Multiple basic science studies have established that atherosclerosis is much more than the mere accumulation of excess lipid in the walls of arteries leading to progressive narrowing of the vessel. Instead, it should be thought of as an inflammatory disease involving many cellular and molecular responses. Inflammatory cells and mediators participate at every stage of atherogenesis, from the earliest fatty streak to the most advanced fibrous lesion . Elevated glucose, increased blood pressure, and inhaled cigarette by-products can trigger and perpetuate inflammation. However, one of the key factors triggering this inflammation is oxidized LDL (low density lipoprotein). When excess LDL is taken up by macrophages, it triggers the release of inflammatory mediators that can lead to thickening and/or rupture of plaque lining the arterial walls. Ruptured or unstable plaques are responsible for clinical events such as myocardial infarction and stroke. Lipid lowering, whether by diet or medication, can therefore be thought of as an antiinflammatory and plaquestabilizing therapy .