Abstract

Coronary artery disease (CAD) progression leading to acute coronary syndrome (ACS) is a rather unpredictable phenomenon. Clinicians currently depend on relatively crude risk scores to identify individuals at risk of developing serious cardiovascular events. Conventional risk factors are able to single out only a proportion of those individuals at a high risk of developing fatal cardiac events. The fact that both atherogenesis and atherosclerotic cardiovascular disease progression are directly linked to inflammatory mechanisms has generated interest among scientists as to the potential role of inflammatory molecules as markers of cardiovascular risk. C-reactive protein, a marker of inflammation, has been shown to add value to the predictive ability of conventional risk factors. However, given the complexity of the mechanisms responsible for both disease progression and acute events, it is unlikely that a single molecule can provide clinicians with an accurate prediction of cardiovascular risk. Current markers, including C-reactive protein, are non-specific and the search should continue for better markers of both atheromatous plaque activity and patient vulnerability. New markers of CAD progression have been identified in recent years, among which, pregnancy-associated plasma protein-A (PAPP-A) appears to offer an interesting profile. Studies have shown that increased plasma PAPP-A levels correlate with the presence of vulnerable coronary artery stenoses and the extent of angiographic CAD1–3 and predict clinical outcome in patients with ACS.4,5 Elesber et al .6 report that in patients with chronic stable CAD, increased plasma PAPP-A levels predict the occurrence of serious cardiovascular events. Findings in this study are of interest as they confirm and expand previous observations, suggesting a role for PAPP-A in atherogenesis and the prediction of cardiovascular risk. PAPP-A is a zinc-binding proteinase produced by different cell types, which circulates as an active homodimer covalenty bound to the proform of oeosinophil major … *Corresponding author. Tel: +44 20 8725 5901; fax: +44 20 8725 3328. E-mail address : jkaski{at}sgul.ac.uk

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