Association between myeloperoxidase polymorphisms and its plasma levels with severity of coronary artery disease

Wainstein, Rodrigo Vugman; Wainstein, Marco Vugman; Ribeiro, Jorge Pinto; Dornelles, Laura Vargas; Tozzati, Paula; Ashton‐Prolla, Patrícia; Ewald, Ingrid Petroni; Vietta, Giovana; Polanczyk, Carísi Anne

doi:10.1016/j.clinbiochem.2009.07.022

Cited by 28 publications

(19 citation statements)

References 35 publications

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“…Its suitability as a potential biomarker for CVD is supported by the demonstration of 30-fold higher amounts of 3-chlorotyrosine LDL present in human atherosclerotic lesions compared with that in Peroxidase activity by guaiacol oxidation [91] Plasma Sandwich ELISA [100] Serum ELISA [175] Plasma EIA [92] EDTA plasma [97] Plasma ELISA [98] Plasma ELISA [93] Serum Sandwich ELISA [96] EDTA plasma Microparticle immunoassay [101] [94] Plasma ELISA [89] Plasma ELISA [88] Serum ELISA [95] Serum Microparticle immunoassay [90] Isolated leukocytes FACS [99] EDTA plasma ELISA Studies contradicting [103] EDTA plasma ELISA [104] Heparin plasma ELISA [107] EDTA plasma Sandwich ELISA [102] Plasma Sandwich ELISA [105] Plasma ELISA Table 8. Association between MPO and MACE prediction.…”

Section: Surrogate Biomarkersmentioning

confidence: 87%

“…Similarly, Wainstein et al determined CAD severity using a six-tier scoring system. They defined non-significant CAD as <70% stenosis in ≥1 epicardial vessel and <50% stenosis of the left main coronary [104], whereas most studies considered >50% stenosis in an epicardial vessel to be significant disease [1,88,[92][93][94][95]98,102,103]. MPO was reported in one study not to correlate with coronary artery calcification as determined by electron beam computed tomography [107].…”

Section: Evidence For Association Between Circulating Mpo and Cadmentioning

confidence: 99%

“…Patients who were scheduled for an elective coronary angiography 135 CAD severity was assessed angiographically using a six-level score based on degree of stenosis and number of diseased vessels Insignificant trend towards elevated MPO plasma levels in patients with higher CAD severity score P = 0.15 [104] There are also studies reporting a lack of association between circulating MPO and CAD. Two studies reported plasma MPO concentration not to be elevated in patients with stable CAD [102,103].…”

Section: Evidence For Association Between Circulating Mpo and Cadmentioning

confidence: 99%

“…This suggests that systemic release of MPO is not a characteristic feature of asymptomatic CAD, although a possible confounding factor in one of these two studies is that the absence of CAD in the control group of volunteers was not ruled out angiographically [102]. Two other studies reporting a lack of significant association between MPO and CAD [104,105] used unusual definitions of disease severity. Specifically, in a study consisting of 3036 patients hospitalized for coronary angiography, CAD was diagnosed as >20% stenosis [105] rather than the 50% benchmark considered to be relevant for CAD outcome [106].…”

Section: Evidence For Association Between Circulating Mpo and Cadmentioning

confidence: 99%

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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: Surrogate Biomarkersmentioning

confidence: 87%

Section: Evidence For Association Between Circulating Mpo and Cadmentioning

confidence: 99%

Section: Evidence For Association Between Circulating Mpo and Cadmentioning

confidence: 99%

Section: Evidence For Association Between Circulating Mpo and Cadmentioning

confidence: 99%

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

et al. 2016

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“…Another possible mechanism responsible for this phenomenon is polymorphism in the promoter region of the MPO gene. Several genetic polymorphisms in the MPO gene were described (Wainstein et al, 2010;Scharnagi et al, 2014;Nikpoor et al, 2001). Some studies suggest that MPO polymorphism in the promoter region (-463G/A) might be associated with coronary artery disease (Castellani et al, 2006;Reynolds et al, 2006;Yang et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Interindividual variability of atorvastatin treatment influence on the MPO gene expression in patients after acute myocardial infarction.

