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Impact of Mon2 monocyte-platelet aggregates on human coronary artery disease

Richard A Brown1,2, Gregory Y H Lip1,3, Chetan Varma3

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

European Journal of Clinical Investigation
|February 10, 2018
PubMed

Insights

Monocyte-platelet aggregates (MPAs) involving the Mon2 subset are elevated in diffuse coronary artery disease (CAD). These MPAs are linked to microvascular endothelial dysfunction, suggesting a role in CAD progression.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Vascular Biology

Background:

  • Monocyte-platelet aggregates (MPAs) are formed by the adhesion of monocyte subsets (Mon1, Mon2, Mon3) to platelets.
  • MPAs are implicated in the pathophysiology of coronary artery disease (CAD).
  • The specific roles of different monocyte subsets in forming MPAs and their association with diffuse CAD remain unclear.

Purpose of the Study:

  • To investigate the association between specific monocyte subsets forming MPAs and the presence of diffuse CAD.
  • To evaluate the relationship between MPAs and microvascular endothelial function in patients with CAD.
  • To assess the longitudinal changes in MPAs and microvascular function in CAD patients.

Main Methods:

  • Flow cytometry was used to quantify MPAs associated with individual monocyte subsets in patients with diffuse CAD, focal CAD, and normal coronary arteries.
  • Cutaneous microcirculation was assessed using laser Doppler flowmetry to measure endothelium-dependent and -independent vasodilation.
  • Patients with CAD underwent repeat assessments at 6 and 12 months.

Main Results:

  • Patients with diffuse CAD exhibited significantly higher baseline counts of MPAs involving the Mon2 subset compared to those with focal CAD and normal arteries.
  • MPAs with the Mon2 subset independently predicted the presence of diffuse CAD.
  • A negative correlation was observed between MPAs with Mon2 and endothelium-dependent microvascular vasodilation, which persisted longitudinally.

Conclusions:

  • Elevated levels of monocyte-platelet aggregates involving the Mon2 subset are associated with diffuse CAD.
  • These MPAs may contribute to accelerated coronary atherosclerotic progression.
  • A potential mechanism involves microvascular endothelial dysfunction.
Abstract

Keywords:
diffuse coronary artery diseasemicrovascular functionmonocyte-platelet aggregates

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