1Mona H. El-Sayed, 2Kamal M. Ahmed, 1Lobna A. Abou
Shamaa and 3Abdul Aziz H. Ghaleb.
Department of 1Immunology and 2Cardiology
Unit Medical
Research Institute, Alexandria University and 3Faculty of Medicine
and Health Sciences, Republic of Yemen.
Immune mechanisms
and inflammation have been suggested to play an important role in the
development of coronary atherosclerosis and its thrombotic complications. Since
the recognition of antiphospholipid syndrome, a great number of cardiac
manifestations have been reported in association with those antibodies. The
purpose of this study was to evaluate the role of anticardiolipin antibody and
T cell activation in the pathogenesis and development of acute coronary
syndromes. 20 patients with myocardial infarction (GpI), 20 with unstable
angina (GpII) and another ten normal subjects were included in the study.
Soluble IL-2R and anticardiolpin antibodies (ACAs) were assessed in the serum
by ELISA. Results revealed a significant increase in ACAs in acute myocardial
infarction (37.14±30.18) when
compared to control (13.14±3.02).
Regarding sIL-2R, a significant increase was observed in patients with unstable
angina (571.42±408.50) when
compared to normals (207.1±127.33). sIL-2R
and ACAs correlated positively with creatine phosphokinase (CPK) level in
myocardial infarction (GpI). We concluded that ACAs is a risk factor for
ischaemic heart disease and should be considered as a marker for subsequent
thrombotic vascular complications. In addition, T cell activity represented by
sIL-2R level is increased with the severity of the ischaemic coronary syndrome.