2015
DOI: 10.1378/chest.15-0484
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Community-Acquired Pneumonia

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Cited by 46 publications
(21 citation statements)
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“…The potential biological mechanism leading to HF or COPD progression following an acute pneumonia episode have not yet been precisely defined. Speculation that the inflammatory response is, in part, harmful underlies the current thinking as prior studies have identified inflammation as a risk factor for development of coronary artery disease [ 19 , 20 ]. In support of the role of inflammation, levels of interleukin 6 measured at the time of hospital discharge in patients with pneumonia identify patients at greater risk of cardiovascular related mortality within a one year follow-up [ 21 ].…”
Section: Discussionmentioning
confidence: 99%
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“…The potential biological mechanism leading to HF or COPD progression following an acute pneumonia episode have not yet been precisely defined. Speculation that the inflammatory response is, in part, harmful underlies the current thinking as prior studies have identified inflammation as a risk factor for development of coronary artery disease [ 19 , 20 ]. In support of the role of inflammation, levels of interleukin 6 measured at the time of hospital discharge in patients with pneumonia identify patients at greater risk of cardiovascular related mortality within a one year follow-up [ 21 ].…”
Section: Discussionmentioning
confidence: 99%
“…These data, if confirmed, suggest successful pneumonia prevention in cardiac and pulmonary disease patients could alter longer term outcomes. Alternatively, addressing the underlying mechanisms, such as chronic inflammation and/or platelet activation, could potentially alter the frequency of exacerbations of HF or COPD [ 20 ]. Smoking cessation and vaccination against influenza and pneumococcal disease are currently recommended for the prevention of CAP [ 28 ].…”
Section: Discussionmentioning
confidence: 99%
“…In this setting, activated platelets act as bridges promoting neutrophil clusters, as well as binding of neutrophils to vascular endothelium mediated by CD62P and other pro-adhesive mechanisms [30, 32, 42]. If poorly controlled, systemic inflammatory mechanisms involving platelets, neutrophils and vascular endothelium predispose to endothelial damage and dysfunction, promoting microvascular damage and coagulation [31]. …”
Section: Pathogenic Mechanisms Of Cap-associated Cvesmentioning
confidence: 99%
“…These have been covered extensively in recent reviews [31, 48] and will be considered briefly here. Agents which target platelet activation fall into several categories, targeting both mediators of activation and their receptors, and include, but are not limited to, the following:

inhibitors of production of thromboxane A 2

antagonists of thromboxane A 2 receptors

antagonists of ADP-activated P2Y12 receptors

antagonists of thrombin-activated proteinase-activated receptor 1

GPIIb/IIIa inhibitors.

…”
Section: Treatment And/or Prevention Of Cap-associated Cvesmentioning
confidence: 99%
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