Most acute coronary syndromes (ACS) are caused by thromboses occurring over ruptured vulnerable plaques (1). While the role of classical risk factors in atherogenesis is consolidated (2,3), their direct effect in acute plaque rupture and thrombosis is unproven: ACS can occur in individuals without risk factors (4), and most individuals with coronary atherosclerosis do not develop ACS (5). The peripheral biochemical phenotype of patients with ACS is progressively diverging from that of patients with chronic ischemic syndromes, and although the biology of ACS is highly subordinated to local factors, risk is better predicted by new sensitive, specific biomarkers of plaque instability (6) than by classical risk factors. These include acute phase reactants, cytokines, markers of platelet activation and oxidative stress, angiogenic growth factors, increased cell adhesiveness, and matrix metalloproteases (7), and they are markers of ACS and players in plaque instability (e.g., highsensitivity C-reactive protein [hs-CRP] actively participates in endothelial dysfunction, atherosclerotic plaque formation, plaque maturation, plaque destabilization, and eventual rupture) (8). High values of CRP are associated with rapid disease progression (9) and higher number of vulnerable plaques (10).