Low CVD Risk: <470
Moderate Risk: 470 - 539
High Risk: >539
Elevated MPO levels have been shown to be a significant independent risk factor for a major adverse cardiac event (MACE) over the ensuing one to six months.
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MPO is a white blood cell-derived inflammatory enzyme that measures disease activity from the luminal aspect of the arterial wall.
Briefly, when the artery wall is damaged, or inflamed, MPO is released by invading macrophages where it accumulates.
MPO mediates the vascular inflammation that propagates plaque formation and activates protease cascades that are linked to plaque vulnerability. White blood cell activation in the bloodstream, in response to luminal injury of the artery wall including fissures, erosions or a degrading collagen cap, leads to MPO release in the bloodstream. This combination of detrimental effects demonstrates that MPO is actively involved in the progression of atherosclerosis.
References:
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Fu X et al. Hypochlorous acid oxygenates the cysteine switch domain of pro-matrilysin (MMP-7). A mechanism for matrix metalloproteinase activation and atherosclerotic plaque rupture by myeloperoxidase. J Biol Chem. 2001; 276: 41279-41287. [L]
Meuwese MC et al. Serum myeloperoxidase levels are associated with the future risk of coronary artery disease in apparently healthy individuals: The EPIC-Norfolk Prospective Population Study. J Am Coll Cardiol. 2007; 50: 159-165. [L]
Karakas M et al. Myeloperoxidase is associated with incident coro¬nary heart disease independently of traditional risk factors: Results from the MONICA/KORA Augsburg study. J Intern Med. 2012; 271: 43-50. [L]
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Cavusoglu E et al. Usefulness of baseline plasma myeloperoxidase levels as an independent predictor of myocardial infarction at two years in patients presenting with acute coronary syndrome. Am J Cardiol. 2007; 99: 1364-1368. [L]
Heslop CL et al. Myeloperoxidase and C-reactive protein have combined utility for long-term prediction of cardiovascular mortality after coronary angiography. J Am Coll Cardiol. 2010; 55: 1102-1109. [L]
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