Association of the serum myeloperoxidase/high-density lipoprotein particle ratio and incident cardiovascular events in a multi-ethnic population: Observations from the Dallas Heart Study

Khine, Htet; Teiber, John F.; Haley, Robert W.; Khera, Amit; Ayers, Colby; Rohatgi, Anand

doi:10.1016/j.atherosclerosis.2017.06.007

Cited by 36 publications

(27 citation statements)

References 43 publications

(55 reference statements)

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“…In humans, serum MPO/HDL particle ratio was directly associated to incident cardiovascular disease (CVD) in a population-based cohort free from CVD at baseline [154]. The observation that MPO/HDL particle ratio was directly associated with high-sensitivity C-reactive protein and IL-18, and inversely associated with PON1 arylesterase activity [155] further linked MPO-HDL with increased vascular inflammation.…”

Section: Myeloperoxidase-induced Modification Of Hdlmentioning

confidence: 99%

Biological Consequences of Dysfunctional HDL

Pirillo

Catapano

Norata

2019

CMC

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Epidemiological studies have suggested an inverse correlation between high density lipoprotein (HDL) cholesterol levels and the risk of cardiovascular disease. HDLs promote reverse cholesterol transport (RCT) and possess several putative atheroprotective functions, associated to the anti-inflammatory, anti-thrombotic and anti-oxidant properties as well as to the ability to support endothelial physiology. The assumption that increasing HDL-C levels would be beneficial on cardiovascular disease (CVD), however, has been questioned as, in most clinical trials, HDL-C-raising therapies did not result in improved cardiovascular outcomes. These findings, together with the observations from Mendelian randomization studies showing that polymorphisms mainly or solely associated with increased HDL-C levels did not decrease the risk of myocardial infarction, shift the focus from HDL-C levels toward HDL functional properties. Indeed, HDL from atherosclerotic patients not only exhibit impaired atheroprotective functions but also acquire pro-atherogenic properties and are referred to as "dysfunctional" HDL; this occurs even in the presence of normal or elevated HDL-C levels. Pharmacological approaches aimed at restoring HDL functions may therefore impact more significantly on CVD outcome than drugs used so far to increase HDL-C levels. Aims of this review is to discuss the pathological conditions leading to the formation of dysfunctional HDL and their role in atherosclerosis and beyond.

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Section: Myeloperoxidase-induced Modification Of Hdlmentioning

confidence: 99%

Biological Consequences of Dysfunctional HDL

Pirillo

Catapano

Norata

2019

CMC

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“…Patients with stable coronary artery disease (SCAD) are a heterogenous group in terms of the progression rate of the disease, the severity of coronary lesions and the occurrence of acute coronary syndromes (ACS) [ 1 – 3 ]. Oxidative stress and inflammation play the direct role in the initial and progression of atherosclerosis plaques and development of cardiovascular artery disease (CAD) [ 4 , 5 ]. A high density lipoprotein (HDL) protects against coronary artery disease (CAD) mainly by reverse cholesterol transport.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, HDL has anti-inflammatory, anti-oxidative, in part via paraoxonase-1 (PON-1), anti-thrombotic and anti-apoptotic properties, increased endothelial cells (EC), nitric oxide synthase, enhanced endothelial progenitor cells (EPC) mediating vasculoprotection, stimulation of endothelial cell proliferation and migration [ 6 ]. Myeloperoxidase (MPO), a product of systemic inflammation plays important role both in the process of oxidative stress and inflammation and promotes oxidation of lipoproteins [ 5 ]. MPO is a leukocyte-derived enzyme that catalyzes the formation of oxidative reactants and participates in innate immunity against infections.…”

Section: Introductionmentioning

confidence: 99%

Myeloperoxidase level and inflammatory markers and lipid and lipoprotein parameters in stable coronary artery disease

