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Nature Medicine 14, 1059-1066 (1 October 2008) | doi:10.1038/nm.1870;

Inhibition of lipoprotein-associated phospholipase A2 reduces complex coronary atherosclerotic plaque development

Robert L Wilensky , Yi Shi , Emile R Mohler , Damir Hamamdzic , Mark E Burgert , Jun Li , Anthony Postle , Robert S Fenning , James G Bollinger , Bryan E Hoffman , Daniel J Pelchovitz , Jisheng Yang , Rosanna C Mirabile , Christine L Webb , LeFeng Zhang , Ping Zhang , Michael H Gelb , Max C Walker , Andrew Zalewski & Colin H Macphee

Increased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity is associated with increased risk of cardiac events, but it is not known whether Lp-PLA2 is a causative agent. Here we show that selective inhibition of Lp-PLA2 with darapladib reduced development of advanced coronary atherosclerosis in diabetic and hypercholesterolemic swine. Darapladib markedly inhibited plasma and lesion Lp-PLA2 activity and reduced lesion lysophosphatidylcholine content. Analysis of coronary gene expression showed that darapladib exerted a general anti-inflammatory action, substantially reducing the expression of 24 genes associated with macrophage and T lymphocyte functioning. Darapladib treatment resulted in a considerable decrease in plaque area and, notably, a markedly reduced necrotic core area and reduced medial destruction, resulting in fewer lesions with an unstable phenotype. These data show that selective inhibition of Lp-PLA2 inhibits progression to advanced coronary atherosclerotic lesions and confirms a crucial role of vascular inflammation independent from hypercholesterolemia in the development of lesions implicated in the pathogenesis of myocardial infarction and stroke.

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