase of neutrophils and macrophages at 6 h IRB (p = 0.01 and p = 0.005 to 6 h IRB) but not the increase in BAL protein and elasticity. TNF-α, MIP-2α, and injury score at 6 h IRB returned to control. p38 activation contributes to IRB-induced pulmonary inflammation.
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