American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Apr 2015
Comparative StudyCT Predictors of Response to Endobronchial Valve Lung Reduction Treatment: Comparison with Chartis™
Chartis Pulmonary Assessment System (Pulmonx Inc., Redwood, CA) is an invasive procedure used to assess collateral ventilation and select candidates for valve-based lung volume reduction (LVR) therapy. Quantitative computed tomography (QCT) is a potential alternative to Chartis and today consists primarily of assessing fissure integrity (FI). ⋯ Quantitative CT led to comparable results to Chartis for classifying LVR and is a promising tool to effectively select patients for valve-based LVR procedures.
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Am. J. Respir. Crit. Care Med. · Apr 2015
Randomized Controlled Trial Comparative StudyRandomized Trial of Endobronchial Ultrasound-guided Transbronchial Needle Aspiration under General Anesthesia versus Moderate Sedation.
Data about the influence of the type of sedation on yield, complications, and tolerance of endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) are based mostly on retrospective studies and are largely inconsistent. ⋯ EBUS-TBNA performed under MS results in comparable diagnostic yield, rate of major complications, and patient tolerance as under GA. Future prospective multicenter studies are required to corroborate our findings. Clinical trial registered with www.clinicaltrials.gov (NCT 01430962).
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Am. J. Respir. Crit. Care Med. · Apr 2015
ReviewCardiotoxicity During Invasive Pneumococcal Disease.
Streptococcus pneumoniae is the leading cause of community-acquired pneumonia and sepsis, with adult hospitalization linked to approximately 19% incidence of an adverse cardiac event (e.g., heart failure, arrhythmia, infarction). Herein, we review the specific host-pathogen interactions that contribute to cardiac dysfunction during invasive pneumococcal disease: (1) cell wall-mediated inhibition of cardiomyocyte contractility; (2) the new observation that S. pneumoniae is capable of translocation into the myocardium and within the heart, forming discrete, nonpurulent, microscopic lesions that are filled with pneumococci; and (3) the bacterial virulence determinants, pneumolysin and hydrogen peroxide, that are most likely responsible for cardiomyocyte cell death. Pneumococcal invasion of heart tissue is dependent on the bacterial adhesin choline-binding protein A that binds to laminin receptor on vascular endothelial cells and binding of phosphorylcholine residues on pneumococcal cell wall to platelet-activating factor receptor. ⋯ We discuss these interactions and how their neutralization, either with antibody or therapeutic agents that modulate platelet-activating factor receptor expression, may confer protection against cardiac damage and meningitis. Considerable collagen deposition was observed in hearts of mice that had recovered from invasive pneumococcal disease. We discuss the possibility that cardiac scar formation after severe pneumococcal infection may explain why individuals who are hospitalized for pneumonia are at greater risk for sudden death up to 1 year after infection.