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Published on: February 14, 2017

Macrophage migration inhibitory factor is enhanced in acute coronary syndromes and is associated with the

Iris I Müller1, Karin A L Müller, Heiko Schönleber

  • 1Kardiologie und Kreislauferkrankungen, Medizinische Klinik III, Eberhard Karls Universität, Tübingen, Germany.

Plos One
|June 14, 2012
PubMed

Insights

Macrophage migration inhibitory factor (MIF) is elevated in patients with acute coronary syndromes (ACS), indicating its role in cardiovascular disease. Higher MIF levels correlate with inflammation and cardiac damage, suggesting potential for risk assessment in ACS patients.

Area of Science:

  • Cardiology
  • Immunology
  • Biochemistry

Background:

  • Chronic inflammation is a key driver of atherosclerosis and a prognostic factor in percutaneous coronary intervention (PCI).
  • Macrophage migration inhibitory factor (MIF) is implicated in atherosclerosis progression and plaque instability, contributing to acute coronary syndromes (ACS).
  • The clinical significance of MIF in symptomatic coronary artery disease (CAD) remains largely unexplored.

Purpose of the Study:

  • To investigate the clinical impact and expression levels of MIF in patients with symptomatic coronary artery disease (CAD) undergoing PCI.
  • To assess the association of MIF with established inflammatory markers and cardiac necrosis markers in ACS patients.

Main Methods:

  • A pilot study evaluated 286 symptomatic CAD patients (119 ACS, 167 stable CAD) and 25 healthy controls undergoing PCI.
  • MIF expression was measured at the time of PCI.
  • Plasma levels of interleukin-6 (IL-6), RANTES, monocyte chemoattractant protein-1 (MCP-1), and C-reactive protein (CRP) were quantified.

Main Results:

  • Patients with ACS exhibited significantly higher plasma MIF levels compared to stable CAD patients and controls (p<0.001).
  • Elevated MIF levels correlated with CRP and IL-6, and with troponin I (TnI) release post-PCI (spearman rank coefficient: 0.31, p<0.001).
  • ACS patients with plaque rupture demonstrated higher MIF levels than those with stenotic lesions (p=0.002).

Conclusions:

  • This study is the first to demonstrate enhanced MIF expression in ACS.
  • MIF is associated with inflammatory markers, cardiac necrosis, and culprit lesions in ACS.
  • Further research is warranted to explore MIF's role in risk stratification for ACS.
Abstract

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