Since the early 1990 s, both experimental and clinical data have clearly demonstrated that inflammatory processes accompany atherosclerotic disease from its initiation to the development of clinical complications. Numerous biomarkers involved at various levels of the inflammation cascade have been shown to be associated with adverse cardiovascular outcomes. Among them, the classical acute phase reactant C-reactive protein (CRP) has been most intensively investigated. Recent research in this field has been driven by the observation that despite low LDL-cholesterol levels, a remarkably high number of patients are still at increased risk for recurrent cardiovascular events. This is argued to be attributable to the presence of a prolonged inflammatory response (reflected by a persistently elevated hsCRP), a concept, which is currently known as "residual inflammatory risk". The unequivocal proof that the inflammatory process is not only a simple bystander but is also causally involved in atherogenesis, came from the recent CANTOS trial, showing a 15 % reduction of primary MACE outcomes despite aggressive statin therapy and lower LDL-cholesterol levels. Thus, an anti-inflammatory treatment strategy might represent a promising tool to improve the outcome of this still deadly disease.
