Journal
REDOX REPORT
Volume 22, Issue 2, Pages 51-73Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/13510002.2016.1256119
Keywords
Atherosclerosis; cardiovascular disease; coronary artery disease; imaging; myeloperoxidase; plaque rupture; reactive oxygen species; vulnerable plaques
Categories
Funding
- National Health and Medical Research Council of Australia [1020776, 1080604, 1052616]
- St Vincent's Clinic Foundation Tancred Research Grant
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Atherosclerosis is the main pathophysiological process underlying coronary artery disease (CAD). Acute complications of atherosclerosis, such asmyocardial infarction, are caused by the rupture of vulnerable atherosclerotic plaques, which are characterized by thin, highly inflamed, and collagen-poor fibrous caps. Several lines of evidence mechanistically link the heme peroxidase myeloperoxidase (MPO), inflammation as well as acute and chronic manifestations of atherosclerosis. MPO and MPO-derived oxidants have been shown to contribute to the formation of foam cells, endothelial dysfunction and apoptosis, the activation of latent matrix metalloproteinases, and the expression of tissue factor that can promote the development of vulnerable plaque. As such, detection, quantification and imaging of MPO mass and activity have become useful in cardiac risk stratification, both for disease assessment and in the identification of patients at risk of plaque rupture. This review summarizes the current knowledge about the role of MPO in CAD with a focus on its possible roles in plaque rupture and recent advances to quantify and image MPO in plasma and atherosclerotic plaques.
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