Chest
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Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. It is estimated that about 500,000 lung cancer deaths and 1.6 million COPD deaths can be attributed to air pollution, but air pollution may also account for 19% of all cardiovascular deaths and 21% of all stroke deaths. Air pollution has been linked to other malignancies, such as bladder cancer and childhood leukemia. ⋯ It is also associated with osteoporosis and bone fractures, conjunctivitis, dry eye disease, blepharitis, inflammatory bowel disease, increased intravascular coagulation, and decreased glomerular filtration rate. Atopic and urticarial skin disease, acne, and skin aging are linked to air pollution. Air pollution is controllable and, therefore, many of these adverse health effects can be prevented.
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Chronic anticoagulation is recommended in patients with hypertrophic cardiomyopathy (HCM) and atrial fibrillation (AF). Non-vitamin K antagonist oral anticoagulants (NOACs) are an alternative to warfarin, but there are limited data to support their use in patients with HCM and AF. We sought to compare thromboembolic events, bleeding, and mortality between NOAC and warfarin in patients with HCM and AF. ⋯ Compared with warfarin, patients with HCM and AF on NOACs had similar stroke and major bleeding risks, but lower all-cause mortality and composite fatal cardiovascular events. Our data suggest that patients with HCM and AF can be safely and effectively treated with NOACs.
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The natural history of lymphangioleiomyomatosis (LAM) is mainly derived from retrospective cohort analyses, and it remains incompletely understood. A National Institutes of Health LAM Registry was established to define the natural history and identify prognostic biomarkers that can help guide management and decision-making in patients with LAM. ⋯ The median transplant-free survival in patients with LAM is > 20 years. Menopausal status, as well as structural and physiologic markers of disease severity, significantly affect the rate of decline of FEV1 and progression to death or lung transplantation in LAM.
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Developing an effective treatment for COPD, and especially pulmonary emphysema, will require an understanding of how fundamental changes at the molecular level affect the macroscopic structure of the lung. Currently, there is no accepted model that encompasses the biochemical and mechanical processes responsible for pulmonary airspace enlargement. We propose that pulmonary emphysematous changes may be more accurately described as an emergent phenomenon, involving alterations at the molecular level that eventually reach a critical structural threshold where uneven mechanical forces produce alveolar wall rupture, accompanied by advanced clinical signs of COPD. The coupling of emergent morphologic changes with biomarkers to detect the process, and counteract it therapeutically, represents a practical approach to the disease.
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Meta Analysis
Change in FEV1 and Feno Measurements as Predictors of Future Asthma Outcomes in Children.
Repeated measurements of spirometry and fractional exhaled nitric oxide (Feno) are recommended as part of the management of childhood asthma, but the evidence base for such recommendations is small. We tested the hypothesis that reducing spirometric indices or increasing Feno will predict poor future asthma outcomes. ⋯ Repeated measurements of %FEV1 that are typically within the "normal" range add to clinical risk assessment of future asthma outcomes in children. The role of repeated Feno measurements is less certain because large changes were associated with small changes in outcome risk.