Malondialdehyde-Modified LDL as a Marker of Acute Coronary Syndromes

Holvoet, Paul; Collen, Désiré; Werf, Frans Van de

doi:10.1001/jama.281.18.1718

Cited by 118 publications

(64 citation statements)

References 18 publications

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“…However, when both are high, they increase the predictive value for diagnosis of acute coronary event 39 . We tried to control the different biases of confusion in the statistical analysis.…”

Section: -Specificitymentioning

confidence: 99%

Anticorpos contra LDL-ox e síndrome coronariana aguda

Medeiros¹,

Mühlen²,

Gidlund³

et al. 2010

Arq. Bras. Cardiol.

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Section: -Specificitymentioning

confidence: 99%

Anticorpos contra LDL-ox e síndrome coronariana aguda

Medeiros¹,

Mühlen²,

Gidlund³

et al. 2010

Arq. Bras. Cardiol.

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“…The serum concentration of malondialdehyde-modified LDL was assayed by a murine monoclonal antibody 4E6 -based sandwich ELISA (Mercodia AB) as described previously. 22 …”

Section: Biochemical Analysismentioning

confidence: 99%

Restoration of Endothelial Function by Increasing High-Density Lipoprotein in Subjects With Isolated Low High-Density Lipoprotein

et al. 2003

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Background-Loss-of-function mutations in the ATP-binding cassette (ABCA)-1 gene locus are the underlying cause for familial hypoalphalipoproteinemia, providing a human isolated low-HDL model. In these familial hypoalphalipoproteinemia subjects, we evaluated the impact of isolated low HDL on endothelial function and the vascular effects of an acute increase in HDL. Methods and Results-In 9 ABCA1 heterozygotes and 9 control subjects, vascular function was assessed by venous occlusion plethysmography. Forearm blood flow responses to the endothelium-dependent and -independent vasodilators serotonin (5HT) and sodium nitroprusside, respectively, and the inhibitor of nitric oxide synthase N G -monomethyl-Larginine (L-NMMA) were measured. Dose-response curves were repeated after systemic infusion of apolipoprotein A-I/phosphatidylcholine (apoA-I/PC) disks. At baseline, ABCA1 heterozygotes had decreased HDL levels (0.4Ϯ0.2 mmol/L; PϽ0.05), and their forearm blood flow responses to both 5HT (maximum, 49.0Ϯ10.4%) and L-NMMA (maximum, Ϫ22.8Ϯ22.9%) were blunted compared with control subjects (both PՅ0.005). Infusion of apoA-I/PC disks increased plasma HDL to 1.3Ϯ0.4 mmol/L in ABCA1 heterozygotes, which resulted in complete restoration of vasomotor responses to both 5HT and L-NMMA (both PՅ0.001). Endothelium-independent vasodilation remained unaltered throughout the protocol. Conclusions-In ABCA1 heterozygotes, isolated low HDL is associated with endothelial dysfunction, attested to by impaired basal and stimulated NO bioactivity. Strikingly, both parameters were completely restored after a single, rapid infusion of apoA-I/PC. These findings indicate that in addition to its long-term role within reverse cholesterol transport, HDL per se also exerts direct beneficial effects on the arterial wall. (Circulation. 2003;107:2944-2948.)

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“…[5][6][7] In humans, plaque specimens from carotid and coronary arteries are significantly enriched in OxLDL 1,3 and become depleted in OxLDL after treatment with statins. 8 In particular, unstable plaques appear to be preferentially enriched in OxLDL, 9,10 and OxLDL in plasma has been shown to be associated with acute coronary syndromes 9,11,12 and endothelial dysfunction. 13,14 In the present study, we measured plasma levels of several OxLDL markers immediately before and serially up to 6 months after percutaneous coronary intervention (PCI) to evaluate the role of OxLDL in PCI.…”

mentioning

confidence: 99%

Percutaneous Coronary Intervention Results in Acute Increases in Oxidized Phospholipids and Lipoprotein(a)

et al. 2004

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Background-This study was performed to assess whether oxidized low-density lipoprotein (OxLDL) levels are elevated after percutaneous coronary intervention (PCI). Methods and Results-Patients (nϭ141) with stable angina pectoris undergoing PCI had serial venous blood samples drawn before PCI, after PCI, and at 6 and 24 hours, 3 days, 1 week, and 1, 3, and 6 months. Plasma levels of OxLDL-E06, a measure of oxidized phospholipid (OxPL) content on apolipoprotein B-100 detected by antibody E06, lipoprotein(a) [Lp(a)], autoantibodies to malondialdehyde (MDA)-LDL and copper-oxidized LDL (Cu-OxLDL), and apolipoprotein B-100 -immune complexes (apoB-IC) were measured. OxLDL-E06 and Lp(a) levels significantly increased immediately after PCI by 36% (PϽ0.0001) and 64% (PϽ0.0001), respectively, and returned to baseline by 6 hours. In vitro immunoprecipitation of Lp(a) from selected plasma samples showed that almost all of the OxPL detected by E06 was bound to Lp(a) at all time points, except in the post-PCI sample, suggesting independent release and subsequent reassociation of OxPL with Lp(a) by 6 hours. Strong correlations were noted between OxLDL-E06 and Lp(a) (rϭ0.68, PϽ0.0001). MDA-LDL and Cu-OxLDL autoantibodies decreased, whereas apoB-IC levels increased after PCI, but both returned to baseline by 6 hours. Subsequently, IgM autoantibodies increased and peaked at 1 month and then returned to baseline, whereas IgG autoantibodies increased steadily over 6 months. Conclusions-PCI results in acute plasma increases of Lp(a) and OxPL and results in short-term and long-term immunologic responses to OxLDL. OxPL that are released or generated during PCI are transferred to Lp(a), suggesting that Lp(a) may contribute acutely to a protective innate immune response. In settings of enhanced oxidative stress and chronically elevated Lp(a) levels, the atherogenicity of Lp(a) may stem from its capacity as a carrier of proinflammatory oxidation byproducts.

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Malondialdehyde-Modified LDL as a Marker of Acute Coronary Syndromes

Cited by 118 publications

References 18 publications

Anticorpos contra LDL-ox e síndrome coronariana aguda

Anticorpos contra LDL-ox e síndrome coronariana aguda

Restoration of Endothelial Function by Increasing High-Density Lipoprotein in Subjects With Isolated Low High-Density Lipoprotein

Percutaneous Coronary Intervention Results in Acute Increases in Oxidized Phospholipids and Lipoprotein(a)

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