Growing evidence suggests that the immune system plays a critical role in all the stages of atherogenesis, from lesion formation to plaque rupture.¹ The inflammatory component of atherothrombosis is a topic of intensive research, since it is still unclear whether inflammatory markers measurable in peripheral blood can be useful tools for risk assessment in the general population; it is also unknown whether therapeutic strategies leading to a decrease of these inflammatory markers can modify cardiovascular risk.^w1

INFLAMMATORY MECHANISMS IN ATHEROSCLEROSIS

Early in the atherogenesis process, resident or circulating leucocytes bind to the site of a developing lesion in response to oxidised low density lipoprotein cholesterol (LDL-C), injury, or infection. Proinflammatory cytokines play a central regulatory role in this early stage of atherogenesis, since they induce the migration of these inflammatory cells to the subendothelial space, both by acting directly on these leucocytes and by upregulating the expression of several adhesion molecules (such as vascular cells adhesion molecules, intercellular adhesion molecules and selectins) which participate in leucocyte adhesion, rolling and subendothelial migration (fig 1⇓).^w2

As these monocytes accumulate in the subendothelial space, they continue to ingest chemically modified lipids and lipoproteins, they become macrophages and finally develop into foam cells, and initiate fatty streaks. At the same time, other inflammatory cells, such as activated T cells and mast cells, also attach themselves to the endothelium, contributing to the formation of the atheromatous lesion, which consists of a lipid pool covered …