Atherosclerosis, and the clinical presentation of atherosclerosis, both have their basic pathogenesis in inflammatory mechanisms. The use of mouse models of atherosclerosis has emphasised the importance of inflammation in atherogenesis, and the use of serum markers of inflammation in epidemiological studies has shown the importance of inflammatory status in determining the presentation of atherosclerotic disease. Therapeutic opportunities will arise from the manipulation of these inflammatory mechanisms. Proof of this principle has been shown with the use of aspirin and statin drugs as well as the emerging roles for peroxisome proliferator-activated receptor (PPAR) agonists. It is likely that both refinement of existing anti-inflammatory agents and the identification of new inflammatory mechanisms will afford real opportunities for the treatment of atherosclerotic cardiovascular disease.