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Published on: October 17, 2017
Small high-density lipoprotein is associated with monocyte subsets in stable coronary artery disease
Konstantin A Krychtiuk1, Stefan P Kastl2, Stefan Pfaffenberger2
1Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria.
Insights
Small high-density lipoprotein (HDL) levels are linked to pro-inflammatory monocytes in coronary artery disease patients. This suggests small HDL may have impaired anti-inflammatory functions, impacting atherosclerosis progression.
Area of Science:
- Cardiovascular Research
- Immunology
- Lipid Metabolism
Background:
- High-density lipoprotein (HDL) particles exhibit structural and functional heterogeneity, with their role in atherogenesis remaining incompletely understood.
- Small HDL subfractions may be dysfunctional in patients with coronary artery disease (CAD).
- Monocyte subsets, including classical (CM), intermediate (IM), and non-classical (NCM), play a critical role in atherosclerotic diseases.
Purpose of the Study:
- To investigate the association between HDL subfractions and monocyte subsets in patients with established atherosclerosis.
- To determine if small HDL levels correlate with specific monocyte populations in CAD patients.
Main Methods:
- Analysis of 90 patients with angiographically stable coronary artery disease (CAD).
- Monocyte subsets were phenotyped as classical (CD14++CD16-), intermediate (CD14++CD16+), and non-classical (CD14+CD16++).
- HDL subfractions were quantified using polyacrylamide gel electrophoresis.
Main Results:
- Serum levels of small HDL were positively correlated with pro-inflammatory non-classical monocytes (NCM) and inversely correlated with classical monocytes (CM).
- Patients in the highest tertile of small HDL showed significantly increased NCM and decreased CM proportions.
- No significant associations were found between intermediate or large HDL, or total HDL, and monocyte subset distribution.
Conclusions:
- Small HDL levels are significantly associated with pro-inflammatory NCM and inversely with CM in CAD patients.
- These findings suggest that small HDL particles may possess dysfunctional anti-inflammatory properties in the context of established coronary artery disease.
Objective:
High-density lipoprotein (HDL) particles are heterogeneous in structure and function and the role of HDL subfractions in atherogenesis is not well understood. It has been suggested that small HDL may be dysfunctional in patients with coronary artery disease (CAD). Monocytes are considered to play a key role in atherosclerotic diseases. Circulating monocytes can be divided into three subtypes according to their surface expression of CD14 and CD16. Our aim was to examine whether monocyte subsets are associated with HDL subfractions in patients with atherosclerosis.
Methods:
We included 90 patients with angiographically stable CAD. Monocyte subsets were defined as classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14+CD16++; NCM). HDL subfractions were measured by electrophoresis on polyacrylamide gel.
Results:
Serum levels of small HDL correlated with circulating pro-inflammatory NCM and showed an inverse relationship to circulating CM independently from other lipid parameters, risk factors, inflammatory parameters or statin treatment regime, respectively. IM were not associated with small HDL. In particular, patients with small HDL levels in the highest tertile showed dramatically increased levels of NCM (14.7 ± 7% vs. 10.7 ± 5% and 10.8 ± 5%; p = 0.006) and a decreased proportion of CM (79.3 ± 7% vs. 83.7 ± 6% and 83.9 ± 6%; p = 0.004) compared to patients in the two lower tertiles. In contrast, intermediate HDL, large HDL and total HDL were not associated with monocyte subset distribution.
Conclusion:
Small HDL levels are associated with pro-inflammatory NCM and inversely correlated with CM. This may suggest that small HDL could have dysfunctional anti-inflammatory properties in patients with established CAD.
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