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The effect of statin therapy withdrawal on monocyte subsets

Anthony S Jaipersad1, Eduard Shantsila, Andrew Blann

  • 1University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK.

European Journal of Clinical Investigation
|October 19, 2013
PubMed

Insights

Statin withdrawal in patients with coronary artery disease did not alter monocyte subset counts but reduced expression of Toll-like receptor-4 (TLR4) and pro-angiogenic receptors. These findings highlight statins' pleiotropic effects on monocyte function.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Three distinct monocyte subsets are known.
  • Statins are effective in atherosclerosis, with known pleiotropic effects.
  • The impact of statins on monocyte subsets remains unclear.

Purpose of the Study:

  • To investigate the effect of statin cessation on monocyte subsets.
  • To examine changes in receptor expression on monocyte subsets after statin withdrawal.
  • To explore statins' pleiotropic effects on monocyte characteristics.

Main Methods:

  • 66 patients with stable coronary artery disease ceased statin therapy for 2 weeks.
  • Monocyte subsets (Mon1, Mon2, Mon3) and their platelet aggregates were analyzed.
  • Flow cytometry assessed expression of receptors involved in inflammation, adhesion, angiogenesis, and repair.

Main Results:

  • Statin cessation did not significantly alter monocyte subset counts or platelet aggregation.
  • All monocyte subsets showed significant downregulation of vascular endothelial growth factor receptor 2, Tie2, and Toll-like receptor-4 (TLR4).
  • CXCR4 expression decreased in Mon1 cells; CD14, CD16, CCR4, IL6 receptor, and VCAM expression remained unchanged.

Conclusions:

  • Statin withdrawal impacts monocyte subsets by downregulating TLR4 and pro-angiogenic receptors.
  • A decrease in CXCR4 expression on 'classical' Mon1 cells was observed.
  • These findings support the pleiotropic effects of statins on monocyte pro-angiogenic and pro-reparative functions.
Abstract

Keywords:
Coronary artery diseasemonocyte subsetsmonocytesstatins

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