In the last decades, the role of inflammation in the pathogenesis of atherosclerosis has been the topic of
intense research. Several markers of inflammation have shown predictive value for first and recurrent coronary
events in patients without and with established Coronary Heart Disease (CHD). Among these markers, lipoprotein-
associated phospholipase A2 (Lp-PLA2) has recently received considerable attention. In the present review,
the potential role of Lp-PLA2 as a marker of CHD risk and as a therapeutic target is discussed. Elevated Lp-
PLA2 mass and activity appears to be associated with increased risk for CHD, both in the general population and
in patients with established CHD. However, it is unclear whether the measurement of Lp-PLA2 improves risk
discrimination when incorporated in models that include traditional cardiovascular risk factors. Moreover, the
lack of effect on CHD events of darapladib, a potent, selective Lp-PLA2 inhibitor, in two large, randomized,
placebo-controlled trials and the mostly negative findings of genetic association studies suggest that Lp-PLA2 is
unlikely to represent a causal factor in atherogenesis. Therefore, it is doubtful whether Lp-PLA2 will constitute a
therapeutic target for the prevention of CHD.
Keywords: Coronary heart disease, lipoprotein-associated phospholipase A2, darapladib, inflammation, myocardial infarction, atherosclerosis.
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