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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1143.)
© 2004 American Heart Association, Inc.

Editorials

Myeloperoxidase and Plaque Vulnerability

Stanley L. Hazen

From the Departments of Cell Biology, Cardiovascular Medicine, and the Center for Cardiovascular Diagnostics and Prevention, Cleveland Clinic Foundation, Cleveland, Ohio 44195

Correspondence to Stanley L. Hazen, MD, PhD, Preventive Cardiology, Cleveland Clinic Foundation, 9500 Euclid Avenue, C51, Cleveland, OH 44195. E-mail hazens@ccf.org

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

Inflammation and the Vulnerable Plaque

Sudden cardiac death remains the leading cause of mortality in industrialized societies, outpacing all cancer related deaths combined. The majority of sudden cardiac deaths arise from acute myocardial infarction secondary to intracoronary artery thromboses. Remarkably, the culprit lesions involved are typically not flow-limiting stenoses,^1,2 but rather inflamed lipid-laden lesions.^3,4 Whereas plaque fissuring or rupture, which exposes the intensely prothrombogenic lipid core, occurs in a majority of cases, fully 40% of intracoronary artery thromboses arise at sites of superficial erosions, where endothelial cell (EC) loss and denudation occurs.³ The mechanisms responsible for plaque vulnerability leading to acute coronary artery thrombosis remain poorly understood. Mounting evidence, however, points toward a critical role for inflammatory processes.^5–8 Macrophages serve as the dominant cell type in the immediate site of both plaque ruptures and superficial erosions in subjects who experience acute coronary thrombosis,⁸ and recent clinical investigations reveal important associations between leukocytes,^9,10 their enzymes,^11–13 and their activation,^14,15 in subjects with unstable angina and acute coronary syndromes. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Sugiyama and colleagues significantly extend our knowledge of potential pathophysiologic inflammatory processes within vulnerable atheroma.¹⁶ Using a combination of biochemical, cellular, and immunohistologic studies, they describe unifying mechanistic links between the activity of the leukocyte enzyme myeloperoxidase (MPO) and two cardinal features of vulnerable plaque: EC loss/denudation and development of a prothrombotic phenotype.

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Myeloperoxidase: an Inflammatory Mediator of Atherosclerosis

First identified within human atherosclerotic plaque nearly a decade ago,¹⁷ MPO has emerged as an important potential participant in the atherosclerotic process. MPO, . . . [Full Text of this Article]

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