Coronary artery disease (CAD) is associated with risk factors such as smoking, diabetes mellitus, dyslipidaemia and hypertension, and represents the major cause of morbidity and mortality in the Western world [1]. In recent years, it has become apparent that inflammation plays a major pathogenic role in both atherogenesis and rapid CAD progression [2,3].

Inflammation and atherosclerosis

Despite important observations regarding an association between inflammation and atherosclerosis in the past, it has been only in the last two decades that scientists have specifically focused their attention on inflammation as a major player in the development of atherosclerosis. As reviewed recently by Ross [3], the atherogenic process involves inflammatory mechanisms with pro- and anti-inflammatory cytokine production, and increased blood concentrations of acute phase reactants. Acute phase reactants, such as fibrinogen, C-reactive protein (CRP), serum amyloid A protein, syalic acid, caeruloplasmin and albumin, have been noted as markers of coronary disease activity, similar to other inflammatory disease processes. Typically, cells involved in chronic inflammation include macrophages, lymphocytes, mast cells and plasma cells. Different cell types, i.e. endothelial cells, vascular smooth muscle cells, macrophages and lymphocytes, as well as numerous families of cytokines and growth factors, are involved in the atherosclerotic process [3]. Cytokines and growth factors have effects on the vasculature, inducing a variety of responses by activated endothelial cells.