Current evidence supports that
inflammation is a major driving force underlying the initiation of coronary plaques, their unstable progression, and eventual disruption; patients with a more pronounced vascular inflammatory response have a poorer outcome.
Biomarkers are generally considered to be
proteins or
enzymes - measured in serum, plasma, or blood - that provide independent diagnostic and prognostic value by reflecting an underlying disease state. In the case of
coronary artery disease (CAD), inflammatory
biomarkers, have been extensively investigated; more evidence exists for
C-reactive protein (CRP). Using high sensitivity (hs) assays, epidemiologic data demonstrate an association between
hs-CRP and risk for future cardiovascular morbidity and mortality among those at high risk or with documented CAD. Moreover, a series of prospective studies provide consistent data documenting that mild elevation of baseline levels of
hs-CRP among apparently healthy individuals is associated with higher long-term risk for cardiovascular events. Yet, the predictive value of
hs-CRP is found to be independent of traditional cardiovascular risk factors. Recent studies suggest that, besides CRP, other inflammatory
biomarkers such as
cytokines [
interleukin (IL)-1,
IL-6,
IL-8,
monocyte chemoattractant protein-1 (MCP-1)], soluble
CD40 ligand,
serum amyloid A (SAA),
selectins (
E-selectin,
P-selectin),
myeloperoxidase (MPO),
matrix metalloproteinases (
MMPs), cellular
adhesion molecules [intercellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule 1 (VCAM-1)], placental
growth factor (PlGF) and A(2)
phospholipases may have a potential role for the prediction of risk for developing CAD and may correlate with severity of CAD. Finally, indications suggest that the increased risk associated with
inflammation may be modified with certain preventive
therapies and
biomarkers may help to identify the individuals who would benefit most from these interventions.