Inflammation, atherosclerosis, and cardiovascular risk: an epidemiologic view.

Based on laboratory and experimental evidence, it has been hypothesized that inflammation plays a fundamental role in atherogenesis and acute thrombosis. From an epidemiologic perspective, corroboration of this hypothesis has been provided by a series of prospective cohort studies which demonstrate that inflammatory parameters (such as fibrinogen, C reactive protein, and serum amyloid A), cellular adhesion molecules [such as intercellular adhesion molecule (ICAM)-1], and cytokines (such as interleukin-6) are all elevated at baseline among patients at risk for future coronary occlusion. Furthermore, data deriving from randomized clinical trials suggest that the efficacy of common preventive agents such as aspirin and hydroxy-methylglutaryl (HMG) CoA reductase inhibition may derive in part from interactions with the inflammatory system. Taken together, these data raise the possibility that therapies targeting chronic low-grade inflammation may provide novel future strategies for cardiovascular disease prevention.