patients with COPD corrected for other risk factors. The underlying mechanism for this remains unknown.The goal of this study was to assess vascular reactivity as mediated through both brachial artery flow-mediated (endothelium dependent) and nitrogen-mediated (endothelium independent) dilatation of the brachial artery in patients with COPD and controls, and to investigate a potential relationship between vascular function and airflow obstruction and systemic inflammation. There were 60 patients with stable COPD studies, of these, 20 were smokers with normal lung function matched for age, sex, and body weight, and 20 were similarly matched nonsmokers. Patients with known cardiovascular morbidities were excluded. Systemic inflammatory markers, including interleukin-6, C-reactive protein, and fibrinogen, were measured.In patients with stable COPD, flow-mediated and nitrogen-mediated dilatation of the brachial artery was impaired compared with smoking and nonsmoking controls. Levels of inflammatory markers such as fibrinogen and interleukin-6 were higher in COPD patients than in controls. Stepwise multiple regression analysis showed that baseline brachial diameter, Creactive protein level, leukocyte count, blood glucose level, age, sex, and percentage of predicted forced expiratory volume in 1 second were independent predictors of flow-mediated dilatation. Pack-years of smoking did not have a relationship with flow-mediated dilatation. Baseline brachial artery diameter was the only independent predictor of nitrogen-mediated dilatation in patients with COPD.Comment: This study tells us that impaired flow-mediated dilatation is strongly related to systemic inflammation in airway obstruction. Systemic inflammation is also related to atherosclerosis. Cardiovascular morbidity and endothelial dysfunction as measured by flow-mediated brachial artery dilatation is an early sign of atherosclerotic risk. Therefore, the study suggests a link between COPD and atherosclerosis, with both mediated by way of systemic markers of inflammation. Diabetes also may be a chronic inflammatory disease. The precise elements of chronic inflammation that contribute to all these processes now associated with atherosclerosis certainly require further investigation.
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