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      Morphological changes in small pulmonary vessels are associated with severe acute exacerbation in chronic obstructive pulmonary disease

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          Abstract

          Background

          Pulmonary vascular remodeling is essential for understanding the pathogenesis of chronic obstructive pulmonary disease (COPD). The total cross-sectional area (CSA) of small pulmonary vessels has been reported to correlate with the pulmonary artery pressure, and this technique has enabled the assessment of pulmonary vascular involvements. We investigated the contribution of morphological alterations in the pulmonary vessels to severe acute exacerbation of COPD (AE-COPD).

          Methods

          This study enrolled 81 patients with COPD and 28 non-COPD subjects as control and assessed the percentage of CSA (%CSA) less than 5 mm 2 (%CSA <5) and %CSA in the range of 5–10 mm 2 (%CSA 5–10) on high-resolution computed tomography images.

          Results

          Compared with the non-COPD subjects, the COPD patients had lower %CSA <5. %CSA <5 was positively correlated with airflow limitation and negatively correlated with the extent of emphysema. COPD patients with lower %CSA <5 showed significantly increased incidences of severe AE-COPD (Gray’s test; P=0.011). Furthermore, lower %CSA <5 was significantly associated with severe AE-COPD (hazard ratio, 2.668; 95% confidence interval, 1.225–5.636; P=0.010).

          Conclusion

          %CSA <5 was associated with an increased risk of severe AE-COPD. The distal pruning of the small pulmonary vessels is a part of the risk associated with AE-COPD, and %CSA <5 might be a surrogate marker for predicting AE-COPD.

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          Most cited references 33

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          Endothelial dysfunction, oxidative stress, and risk of cardiovascular events in patients with coronary artery disease.

          Endothelial function is impaired in coronary artery disease and may contribute to its clinical manifestations. Increased oxidative stress has been linked to impaired endothelial function in atherosclerosis and may play a role in the pathogenesis of cardiovascular events. This study was designed to determine whether endothelial dysfunction and vascular oxidative stress have prognostic impact on cardiovascular event rates in patients with coronary artery disease. Endothelium-dependent and -independent vasodilation was determined in 281 patients with documented coronary artery disease by measuring forearm blood flow responses to acetylcholine and sodium nitroprusside using venous occlusion plethysmography. The effect of the coadministration of vitamin C (24 mg/min) was assessed in a subgroup of 179 patients. Cardiovascular events, including death from cardiovascular causes, myocardial infarction, ischemic stroke, coronary angioplasty, and coronary or peripheral bypass operation, were studied during a mean follow-up period of 4.5 years. Patients experiencing cardiovascular events (n=91) had lower vasodilator responses to acetylcholine (P<0.001) and sodium nitroprusside (P<0.05), but greater benefit from vitamin C (P<0.01). The Cox proportional regression analysis for conventional risk factors demonstrated that blunted acetylcholine-induced vasodilation (P=0.001), the effect of vitamin C (P=0.001), and age (P=0.016) remained independent predictors of cardiovascular events. Endothelial dysfunction and increased vascular oxidative stress predict the risk of cardiovascular events in patients with coronary artery disease. These data support the concept that oxidative stress may contribute not only to endothelial dysfunction but also to coronary artery disease activity.
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            Inflammation, growth factors, and pulmonary vascular remodeling.

            Inflammatory processes are prominent in various types of human and experimental pulmonary hypertension (PH) and are increasingly recognized as major pathogenic components of pulmonary vascular remodeling. Macrophages, T and B lymphocytes, and dendritic cells are present in the vascular lesions of PH, whether in idiopathic pulmonary arterial hypertension (PAH) or PAH related to more classical forms of inflammatory syndromes such as connective tissue diseases, human immunodeficiency virus (HIV), or other viral etiologies. Similarly, the presence of circulating chemokines and cytokines, viral protein components (e.g., HIV-1 Nef), and increased expression of growth (such as vascular endothelial growth factor and platelet-derived growth factor) and transcriptional (e.g., nuclear factor of activated T cells or NFAT) factors in these patients are thought to contribute directly to further recruitment of inflammatory cells and proliferation of smooth muscle and endothelial cells. Other processes, such as mitochondrial and ion channel dysregulation, seem to convey a state of cellular resistance to apoptosis; this has recently emerged as a necessary event in the pathogenesis of pulmonary vascular remodeling. Thus, the recognition of complex inflammatory disturbances in the vascular remodeling process offers potential specific targets for therapy and has recently led to clinical trials investigating, for example, the use of tyrosine kinase inhibitors. This paper provides an overview of specific inflammatory pathways involving cells, chemokines and cytokines, cellular dysfunctions, growth factors, and viral proteins, highlighting their potential role in pulmonary vascular remodeling and the possibility of future targeted therapy.
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              Computed tomographic measurements of airway dimensions and emphysema in smokers. Correlation with lung function.

              Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow obstruction caused by emphysema or airway narrowing, or both. Low attenuation areas (LAA) on computed tomography (CT) have been shown to represent macroscopic or microscopic emphysema, or both. However CT has not been used to quantify the airway abnormalities in smokers with or without airflow obstruction. In this study, we used CT to evaluate both emphysema and airway wall thickening in 114 smokers. The CT measurements revealed that a decreased FEV(1) (%predicted) is associated with an increase of airway wall area and an increase of emphysema. Although both airway wall thickening and emphysema (LAA) correlated with measurements of lung function, stepwise multiple regression analysis showed that the combination of airway and emphysema measurements improved the estimate of pulmonary function test abnormalities. We conclude that both CT measurements of airway dimensions and emphysema are useful and complementary in the evaluation of the lung of smokers.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2016
                28 June 2016
                : 11
                : 1435-1445
                Affiliations
                [1 ]Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan
                [2 ]Department of Respiratory Medicine, Iwata City Hospital, Iwata, Japan
                Author notes
                Correspondence: Yuzo Suzuki, Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama Higashi-ku, Hamamatsu, Shizuoka 431-3129, Japan, Tel +81 53 435 2263, Fax +81 53 435 2354, Email yuzosuzu@ 123456hama-med.ac.jp
                Article
                copd-11-1435
                10.2147/COPD.S107424
                4934566
                27418816
                © 2016 Yoshimura et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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