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Acute coronary syndromes (ACS), which include unstable angina, myocardial infarction, and sudden cardiac death, continue to be a significant public health problem in industrialized countries. A growing body of research is directed at understanding the etiology of ACS and at identifying biomarkers of high risk. The results from angiographic and angioscopic studies suggest that the disruption of an atherosclerotic plaque with subsequent thrombosis may represent a common, although not the only, pathogenetic mechanism for ACS (1).The definitive reasons for plaque rupture are unknown, but inflammation appears to play a major role (2). Indeed, the main features that distinguish unstable from stable plaques include the presence of wide inflammatory infiltration, plaque fissures, and fresh thrombi (3). Early studies reported evidence of local activation of inflammatory cells in the shoulder region of coronary plaques, with release of proteolytic enzymes (metalloproteinases) that degrade the extracellular matrix and contribute to the fibrous cap weakening and plaque instability (1)(2)(3). More recently, however, it has been demonstrated that patients with ACS have widespread inflammation of the coronary tree as well as systemic activation of the inflammatory system (4)(5). These findings have stimulated the search for an ideal marker of plaque instability.Liuzzo et al. (5) reported for the first time that systemic concentrations of C-reactive protein (CRP), a prototypic marker of inflammation, were increased in a population of patients with unstable angina and were associated with a high recurrence of cardiac events. Larger studies confirmed the predictive value of …

Pregnancy-Associated Plasma Protein-A: Do Specific Markers of Vascular or Plaque Activation Exist, and Do We Really Need Them?