Lipoprotein-Associated Phospholipase A2
Novel Biomarker and Causal Mediator of Atherosclerosis?
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Inflammation is clearly recognized as a central component in the development and progression of cardiovascular disease (CVD). What is not clear, however, is how to best identify and monitor pathophysiologic inflammatory processes leading to acute coronary events. Many studies have focused on the potential of circulating biomarkers of inflammation to define risk of incident CVD events and morbidity and mortality following events.
See pages 2517 and 2523
Lipoprotein-associated phospholipase A2 (Lp-PLA2) holds promise as a biomarker specifically associated with several key aspects of atherogenesis. Lp-PLA2, also known as platelet-activating factor acetylhydrolase (PAF-AH), is an enzyme produced primarily by macrophages and lymphocytes.1 Although Lp-PLA2 has been reported to exhibit both pro- and antiinflammatory activities, its primary role appears to be proatherogenic. In this context, Lp-PLA2 hydrolyzes oxidized phospholipids such as those within oxidized LDL, generating proinflammatory moieties lysophosphatidylcholine and oxidized fatty acids.1 In addition, approximately 80% of circulating Lp-PLA2 is sequestered on LDL particles which serve to modulate enzyme activity.1 Enzyme activity is reported to be increased when Lp-PLA2 bound to more atherogenic small dense LDL versus larger particles.2
In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Kolodgie and colleagues3 and Gerber and colleagues4 provide important new evidence on the role of Lp-PLA2 in atherosclerosis development and prognostic value of this novel biomarker after myocardial infarction (MI). In an immunohistochemical study of …