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Recent activation of the plaque immune response in coronary lesions underlying acute coronary syndromes

A C van der Wal1, J J Piek, O J de Boer

  • 1Department of Cardiovascular Pathology, University of Amsterdam, Netherlands.

Heart (British Cardiac Society)
|October 9, 1998
PubMed

Insights

Increased interleukin 2 receptor (IL-2R) positive T cells in coronary lesions indicate acute immune activation in acute coronary syndromes. This immune response may trigger plaque rupture and subsequent cardiovascular events.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Pathology

Background:

  • Atherosclerotic plaques harbor immune cells, but distinguishing chronic inflammation from acute immune activation is challenging.
  • Acute coronary syndromes (ACS) involve complex plaque rupture dynamics influenced by local immune responses.

Purpose of the Study:

  • To differentiate chronic inflammation from acute immune activation within culprit lesions of ACS patients.
  • To assess the role of T-lymphocyte activation in the pathogenesis of ACS.

Main Methods:

  • Retrospective analysis of 71 patients undergoing coronary atherectomy for various ischemic syndromes.
  • Immunohistochemical analysis of interleukin 2 receptor (IL-2R, CD25) positive T cells in atherectomy specimens.
  • Quantification of CD25/CD3 ratios to determine the percentage of activated T cells.

Main Results:

  • Lesions from patients with more severe ischemic syndromes (refractory unstable angina, acute myocardial infarction) showed a higher percentage of IL-2R positive T cells.
  • The percentage of activated T cells (CD25/CD3 ratio) was significantly higher in lesions associated with refractory unstable angina (7.8%) and acute myocardial infarction (18.5%) compared to stable or stabilized angina (2.2%-3.3%).

Conclusions:

  • Elevated IL-2R positive T lymphocytes in culprit lesions signify recent immune activation within atherosclerotic plaques.
  • This acute immune response may lead to the release of inflammatory mediators, promoting plaque instability and potentially initiating acute coronary events.
Abstract

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