Coronary artery endothelial cells and microparticles increase expression of VCAM-1 in myocardial infarction

Christopher E Radecke, Alexandra E Warrick, Gagan D Singh

  • 1Scott I. Simon, Department of Biomedical Engineering, University of California at Davis, 451 East Health Sciences Drive, Davis, CA 95616, USA, Tel.: +1 530 752 0299, E-mail sisimon@ucdavis.edu.

Thrombosis and Haemostasis
|November 22, 2014
PubMed

Insights

Researchers developed a new method to analyze endothelial cells and microparticles directly from coronary artery plaque during procedures. This analysis revealed higher VCAM-1 expression in myocardial infarction patients, indicating increased vascular inflammation.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Biomedical Engineering

Background:

  • Coronary artery disease (CAD) involves atherosclerotic plaque buildup, potentially leading to myocardial infarction (MI) via plaque rupture.
  • Assessing endothelial inflammation directly at coronary artery stenosis sites has been challenging, often relying on pathology or animal models.
  • Inflammatory pathways significantly impact atherosclerotic plaque stability.

Purpose of the Study:

  • To develop and validate a technique for isolating and characterizing endothelial cells (ECs) and EC microparticles (EMPs) from coronary artery plaque during interventions.
  • To assess the expression of vascular cell adhesion molecule-1 (VCAM-1) on ECs and EMPs at the site of coronary artery stenosis.
  • To investigate the correlation between VCAM-1 expression and the severity of inflammation in patients with CAD and MI.

Main Methods:

  • Developed a novel technique to isolate ECs and EMPs from coronary artery plaque during balloon angioplasty and percutaneous coronary intervention.
  • Utilized imaging flow cytometry (IFC) to identify coronary artery endothelial cells (CAECs).
  • Quantified VCAM-1 expression on individual CAECs and EMPs immediately post-angioplasty.

Main Results:

  • Patients with MI showed significantly higher VCAM-1 expression on CAECs (73% increase) and EMPs (79% increase) compared to stable CAD patients.
  • VCAM-1 expression was notably absent on ECs from the peripheral circulation of the same subjects.
  • Elevated VCAM-1 density on CAECs and EMPs in MI patients positively correlated with markers of myocardial infarct size.

Conclusions:

  • Increased VCAM-1 expression on ECs and EMPs at the coronary plaque site is a strong indicator of vascular inflammation.
  • This novel method allows for direct assessment of endothelial inflammation in human coronary artery disease.
  • Findings suggest VCAM-1 plays a critical role in the inflammatory processes underlying myocardial infarction.