Rahul Kurup,1,2,3 *Sanjay Patel1,2,3
1. Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia
2. Heart Research Institute, Sydney, Australia
3. Sydney Medical School, The University of Sydney, Sydney, Australia
*Correspondence to firstname.lastname@example.org
Disclosure: The authors have declared no conflicts of interest.
Received: 15.05.17 Accepted: 11.08.17
Citation: EMJ Cardiol. 2017;5:79-87.
Acute coronary syndrome (ACS) encompasses a spectrum of clinical disorders of myocardial ischaemia or infarction, with atherosclerosis leading to coronary plaque formation the predominant disease process. Alterations of endothelial cell integrity involving atherosclerotic plaque surfaces, such as plaque rupture or erosion, can lead to atherothrombosis with subsequent interruption to myocardial blood supply. Over the past two decades, it has become increasingly apparent that inflammation plays a pivotal role in the initiation and progression of atherosclerosis. Inflammatory cytokines have been shown to correlate with the risk and burden of coronary artery disease and there is a growing body of evidence demonstrating the presence of various immune cells in atherosclerotic plaques and coronary thrombus specimens. Due to improved cellular detection methods compared to earlier studies, neutrophils are being increasingly recognised as a key player in the process of athero-inflammation. The aim of this review is to: i) outline the role of neutrophils in ACS and atherothrombosis, ii) describe the process of inflammasome-mediated release of inflammatory cytokines from neutrophils, and iii) discuss multiple parameters of neutrophil activity in ACS, including peripheral neutrophil/lymphocyte ratio; neutrophil microparticle release; expression of neutrophilic granular proteins, including myeloperoxidase, neutrophil elastase, and metalloproteinases; neutrophil extracellular traps release; tissue factor; and neutrophil-macrophage interactions.
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