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(Circulation. 2006;113:e152-e155.)
© 2006 American Heart Association, Inc.

Clinician Update

Inflammatory Biomarkers in Acute Coronary Syndromes

Part II: Acute-Phase Reactants and Biomarkers of Endothelial Cell Activation

Ehrin J. Armstrong, MD, MSc; David A. Morrow, MD, MPH; Marc S. Sabatine, MD, MPH

From the Department of Medicine (E.J.A.), Massachusetts General Hospital, and the TIMI Study Group (D.A.M., M.S.S.), Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass.

Correspondence to Marc S. Sabatine, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail msabatine@partners.org

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

	Introduction

 
The inflammatory etiology of atherosclerosis has prompted a search for biomarkers of inflammation that predict risk for coronary artery disease and its sequelae. Within the acute coronary syndromes (ACS), inflammatory biomarkers may provide independent information regarding pathophysiology, prognosis, and optimal therapeutic strategies. On the basis of the hypothesis that different pathophysiological processes provide nonoverlapping information regarding risk stratification and disease management, this review series addresses biomarkers for each step in the inflammatory process that leads to ACS. Part I reviewed cytokines; this part reviews acute-phase reactants and biomarkers of endothelial cell activation; subsequent parts will address biomarkers of oxidative stress, angiogenesis, extracellular matrix degradation, and platelet activation.

	Acute-Phase Reactants

 
In the acute-phase response, cytokines drive production of acute-phase reactants, defined by >25% change in circulating concentration during an inflammatory response. These markers may also remain elevated chronically because of continuing inflammatory stimuli (Table).

View this table: [in this window] [in a new window]   Inflammatory Biomarkers in ACS

C-Reactive Protein
C-reactive protein (CRP) is a pentraxin acute-phase protein, members of which are evolutionarily conserved in most vertebrates.¹ Hepatocytes and possibly smooth muscle cells and macrophages transcriptionally activate production of CRP in response to inflammatory cytokines, including interleukin-1 and interleukin-6.² CRP is a robust clinical marker because of its stability, reproducible results, and ease of assay.

Although it was originally proposed as a nonspecific marker of inflammation, several reports suggest that CRP may play a direct pathophysiological role in the development and progression of atherosclerosis. Proposed mechanisms include induction of endothelial dysfunction,³ promotion of foam cell formation,⁴ inhibition of endothelial progenitor cell survival and . . . [Full Text of this Article]

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