Rationale: Basic research implicates alveolar endothelial cell apoptosis in the pathogenesis of chronic obstructive pulmonary disease (COPD) and emphysema. However, information on endothelial microparticles (EMPs) in mild COPD and emphysema is lacking. Objectives: We hypothesized that levels of CD311 EMPs phenotypic for endothelial cell apoptosis would be elevated in COPD and associated with percent emphysema on computed tomography (CT). Associations with pulmonary microvascular blood flow (PMBF), diffusing capacity, and hyperinflation were also examined. Methods: The Multi-Ethnic Study of Atherosclerosis COPD Study recruited participants with COPD and control subjects age 50-79 years with greater than or equal to 10 pack-years without clinical cardiovascular disease. CD311 EMPs were measured using flow cytometry in 180 participants who also underwent CTs and spirometry. CD62E1 EMPs phenotypic for endothelial cell activation were also measured. COPD was defined by standard criteria. Percent emphysema was defined as regions less than 2950 Hounsfield units on full-lung scans. PMBF was assessed on gadolinium-enhanced magnetic resonance imaging. Hyperinflation was defined as residual volume/total lung capacity. Linear regression was used to adjust for potential confounding factors. Measurements and Main Results: CD311 EMPs were elevated in COPD compared with control subjects (P ¼ 0.03) and were notably increased in mild COPD (P ¼ 0.03). CD311 EMPs were positively related to percent emphysema (P ¼ 0.045) and were inversely associated with PMBF (P ¼ 0.047) and diffusing capacity (P ¼ 0.01). In contrast, CD62E1 EMPs were elevated in severe COPD (P ¼ 0.003) and hyperinflation (P ¼ 0.001). Conclusions: CD311 EMPs, suggestive of endothelial cell apoptosis, were elevated in mild COPD and emphysema. In contrast, CD62E 1 EMPs indicative of endothelial activation were elevated in severe COPD and hyperinflation.Keywords: chronic obstructive pulmonary disease; emphysema; antigens, CD31; endothelium; pulmonary disease Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the United States (1) and is projected to be the third leading cause of death worldwide by 2020 (2). COPD is defined as airflow obstruction that is not fully reversible (3). Many patients with COPD have emphysema, which is characterized by the destruction of alveolar walls with permanent loss of lung architecture and parenchyma (4).Cigarette smoking, the primary cause of COPD (3), is known to cause endothelial dysfunction (5). Cigarette smoke is delivered directly to pulmonary endothelial cells and contains multiple factors including acrolein that cause endothelial apoptosis (6). Increased endothelial cell apoptosis has been observed in the lung tissue of patients with emphysema compared with control subjects (7,8). Additionally, reductions in vascular endothelial growth factor (VEGF) and its receptor have been noted Prior research using animal models has implicated the primary destruction of the pulmonary capillary bed in the patho...

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Background Intensive care unit (ICU)–ward patient transfers are inherently high risk, and clinician miscommunication has been linked to adverse events and negative outcomes. Despite these risks, few educational tools exist to improve resident handoff communication at ICU–ward transfer. Objective We used human-centered design (HCD) methods to cocreate a novel electronic health record ICU–ward transfer tool alongside Internal Medicine residents at three academic hospitals. Methods We conducted HCD workshops at each hospital, performing process mapping, brainstorming, and rapid prototyping. We performed thematic analysis on verbatim-transcribed workshop audio recordings to inform development and adaptation of the final resident prototype into the ICU-PAUSE tool. Results ICU-PAUSE focuses on reasons for ICU admission and problem-based ICU course (I); Code status, goals of care, and family contacts (C); a diagnostic pause acknowledging Uncertainty (U); Pending tests (P); Active consultants (A); high-risk medications, including medications to be Unprescribed (U); Summary of problems and to-dos (S); and a current physical Exam (E). Conclusion We used HCD to cocreate a novel, more user-friendly electronic ICU–ward transfer tool, ICU-PAUSE, alongside Internal Medicine trainees. Future steps will involve formal usability testing, evidence-driven implementation, and clinical evaluation of ICU-PAUSE across multiple hospitals.

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