Monocyte subset distribution in patients with stable atherosclerosis and elevated levels of lipoprotein(a)

Konstantin A Krychtiuk1, Stefan P Kastl2, Sebastian L Hofbauer2

  • 1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Cluster for Cardiovascular Research, Vienna, Austria.

Insights

Elevated lipoprotein(a) (Lp(a)) levels are linked to a proatherogenic shift in monocyte subsets, specifically increasing intermediate monocytes (IMs). This finding suggests a potential mechanism connecting Lp(a) to atherosclerosis progression.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Lipidology

Background:

  • Lipoprotein(a) (Lp(a)) is a known risk factor for atherosclerosis and thrombotic events.
  • Lp(a) carries pro-inflammatory oxidized phospholipids (OxPL), contributing to vascular inflammation.
  • Monocytes, key players in atherosclerosis, are classified into subsets with varying atherogenic potential.

Purpose of the Study:

  • To investigate the association between elevated Lp(a) and OxPL/apoB levels and the distribution of monocyte subsets.
  • To determine if Lp(a) influences the proportions of classical, intermediate, and nonclassical monocytes.

Main Methods:

  • Study included 90 patients with stable coronary artery disease.
  • Lp(a) and OxPL/apoB were quantified.
  • Monocyte subsets (CM, IM, NCM) were identified using flow cytometry based on CD14 and CD16 expression.

Main Results:

  • Patients with elevated Lp(a) (>50 mg/dL) showed a significantly higher proportion of intermediate monocytes (IMs).
  • No significant differences were observed in classical (CM) or nonclassical (NCM) monocyte proportions.
  • The association between Lp(a) and IMs was independent of traditional risk factors and inflammatory markers. OxPL/apoB levels correlated with IMs.

Conclusions:

  • Elevated Lp(a) levels are associated with a proatherogenic monocyte subset distribution in patients with stable atherosclerotic disease.
  • This suggests a potential mechanism linking Lp(a) to increased atherosclerosis risk via monocyte modulation.
Abstract

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