Related Experiment Video
Updated: Jan 18, 2026
Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Oxidized high-density lipoprotein associates with cardiometabolic dysfunction in coronary artery disease and acute
Benjamin Sasko1,2, Nikolaos Pagonas3,4, Martin Christ5
1Medical Department II, Ruhr University Bochum, Marien Hospital Herne, Herne, Germany.
Insights
Oxidized high-density lipoprotein (HDL) is linked to coronary artery disease (CAD) and acute coronary syndrome (ACS). Higher oxidized HDL levels correlate with impaired vascular function and inflammation in CAD and ACS patients.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Immunology
Background:
- High-density lipoprotein (HDL) function, not just concentration, is key in coronary artery disease (CAD).
- Diminished HDL antioxidant properties, marked by elevated oxidized HDL (nHDLox) and reduced paraoxonase-1 (PON-1) activity, may drive vascular dysfunction and inflammation.
- Limited data exist on these associations in CAD and acute coronary syndrome (ACS) patients.
Purpose of the Study:
- To assess the association between oxidized HDL (nHDLox) and markers of vascular health.
- Investigate relationships with PON-1 activity, oxidized low-density lipoprotein (LDL), VCAM-1, IL-6, and nitric oxide (NO) production.
- Clarify the role of HDL function in CAD and ACS pathogenesis.
Main Methods:
- Evaluated HDL function in 90 CAD patients, 90 ACS patients, and 90 healthy controls.
- Quantified oxidized HDL (nHDLox) using a validated biochemical assay.
- Measured plasma PON-1 activity, oxidized LDL, VCAM-1, IL-6, and NO production.
Main Results:
- ACS patients exhibited 140% higher nHDLox levels than controls (p < 0.001).
- Elevated nHDLox correlated significantly with increased VCAM-1, indicating vascular inflammation.
- Reduced PON-1 activity, elevated oxidized LDL, and decreased NO production were observed in ACS patients, suggesting impaired vascular function.
Conclusions:
- Oxidized HDL (HDLox) levels are highest in ACS patients, followed by stable CAD patients compared to healthy controls.
- Measured HDL function parameters indicate a loss of HDL's atheroprotective function.
- The study establishes a novel mechanistic link between oxidized HDL and the occurrence of ACS.
Background:
High-density lipoprotein (HDL) function, rather than its concentration, plays a crucial role in the development of coronary artery disease (CAD). Diminished HDL antioxidant properties, indicated by elevated oxidized HDL (nHDLox) and diminished paraoxonase-1 (PON-1) activity, may contribute to vascular dysfunction and inflammation. Data on these associations in CAD patients, including acute coronary syndrome (ACS), remain limited. The aim of this study is to assess the association of oxidized HDL with PON-1 activity, oxidized low-density lipoprotein (LDL), vascular cell adhesion molecule-1 (VCAM-1), IL-6 levels, and nitric oxide (NO) production as markers of vascular health.
Methods:
We assessed HDL function in three groups: 90 CAD patients, 90 healthy controls, and 90 ACS patients. HDL antioxidant function was measured using a validated biochemical assay to quantify oxidized HDL (nHDLox). Plasma PON-1 activity, oxidized LDL, VCAM-1, IL-6, and NO production were also evaluated.
Results:
ACS patients had nHDLox levels 140% higher than healthy controls (p < 0.001). Higher nHDLox levels were significantly linked to vascular inflammation, reflected by elevated VCAM-1 levels. Additionally, a reduced PON-1 activity indicates an impaired antioxidant protection in ACS patients. Finally, oxidized LDL levels were elevated, and NO production was reduced, suggesting impaired vascular function.
Conclusion:
HDLox levels are highest in patients with ACS. Patients with stable CAD have higher levels than healthy controls. Correspondingly, the parameters of HDL function measured in this study, which all indicate a loss of HDL's atheroprotective function, correlate with these findings. Our study establishes a novel mechanistic pathway linking oxidized HDL to the presence of an ACS.
Clinical Trial Registration:
DRKS00014037.
Related Concept Videos
01:26Coronary Artery Disease II: Pathophysiology
01:30Coronary Artery Disease I: Introduction
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
01:26Coronary Artery Disease IV: Preventive Measures
01:30Atherosclerosis I: Introduction
01:26Atherosclerosis III: Management