Plasma Concentrations of Myeloperoxidase Predict Mortality After Myocardial Infarction

Mocatta, Tessa; Pilbrow, Anna P.; Cameron, Vicky A.; Senthilmohan, Revathy; Frampton, Chris; Richards, A. Mark; Winterbourn, Christine C.

doi:10.1016/j.jacc.2007.02.040

Cited by 295 publications

(200 citation statements)

References 42 publications

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“…Although ELISA is easy to use, only few reports have compared the various kits to determine their accuracy and reliability. Comparisons of in-house MPO ELISA with commercial kits generally show strong positive correlations (Pearson correlation coefficient >0.9) [120,121]. However, there is concern around the accuracy of the assays given that different concentrations of MPO can be obtained in the same samples when applying different ELISA kits/methods [120].…”

Section: Detection Of Mpo Proteinmentioning

confidence: 99%

The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture

et al. 2016

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Atherosclerosis is the main pathophysiological process underlying coronary artery disease (CAD). Acute complications of atherosclerosis, such as myocardial 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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Section: Detection Of Mpo Proteinmentioning

confidence: 99%

The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture

et al. 2016

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“…In addition, serum MPO levels are elevated in human stroke patients compared with normal subjects (12) and can predict future stroke and vasculopathic events in Fabry disease (13). Additionally, serum MPO levels are elevated in other cardiovascular diseases in humans, including myocardial infarction (14), congestive heart failure (15), and peripheral vascular disease (16). Therefore, whereas inflammation is a complex cascade of events involving different types of cells and molecules, MPO could be used as a biomarker for inflammation, and a noninvasive method to identify MPO activity in the ischemic brain could allow clinicians to identify those patients that would most likely benefit from antiinflammatory therapy.…”

mentioning

confidence: 99%

Tracking the inflammatory response in stroke in vivo by sensing the enzyme myeloperoxidase

Breckwoldt

Chen

Stangenberg³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

284

240

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Inflammation can extend ischemic brain injury and adversely affect outcome in experimental animal models. A key difficulty in translating animal studies to humans is the lack of a definitive method to confirm and track inflammation in the brain in vivo. Myeloperoxidase (MPO), a key inflammatory enzyme secreted by activated neutrophils and macrophages/microglia, can generate highly reactive oxygen species to cause additional damage in cerebral ischemia. We report here that a functional, enzyme-activatable MRI agent can accurately track the oxidative activity of MPO noninvasively in stroke in living animals. We found that MPO is widely distributed in ischemic tissues, correlates positively with infarct size, and is detected even 3 weeks postinfarction. The peak level of MPO activity, determined by activation of the MPO-sensing agent in vivo and confirmed by MPO activity and quantitative RT-PCR assays, occurred on day 3 after ischemia. Both neutrophils and macrophages/microglia contribute to secrete MPO in the ischemic brain, although neutrophils peak earlier (days 1-3) whereas macrophages/microglia are most abundant later (days 3-7). In contrast to the conventional MRI agent diethylenetriaminepentatacetate gadolinium, which reports blood-brain barrier disruption, MPO imaging is able to additionally track MPO activity and confirm inflammation on the molecular level in vivo, information that was previously only possible to obtain on ex vivo brain sections and impossible to assess in living human patients. Our findings could allow efficient noninvasive serial screening of therapies targeting inflammation and the use of MPO imaging as an imaging biomarker to risk-stratify patients.inflammation ͉ ischemia ͉ molecular imaging ͉ MRI ͉ brain

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“…Similar findings were observed by Esporcatte et al 16 in a heterogeneous group of chest pain patients. Mocatta et al 17 showed a significant relationship between abovemedian levels of MPO after acute myocardial infarction and increased 5 y mortality. Nonetheless, we were unable to show an association of MPO with cardiovascular events in long-term follow-up.…”

Section: Discussionmentioning

confidence: 97%

Serial Analyses of C‐Reactive Protein and Myeloperoxidase in Acute Coronary Syndrome

Borges¹,

Borges²,

Stella³

et al. 2009

Clinical Cardiology

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Background: C-reactive protein (CRP) and myeloperoxidase (MPO) are involved in the pathogenesis of atherosclerosis, mainly during periods of instabilization. This study aims to test the hypothesis that patients with acute coronary syndrome (ACS) maintain a persistent inflammatory state, and that this is associated with long-term mortality. Hypothesis: We hypothesized that serum C-reactive protein and myeloperoxidase collected at the index event and later, could add to the prognostic information in patients with ACS. Methods: In a prospective cohort of 115 consecutive patients with ACS, myeloperoxidase and C-reactive protein were measured at admission and 2 y later. Patients were followed-up for the occurrence of cardiac death and other major cardiac events. Results: Levels of CRP decreased from 26±34 mg/L in the acute phase to 6±8 mg/L in the chronic phase (p<0.001), and MPO levels decreased from 86±43 pM to 27±32 pM (p<0.001). After 29±12 mo, 27% patients died, 39% had new episode of ACS, and 30% underwent revascularization procedures. Initial CRP levels above 10 mg/L were associated with higher long-term mortality (hazard ratio [HR]

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Plasma Concentrations of Myeloperoxidase Predict Mortality After Myocardial Infarction

Abstract: Myeloperoxidase and protein carbonyl levels are elevated in plasma after acute MI, apparently via independent mechanisms. High MPO is a risk factor for long-term mortality and adds prognostic value to LVEF and plasma NT-proBNP measurements.

Cited by 295 publications

References 42 publications

The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture

The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture

Tracking the inflammatory response in stroke in vivo by sensing the enzyme myeloperoxidase

Serial Analyses of C‐Reactive Protein and Myeloperoxidase in Acute Coronary Syndrome

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