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Circulating MicroRNAs and Monocyte-Platelet Aggregate Formation in Acute Coronary Syndrome

Stefan Stojkovic1, Patricia P Wadowski1, Patrick Haider1

  • 1Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Thrombosis and Haemostasis
|January 20, 2021
PubMed
Abstract

Insights

Platelet microRNAs miR-21 and miR-126 predict monocyte-platelet aggregate formation in acute coronary syndrome patients. No significant differences in microRNAs or aggregates were found between prasugrel and ticagrelor treatments.

Area of Science:

  • Cardiovascular Medicine
  • Molecular Biology
  • Pharmacology

Background:

  • Monocyte-platelet aggregates (MPAs) are key indicators of platelet activation in acute coronary syndrome (ACS).
  • MicroRNAs (miRs) regulate platelet activation and may influence MPA formation.
  • P2Y12 inhibitors can affect both miRs and MPAs.

Purpose of the Study:

  • To investigate the link between platelet-related miRs and MPA formation in ACS patients on dual antiplatelet therapy (DAPT).
  • To compare miR and MPA levels between patients treated with prasugrel versus ticagrelor.

Main Methods:

  • Analysis of 10 circulating platelet-related miRs in 160 ACS patients on DAPT (80 prasugrel, 80 ticagrelor).
  • MPA formation measured by flow cytometry, with and without stimulation (Pam3CSK4, ADP, AA).
  • Multivariate regression analysis to identify predictors of MPA formation.

Main Results:

  • miR-21 and miR-126 were identified as independent predictors of increased MPA formation in vivo and after TLR-1/2 stimulation.
  • No significant association was found between investigated miRs and MPA formation after ADP or AA stimulation.
  • Platelet miR expression and MPA formation levels were comparable between prasugrel and ticagrelor groups.

Conclusions:

  • Platelet-specific miR-21 and miR-126 are associated with MPA formation in ACS patients receiving DAPT.
  • No significant differences in miRs or MPA levels were observed between prasugrel and ticagrelor treatment groups.

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