Immunoglobulin E as a marker of the atherothrombotic process in patients with acute myocardial infarction.

BACKGROUND: Clot formation is a crucial moment in the patophysiology of acute coronary syndromes. The aim of this research was to assess the relationship between immunoglobulin E (IgE), lipid parameters and chosen hemostatic markers. The role of IgE as a possible participant in the atherothrombotic process was also investigated. METHODS: A total of 80 patients with acute myocardial infarction (MI) was enrolled in the study. Concentrations of IgE, plasma lipid parameters, lipoprotein(a), markers of thrombin generation (TAT, AT III), markers of fibrinolysis (tPA:Ag, PAI-1:Ag, PAP, D-dimers) and markers of endothelial damage (von Willebrand factor) were measured in blood samples collected immediately after admission, before any treatment administration. RESULTS: In patients with acute MI and with IgE concentration above 100 kU/l, IgE values were strongly, positively correlated with LDL concentration (p < 0.05), lipoprotein(a) concentration (p < 0.02) and negatively correlated with HDL plasma levels (p < 0.02). Exclusion of patients with IgE concentration lower than 150 kU/l strengthened the correlation between IgE concentration and LDL (p < 0.002) and lipoprotein(a) (p < 0.01) levels. It also revealed a significant correlation between IgE and TAT (p < 0.001), IgE and AT III (p < 0.002), and IgE and D-dimers (p < 0.05). IgE and TAT values measured 7, 14 and 40 days after infarction also showed significant positive correlation between increments of these parameters. CONCLUSIONS: In patients with acute MI, a significant increase of thrombinogenesis and fibrinolysis markers is observed. Positive correlation between IgE concentration above 100 kU/l and markers of thrombinogenesis activation, lipid parameters and lipoprotein(a) levels, with significance increasing with IgE concentration and constant positive correlation between increments of IgE and TAT, can serve as evidence of IgE participation in the atherothrombotic process. (Cardiol J 2007; 14: 266-273).