et al. 2018

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BackgroundMyeloperoxidase (MPO) impairing endothelial functions. We investigated whether increasing concentration of myeloperoxidase (MPO) and inflammatory markers induce progression and incident acute coronary syndrome (ACS) in stable coronary artery disease (SCAD) patients. Therefore, the concentration of MPO, lipids, lipoproteins (apo(apolipoprotein) AI, apoB, lipoprotein associated phospholipase A2 (LpPLA2) level), inflammatory markers (high sensitivity C-reactive protein (hsCRP), tumor necrosis factor-α (TNF-α), interleukine-6 (IL-6) concentration) were examined.MethodsThis study concerned 67 SCAD patients divided into groups: all patients, patients with MPO < 200 ng/ml, MPO 200–300 ng/ml, MPO > 300 ng/ml concentration and 15 controls. ApoAI, apoB and hsCRP levels were examined using the immunonephelometric method, and MPO, LpPLA2, IL-6, TNF-α concentration was performed by using Quantikine ELISA kit R&D Systems.ResultsIn the all patients, and in group with MPO 200–300 ng/ml TC, LDL-C, nonHDL-C, LpPLA2 concentration and TC/HDL-C, LDL-C/HDL-C ratios were insignificant, and significantly higher concentration of TG, apoB, MPO, inflammatory markers and TG/HDL-C, MPO/apoAI, MPO/HDL-C ratios but HDL-C, apoAI level and HDL-C/apoAI ratio were significantly reduced. In the group of patients with MPO < 200 ng/ml, level of TC, LDL-C, nonHDL-C, apoAI, apoAII, LpPLA2 and MPO and LDL-C/HDL-C ratio were in-significant, HDL-C was decreased but apoB, TG, inflammatory markers, apoB/apoAI, TG/HDL-C, MPO/apoAI, MPO/HDL-C ratio were significantly increased. In the group of patients with MPO > 300 ng/ml concentration of TC, LDL-C, nonHDL-C, apoAII, LpPLA2 and LDL-C/HDL-C ratios were not significant, but HDL-C and apoAI concentrations were significantly decreased. The concentrations of TG, apoB, MPO and inflammatory markers and TG/HDL-C, MPO/apoAI, MPO/HDL-C ratios were significantly increased compared to the controls. The apoAI concentration was significantly decreased and the concentration of MPO and hsCRP as well as MPO/apoAI and MPO/HDL-C ratios were significantly higher as compared to the group of patients with MPO < 200 ng/ml.Spearman’s correlation test showed a positive correlation between MPO concentration and MPO/apoAI and MPO/HDL-C ratios in all patients and MPO < 200 ng/ml, MPO 200–300 ng/ml. The patients with MPO > 300 ng/ml showed a positive correlation between the concentration of MPO and the level of hsCRP and IL-6, and a negative correlation between MPO/apoAI ratio and the concentration of HDL-C, apoAI and apoAII.ConclusionThe results suggest that moderate dyslipidemia and dyslipoproteinemia deepening of inflammation, and inflammation slowly induce increase MPO concentration which decrease apoAI and HDL-C level and disturb HDLs function. The increasing MPO level and MPO/HDL-C, MPO/apoAI ratios can differentiate the SCAD patients at the risk of acute coronary syndrome (ACAD) and stroke.

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“…Myeloperoxidase (MPO) mediates the oxidation of ApoA1 that creates a dysfunctional HDL particle, which activates nuclear factor kappa-B and promotes inflammation in the vessel wall [5] . MPO level and its role in oxidative stress and inflammation has been implicated in the pathophysiology of cardiovascular diseases such as coronary artery disease [6] . Human paraoxonase-1 (PON1) is a calcium-dependent lactonase that is produced by the liver and almost exclusively associated with HDL [7] .…”

Section: Introductionmentioning

confidence: 99%

HDL subfraction distribution and HDL function in untreated dyslipidemic patients

Harangi¹,

Szentpéteri²,

Nádró³

et al. 2017

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Aim:The protective role of high-density lipoprotein (HDL) against atherosclerosis is well known. However, both structural and functional changes of the HDL particles may affect its protective efficacy. Increased levels of HDL-associated myeloperoxidase (MPO) and decreased HDL-linked paraoxonase-1 (PON1) activity have been reported in dyslipidemic patients. Some changes in HDL subfraction distributions were also studied previously, but data on structural and functional changes in dyslipidemia are not complete. Therefore, the authors aimed to evaluate these qualitative and quantitative markers of HDL in dyslipidemic patients and healthy control subjects. Methods: Anthropometric parameters, serum levels of lipoproteins and MPO, as well as PON1 activities were investigated in 81 untreated dyslipidemic patients and in 32 healthy gender-matched controls. Additionally, HDL subfractions were detected by an electrophoretic method on polyacrylamide gel (Lipoprint). Results: Significantly higher glucose, hemoglobin A1c, total cholesterol, low-density lipoprotein-cholesterol, triglyceride, lipoprotein(a), apolipoprotein B, C-reactive protein, and MPO levels were found in patients compared to the healthy subjects. There were no significant differences in PON1 paraoxonase and arylesterase activities between the two study groups, but MPO/PON1 ratio was significantly higher in patients. There was a shift towards the smaller HDL subfractions, but only the intermediate HDL ratio was significantly lower in patients compared to controls. Conclusion:The results highlight the importance of HDL-associated pro-and antioxidant enzymes suggesting the possible clinical benefit of MPO/PON1 calculation and confirm that quantification of HDL-C level alone provides limited data regarding HDL's cardioprotective effect. Calculation of MPO/PON1 ratio may be a useful cardiovascular marker in dyslipidemia. Key words:High-density lipoprotein, subfraction, paraoxonase, myeloperoxidase, dyslipidemia ABSTRACTArticle history:

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Association of the serum myeloperoxidase/high-density lipoprotein particle ratio and incident cardiovascular events in a multi-ethnic population: Observations from the Dallas Heart Study

Cited by 36 publications

References 43 publications

Biological Consequences of Dysfunctional HDL

Biological Consequences of Dysfunctional HDL

Myeloperoxidase level and inflammatory markers and lipid and lipoprotein parameters in stable coronary artery disease

HDL subfraction distribution and HDL function in untreated dyslipidemic patients

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