MIR-155 as a potential biomarker for disease severity in st-segment elevation myocardial infarction: insights from a

Ailyn Morales-Rentería1, Amina Ruiz-Santos1, Luis M Amezcua-Castillo2

  • 1School of Medicine, Universidad Autónoma Metropolitana (UAM)-Xochimilco, Mexico City, Mexico.

Abstract

Insights

MicroRNA-155 (miR-155) levels are lower in ST-elevation myocardial infarction (STEMI) patients and linked to more severe atherosclerosis and adverse outcomes, independent of inflammation.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biomarker Discovery

Background:

  • MicroRNA-155 (miR-155) is implicated in inflammatory processes and cardiovascular diseases.
  • Its specific role in ST-elevation myocardial infarction (STEMI), including associations with inflammation, atherosclerosis, and clinical outcomes, requires further elucidation.

Purpose of the Study:

  • To investigate the relationship between miR-155 expression levels and markers of inflammation, atherosclerotic burden, and major adverse cardiovascular events (MACE) in patients with STEMI.

Main Methods:

  • A cohort of 69 STEMI patients and 16 healthy controls underwent miR-155 expression analysis and serum inflammatory marker measurement.
  • Patients were stratified into tertiles based on miR-155 levels, with clinical data, atherosclerotic burden via cardiac catheterization, and in-hospital MACE meticulously recorded.

Main Results:

  • STEMI patients exhibited significantly lower miR-155 levels compared to controls (median 54.2 vs. 152.8 arbitrary units; p = 0.003).
  • Higher miR-155 expression tertiles correlated with increased prevalence of three-vessel coronary artery occlusion (p = 0.007) and a higher incidence of pulmonary edema (p = 0.030).
  • No significant associations were observed between miR-155 levels and inflammatory markers or myocardial damage indicators.

Conclusions:

  • Dysregulated miR-155 expression in STEMI patients may contribute to disease severity and MACE risk.
  • These effects appear to be independent of established markers of inflammation or myocardial injury.