Related Articles

Reduced forced expiratory volume is associated with increased incidence of atrial fibrillation: the Malmo Preventive Project.

Europace. 2013 Aug 19;

Authors: Johnson LS, Juhlin T, Engström G, Nilsson PM

Abstract
AIMS: Reduced forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) have been associated with increased incidence of cardiovascular diseases. However, whether reduced lung function is also a risk factor for incidence of atrial fibrillation (AF) is still unclear. We aimed to determine whether lung function predicted AF in the Malmö Preventive Project, a large population-based cohort with a long follow-up.METHODS AND RESULTS: The study population consisted of 7674 women and 21 070 men, mean age 44.6 years. The cohort was followed on average for 24.8 years, during which time 2669 patients were hospitalized due to AF. The incidence of AF in relationship to quartiles of FEV1 and FVC and per litre decrease at baseline was determined using a Cox proportional hazards model adjusted for age, height, weight, current smoking status, systolic blood pressure, erythrocyte sedimentation rate, and fasting blood glucose. Forced expiratory volume in one second was inversely related to incidence of AF (per litre reduction in FEV1) hazard ratio (HR): 1.39 [95% confidence interval (CI): 1.16-1.68; P = 0.001] for women, and HR: 1.20 (95% CI: 1.13-1.29; P < 0.0001) for men. Forced vital capacity was also inversely related to incidence of AF (per litre reduction in FVC) HR: 1.20 (95% CI: 1.03-1.41; P = 0.020) for women, and HR: 1.08 (95% CI: 1.02-1.14; P = 0.01) for men. This relationship was consistent in non-smokers as well as smokers, and among individuals younger than the median age of 45.8 years or normotensive subjects.CONCLUSION: Impaired lung function is an independent predictor of AF. This may explain some risk of AF that is currently unaccounted for.

PMID: 23960091 [PubMed - as supplied by publisher]

Related Articles

Meta-Analysis of Genetic Programs between Idiopathic Pulmonary Fibrosis and Sarcoidosis.

PLoS One. 2013;8(8):e71059

Authors: Leng D, Huan C, Xie T, Liang J, Wang J, Dai H, Wang C, Jiang D

Abstract
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) and pulmonary sarcoidosis are typical interstitial lung diseases with unknown etiology that cause lethal lung damages. There are notable differences between these two pulmonary disorders, although they do share some similarities. Gene expression profiles have been reported independently, but differences on the transcriptional level between these two entities have not been investigated.
METHODS/RESULTS: All expression data of lung tissue samples for IPF and sarcoidosis were from published datasets in the Gene Expression Omnibus (GEO) repository. After cross platform normalization, the merged sample data were grouped together and were subjected to statistical analysis for finding discriminate genes. Gene enrichments with their corresponding functions were analyzed by the online analysis engine "Database for Annotation, Visualization and Integrated Discovery" (DAVID) 6.7, and genes interactions and functional networks were further analyzed by STRING 9.0 and Cytoscape 3.0.0 Beta1. One hundred and thirty signature genes could potentially differentiate one disease state from another. Compared with normal lung tissue, tissue affected by IPF and sarcoidosis displayed similar signatures that concentrated on proliferation and differentiation. Distinctly expressed genes that could distinguish IPF from sarcoidosis are more enriched in processes of cilium biogenesis or degradation and regulating T cell activations. Key discriminative network modules involve aspects of bone morphogenetic protein receptor two (BMPR2) related and v-myb myeloblastosis viral oncogene (MYB) related proliferation.
CONCLUSIONS: This study is the first attempt to examine the transcriptional regulation of IPF and sarcoidosis across different studies based on different working platforms. Groups of significant genes were found to clearly distinguish one condition from the other. While IPF and sarcoidosis share notable similarities in cell proliferation, differentiation and migration, remarkable differences between the diseases were found at the transcription level, suggesting that the two diseases are regulated by overlapping yet distinctive transcriptional networks.

PMID: 23967151 [PubMed - in process]

Microbiota abnormalities in inflammatory airway diseases - potential for therapy.

