Diabetes is associated with an increased risk of cardiovascular complications, as a reflection of the chronic inflammatory status. Monocytes-macrophages in diabetic subjects present impaired arachidonic acid metabolism. Moreover, atheromatous plaques in diabetic subjects seem to be significantly enriched in 2-AA-LPC (2-arachidonoyl-lysophosphatidylcholine) and are more inflammatory and more likely to rupture than are plaques in non-diabetic subjects. We therefore hypothesize that this vulnerability of atheromatous plaques in diabetic subjects could be explained by impaired 2-AA-LPC metabolism within the plaque.