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Heart 1998;80:14-18 ( July )
a Department of
Cardiovascular Pathology, Academic Medical Center, University of
Amsterdam, PO Box 22700, 1100 DE Amsterdam, Netherlands, b Department of
Cardiology, Academic Medical Center, University of Amsterdam
Correspondence to: Dr van der Wal.
Accepted for publication 30 October 1997
Objective
To
discriminate between chronic inflammation and acute activation of the
plaque immune response in culprit lesions of patients with acute
coronary syndromes.
DesignRetrospective study.
SettingTertiary
referral centre.
Subjects71 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
measuresImmunohistochemical 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.
ResultsThe 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 ×100) 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%).
ConclusionsAn
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.
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