Persistent circulating platelet and endothelial derived microparticle signature may explain on-going

S Koganti1, D Eleftheriou2, R Gurung3

  • 1Citizens Specialty Hospital, Hyderabad, India; UCL Institute of Cardiovascular Science, London, UK.

Thrombosis Research
|August 21, 2021
PubMed
Abstract

Insights

Microparticle (MP) levels, particularly platelet-derived MPs (PMP) and endothelial-derived MPs (EMP), remain elevated for six months post-acute coronary syndrome (ACS). This suggests ongoing inflammation and endothelial injury, contributing to persistent pro-thrombotic risk in ACS patients.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Cell Biology

Background:

  • Microparticles (MPs) are small vesicles released from cells, implicated in coronary artery disease (CAD) and possessing pro-thrombotic properties.
  • Elevated circulating MPs are observed in CAD patients, but their temporal dynamics after an acute coronary event are not well-characterized.

Purpose of the Study:

  • To investigate the longitudinal changes in circulating microparticle (MP) levels and their pro-thrombotic potential following an acute coronary syndrome (ACS).
  • To compare MP signatures between patients with ACS and stable angina (SA).

Main Methods:

  • Quantification of circulating MPs (endothelial, platelet, monocyte, neutrophil, smooth muscle cell origin) using flow cytometry in ACS and SA patients.
  • MP levels were measured at baseline, post-percutaneous coronary intervention (PCI), and at 1, 7, 30, and 6 months.
  • MP-mediated thrombin generation was assessed by analyzing lag phase, velocity index, peak thrombin, and endogenous thrombin potential.

Main Results:

  • Total MP levels peaked immediately after PCI and decreased by day 1, but remained elevated compared to controls up to 6 months.
  • Platelet-derived MPs (PMP) and endothelial-derived MPs (EMP) were significantly elevated in ACS patients at 6 months compared to SA patients.
  • Patients with CAD (ACS and SA) exhibited abnormal thrombin generation compared to healthy controls, with parameters remaining abnormal at 6 months.

Conclusions:

  • PCI significantly increases total MPs and individual phenotypes, indicating endothelial injury.
  • Sustained elevation of PMP and EMP in ACS patients at 6 months suggests ongoing inflammation and endothelial damage.
  • These findings may explain the persistent pro-thrombotic state observed in ACS patients, even with dual antiplatelet therapy.

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