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

A.C. van der Wal, J.J. Piek, O.J. de Boer, K.T. Koch, P. Teeling, C.M. van der Loos, A.E. Becker

Research output: Contribution to journalArticleAcademicpeer-review

98 Citations (Scopus)

Abstract

OBJECTIVE: To discriminate between chronic inflammation and acute activation of the plaque immune response in culprit lesions of patients with acute coronary syndromes. DESIGN: Retrospective study. SETTING: Tertiary referral centre. SUBJECTS: 71 patients having coronary atherectomy were classified according to their ischaemic syndrome: stable angina (n = 23); stabilised unstable angina (n = 18); refractory unstable angina (n = 11); and acute myocardial infarction (n = 19). MAIN OUTCOME MEASURES: Immunohistochemical measurement of interleukin 2 receptor (IL-2R) (CD25) positive cells expressed as a percentage of the total amount of (CD3 positive) T lymphocytes in frozen sections of atherectomy specimens. RESULTS: The number of lesions containing IL-2R (CD25) positive T cells increased with severity of the ischaemic coronary syndrome (stable angina, 52%; stabilised unstable angina, 77.8%; refractory unstable angina, 90.9%; acute myocardial infarction, 89.4%). The percentage of activated T cells (CD25/CD3 ratios x100) increased in lesions associated with refractory unstable angina (7.8%) and acute myocardial infarction (18.5%), compared with those in lesions associated with either chronic stable angina (2.2%) or stabilised unstable angina (3.3%). CONCLUSIONS: An increase in the percentage of IL-2R positive T lymphocytes in culprit lesions of patients with acute coronary syndromes indicates recent activation and amplification of the immune response within plaques. This may result in a burst of inflammatory products with tissue degrading and vasoactive properties and, hence, could initiate or accelerate the onset of an acute coronary event
Original languageUndefined/Unknown
Pages (from-to)14-18
JournalHeart
Volume80
Issue number1
DOIs
Publication statusPublished - 1998

Keywords

  • AMC wi-co
  • AMC wi-eigen

Cite this