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Reciprocal activation of leukocyte-endothelial adhesion molecules in acute coronary syndromes

Ross T Murphy1, J B Foley, Peter Crean

  • 1Department of Cardiology, St James's Hospital, Dublin 8, Ireland. rmurphy@sghms.ac.uk

International Journal of Cardiology
|September 6, 2003
PubMed

Insights

Acute coronary syndromes involve inflammation and leukocyte activation. Studies show elevated monocyte markers and adhesion molecules, suggesting a systemic inflammatory source in acute coronary disease.

Area of Science:

  • Cardiology
  • Immunology
  • Biochemistry

Background:

  • Acute coronary syndromes (ACS) trigger significant inflammation and leukocyte activation.
  • The origin of this inflammation (local coronary vs. systemic) is debated.
  • Inflammation is linked to poor prognosis in ACS.

Purpose of the Study:

  • To investigate the source of inflammation in ACS.
  • To measure markers of leukocyte and endothelial activation in ACS patients.

Main Methods:

  • Measured soluble cell adhesion molecules (sICAM-1, sVCAM-1) and monocyte ligands (CD11b, CD49d) in 21 ACS patients.
  • Used ELISA for soluble molecules and flow cytometry for cell surface expression.

Main Results:

  • ACS patients showed significantly higher levels of monocyte receptor CD11b and soluble intercellular adhesion molecule-1 compared to controls.
  • Elevated levels of CD11b (531 vs. 345 MFI) and sICAM-1 (329 vs. 232 ng/ml) were observed.

Conclusions:

  • Found reciprocal activation of monocyte ligands and endothelial adhesion molecules in ACS patients.
  • Suggests a systemic inflammatory upregulation involving both leukocytes and endothelium.
  • Indicates a systemic, rather than local, source of inflammation in acute coronary disease.
Abstract

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