Abstract

The aims of the study were to determine the pattern of changes in serum IgE and IgG levels and to evaluate their probable implications in the aetiopathogenesis of acute myocardial infarction (AMI). A total of 31 AMI patients were obtained from Coronary Care Unit (CCU) at seventh October Hospital, Benghazi, Libya and Jamahiriya Hospital, Benghazi, Libya during the period of September to December 1998. A total of 11 patients with Angina Pectoris (AP) were obtained as disease control and 26 healthy adult Libyans were also obtained as normal control (NC) subjects. Venous blood specimen was collected in tube with or without anticoagulant as required for routine hematological tests and biochemical investigations and special immunological assays. Serum IgE level (GM±GSD, iu/ml) was significantly elevated in AMI compared to AP and NC at the 1st day (AMI1:102.0±3.2, AP1: 39.9±1.2, NC: 36.8±1.5; ANOVA: P=0.0001) as well as at the 7th day (AMI 7: 119.8±3.7, AP 7: 37.1±1.6, NC: 36.8±1.5; ANOVA: P=0.0000). No significant differences were observed for IgE levels between AP and NC and between AMI1 and AMI7 (P>0.05). Ele- vated serum IgE level in AMI was independent of risk factors such as Hypertension (HTN), Diabetes Mellitus (DM), Smoking (Sm), history Of Previous Coronary Artery Attack (H/OP CAA), complications and streptokinase therapy (P>0.1). Serum IgG level (Mean±SD, mg/dl) was significantly declined both in AMI and AP at the 1st day as well as 7th day as compared to NC (AMI1: 1033±314, AP1: 1056±320, NC: 1258±251, ANOVA: P=0.0144; AMI7: 936±383, AP 7:1042±318, NC: 1258±251, ANOVA; P=0.0002). No significant differences were observed between IgG levels in AMI1 and AP1 (P=0.833) and in AMI7 and AP7 (P=0.307). However, the decline in IgG level at the 7th day compared with 1st day was significant in AMI (P=0.014) and insignificant in AP (P=0.859). The IgG levels at the 1st and 7th day were significantly correlated in AMI patients (r=0.764, P=0.000) and also in AP patients (r=0.658, P=0.028). AMI patients with high IgE levels may be protected from infarction consequences. Other immunological responses, such as IgG, complement, cytokines, and cellular immunity, as well as research on IgG subclasses, are needed to understand their function in the aetiopathogenesis of AMI.

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