et al. 2015

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Myeloperoxidase (MPO) and C-reactive protein (CRP) may play critical roles in generation of oxidative stress and the development of the systemic inflammatory response. The aim of the study was to determine the effect of atorvastatin therapy on the MPO gene expression and its plasma level in relation to lipids level lowering and an anti-inflammatory response in patients after acute myocardial infarction. The research material was represented by 112 samples. Thirty-eight patients with first AMI receiving atorvastatin therapy (40 mg/day) and followed up for one month were involved in the study. The relative MPO gene expression in peripheral blood mononuclear cells (PBMCs) was examined using RT-qPCR in 38 patients before-, 38 patients after-therapy and in 36 patients as the control group. The plasma concentrations of MPO and serum concentrations of biochemical parameters were determined using commercially available diagnostic tests. After one month of atorvastatin therapy, in 60.5% patients a decrease of MPO gene expression, whereas in 39.5% patients an increase, was observed. The plasma MPO levels behaved in the same way as the MPO gene expression. However, the serum lipids and CRP concentrations were significantly lower after one month of atorvastatin therapy in both groups of patients -with decreased and increased MPO gene expression. Atorvastatin exhibited a different effect on MPO gene expression and its plasma level. Short-term atorvastatin therapy resulted in lipid lowering and anti-inflammatory activity in patients after AMI, independently of its effect on MPO gene expression. The molecular mechanisms of this phenomenon are not yet defined and require further research.

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The expression of myeloperoxidase in thrombi is associated with reduced heme oxygenase‐1 induction and worse left ventricular remodeling in patients with acute ST‐elevation myocardial infarction

Shi

Zhu

et al. 2021

Clinical Cardiology

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Background Myeloperoxidase (MPO) secreted by neutrophils is the enzyme that kills bacteria and other pathogens. Acute myocardial infarction (AMI) is usually caused by thrombosis in response to vulnerable plaque rupture. Circulating MPO was found to be associated with increased mortality in AMI patients. However, the relationship between MPO in thrombi and the prognosis of AMI patients remains unknown. Hypothesis MPO expression in thrombi is associated with the prognosis of patients who underwent primary percutaneous coronary intervention (PCI) after AMI. Methods This study included 41 consecutive patients with acute ST‐elevation myocardial infarction, who successfully underwent primary PCI, during which we collected thrombi remaining in the culprit artery using aspiration catheters. These thrombus samples were fixed, and immunohistochemical staining against MPO and heme oxygenase‐1 (HO‐1) was conducted. Enrolled patients were divided into two groups based on the induction of thrombotic MPO, which was quantified using Image J software. Methods We observed that increased MPO was associated with lower left ventricular ejection fraction (LVEF) and worse LV remodeling in AMI patients. Instead, patients with decreased thrombotic MPO induction had a considerable improvement in LVEF 1 month after discharge (54.4 ± 2.0% vs. 61.1 ± 2.3%, p < 0.01). In the MPO group, a reduction in the thrombotic HO‐1 level contributed to the development of adverse LV remodeling. Logistic regression showed that MPO was a considerable risk factor for adverse LV remodeling (adjusted OR 3.70, p < 0.05). Conclusion MPO expression in thrombi is associated with reduced LVEF and deteriorated LV remodeling in AMI patients, which may be due to HO‐1 suppression in thrombi.

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Association between myeloperoxidase polymorphisms and its plasma levels with severity of coronary artery disease

Cited by 28 publications

References 35 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

Interindividual variability of atorvastatin treatment influence on the MPO gene expression in patients after acute myocardial infarction.

The expression of myeloperoxidase in thrombi is associated with reduced heme oxygenase‐1 induction and worse left ventricular remodeling in patients with acute ST‐elevation myocardial infarction

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