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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2417.)
© 2006 American Heart Association, Inc.

Editorials

Lipoprotein-Associated Phospholipase A₂

Novel Biomarker and Causal Mediator of Atherosclerosis?

Nancy Swords Jenny

From the Department of Pathology, University of Vermont College of Medicine, Colchester.

Correspondence to Nancy Swords Jenny, PhD, Department of Pathology, University of Vermont College of Medicine, 208 South Park Drive, Suite 2, Colchester, VT 05446. E-mail Nancy.Jenny@uvm.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 Lp-PLA₂ expression in coronary segments from 25 sudden coronary death patients, Kolodgie et al³ found strong expression of Lp-PLA₂ within the necrotic core and in . . . [Full Text of this Article]

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