The estimation of risk for atherosclerotic cardiovascular (CV) events based
only on the presence of classical risk factors is often insufficient. Therefore, efforts
have been made to find markers that indicate the presence of preclinical or clinical
disease. Inflammation mediates all stages of the disease, from initiation to the thrombotic
complications of atherosclerosis. Raised levels of several circulating markers,
particularly inflammatory mediators, have been reported in subjects with atherosclerosis.
Increased risk for CV events is associated with increased levels of cytokines, celladhesion
molecules, P-selectin and E-selectin, and acute phase reactants, such a highsensitivity
C-reactive protein and serum amyloid-A. Elevation of some of these markers
predicts the outcomes of patients with acute coronary syndromes. However, because
of their non-specificity, these biomarkers represent only a moderate added predicting value after
considering conventional CV risk factors. Consequently, recent research has focused on the detection of
vulnerable plaque, using vascular bed-specific biomarkers that can help identify individuals at highest risk
and help guide how to intervene to prevent CV events.
Considerable progress in the understanding of the role of the inflammation in atherogenesis has opened
new possibilities for the management of atherosclerosis. Recently new drugs mediating the direct inhibition
of circulating markers of inflammation were developed. These drugs could provide a novel therapeutic
approach and further enhance the understanding of the role of inflammation in atherosclerosis.