The role of inflammation in atherothrombosis: current and future strategies of medical treatment.

Atherosclerosis is a pathological process caused by vascular remodeling. It symbolizes one of the major causes for morbidity and mortality in the western world. The causes for these vascular problems are manifold and different etiologies have been discussed. Since the 1980s the role of chronic inflammation has been considered and is now confirmed by many studies and experimental data. Several inflammatory pathways have been shown to participate in the atherosclerotic process. Different markers for inflammation have been found to predict the future risk for developing cardiovascular disease. Among these, high sensitivity C-reactive protein has been the most extensively validated. Newer markers such as CD40 ligand appear also to provide important information regarding risk stratification. Medications have been found to lower levels of inflammatory markers and perhaps decrease the associated clinical risk. Statins particularly appear to have anti-inflammatory mediated benefits, though other classes of drugs are also being evaluated. Lipid-lowering therapy in general has been found to be associated with reductions in inflammatory markers. Antithrombotic therapy, such as intravenous glycoprotein lIb/IIIa inhibitors and clopidogrel, has also been demonstrated to reduce inflammatory marker release. Peroxisome proliferator-activated receptor agonists are being evaluated for possible roles in targeting arterial inflammation. Angiotensin-converting enzyme inhibitors may also have anti-inflammatory properties. In this article we review the existing data in the inflammatory model of atherosclerosis. Furthermore, we discuss the prognostic value of different inflammatory markers and the potential benefit of anti-inflammatory therapies in cardiovascular disease.