Pharmacol Ther. 2013 Aug 19;

Authors: Gollwitzer ES, Marsland BJ

Abstract
Increasingly the development of novel therapeutic strategies is taking into consideration the contribution of the intestinal microbiota to health and disease. Dysbiosis of the microbial communities colonizing the human intestinal tract has been described for a variety of chronic diseases, such as inflammatory bowel disease, obesity and asthma. In particular, reduction of several so-called probiotic species including Lactobacilli and Bifidobacteria that are generally considered to be beneficial, as well as an outgrowth of potentially pathogenic bacteria is often reported. Thus a tempting therapeutic approach is to shape the constituents of the microbiota in an attempt to restore the microbial balance towards the growth of 'health-promoting' bacterial species. A twist to this scenario is the recent discovery that the respiratory tract also harbors a microbiota under steady-state conditions. Investigators have shown that the microbial composition of the airway flora is different between healthy lungs and those with chronic lung diseases, such as asthma, chronic obstructive pulmonary disease as well as cystic fibrosis. This is an emerging field, and thus far there is very limited data showing a direct contribution of the airway microbiota to the onset and progression of disease. However, should future studies provide such evidence, the airway microbiota might soon join the intestinal microbiota as a target for therapeutic intervention. In this review, we highlight the major advances that have been made describing the microbiota in chronic lung disease and discuss current and future approaches concerning manipulation of the microbiota for the treatment and prevention of disease.

PMID: 23969226 [PubMed - as supplied by publisher]

Publication date: June 2013 Source:Revue de Pneumologie Clinique, Volume 69, Issue 3

Author(s): P. Mordant , A. Arame , A. Legras , F. Le Pimpec Barthes , M. Riquet

Le système lymphatique de la plèvre est un lieu de résorption majeur. L’action la mieux connue concerne la résorption des liquides. La plèvre, qui tapisse les poumons (plèvre viscérale), le médiastin, le diaphragme et la paroi thoracique osseuse intercostale (plèvre pariétale) est constituée d’une couche de cellules mésothéliales (mésothélium). La perméabilité du mésothélium pleural est voisine de celle de l’endothélium vasculaire. Le mésothélium est sous-tendu par un tissu conjonctif (interstitium) contenant des vaisseaux sanguins et lymphatiques. Les lymphatiques initiaux drainent cet interstitium, mais communiquent aussi directement avec l’espace pleural par des ouvertures ou stoma qui siègent au niveau des parties déclives de la plèvre pariétale, et sur la plèvre diaphragmatique. Ainsi, une partie du liquide interstitiel pulmonaire diffuse dans la cavité pleurale à travers la plèvre viscérale et est réabsorbée par les stoma de la plèvre pariétale. Cette réabsorption est active, directement en rapport avec l’activité musculaire lisse du système lymphatique. En marge de la résorption liquidienne, il faut souligner que cette activité de « pompage » est permanente et à l’origine des pressions négatives et du « vide pleural » propre à cette cavité. D’autres éléments sont réabsorbés, molécules, débris bactériens et cellulaires, cellules entières, érythrocytes et cellules cancéreuses. The pleural lymphatic system has a great absorption capacity. Its most known function is fluid resorption. The pleura which cover the lungs (visceral pleura), the mediastinum, diaphragm and thoracic wall (parietal pleura) are formed by a mesothelial cell layer (mesothelium). This permeable layer is in direct contact with the vascular endothelium. The mesothelium is based over a connective tissue (interstitium) containing the blood and lymphatic vessels. The primary lymphatic vessels drain interstitium but are also in direct contact with pleural space by the stoma or openings, situated in the lower parts of parietal pleura, i.e: diaphragm, over lower ribs and mediastinum but not existing in the adjacent visceral pleura. In addition, a part of interstitial pulmonary fluid entered in the pleural cavity by passing the visceral pleura would be absorbed by these openings. The resorption process is active and directly related to the function of smooth muscles of lymphatic vessels. Besides resorption, we must emphasize that this “pumping” activity is permanent and the origin of negative pressure (the pleural void) in pleural cavity, a unique property. The other resorbed elements are molecules, bacterial and cellular debris, cells, red blood and cancer cells.