Serum IgE levels in coronary artery disease

The development and progression of atherosclerosis and its predisposition for unstable angina, myocardial infarction and stroke is associated with traditional risk factors such as family history, cigarette smoking, hypertension, dyslipidemia, diabetes mellitus, obesity, imbalance of the hemostatic/fibrinolytic system and sedentary lifestyle. However, much of the variability in atherosclerosis and its manifestations still remains unexplained. Nowadays, there is increasing evidence that immunologic mechanisms play a major role in etiology, prediction of coronary plaque instability and foreseeing severe reaction leading to an actual coronary event. Cells of the immune system such as macrophages, mast cells and T-lymphocytes are major components of human atheromatous plaque. These cells participate in a vicious immune cycle and activate each others via bidirectional stimuli. For example, mast cells can activate macrophages and may enhance T-cell activation. Inducible macrophage protein 1a may activate mast cells, while CD169+ macrophages activate CD8 T cells. T cells may mediate mast-cell activation and proliferation and regulate macrophage activity. Mediators secreted by these cells, including histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines and chemokines, can induce coronary artery spasm and atheromatous plaque erosion and rupture, culminating in the development of acute coronary syndromes.