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.