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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1091.)
© 2005 American Heart Association, Inc.

Editorials

CRP or not CRP? That Is the Question

Mark B. Pepys

From the Centre for Amyloidosis and Acute Phase Proteins, Department of Medicine, Royal Free and University College Medical School, London, United Kingdom.

Correspondence to Professor Mark B. Pepys, Centre for Amyloidosis and Acute Phase Proteins, Department of Medicine, Royal Free and University College Medical School, Rowland Hill Street, London NW3 2PF, United Kingdom. E-mail m.pepys@rfc.ucl.ac.uk

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

C-reactive protein (CRP) and cardiovascular disease is a very hot topic at present. Excitement and interest have spilled over dramatically from the scientific literature into the media and popular press leading to much speculative comment. However, rigorously controlled and reproducible studies are now laying the basis for a more realistic consensus. The article in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology from Carmen van den Berg’s laboratory makes a notable contribution to this process.¹

See page 1225

Shortly after its discovery in 1929 as "the acute phase protein," increased production of CRP was recognized as a characteristic feature of the response to acute myocardial infarction, and until the 1960’s detection of CRP was widely used for routine monitoring of acute rheumatic fever. In 1961 Irving Kushner, in one of the first applications of the then new technique of immunofluorescence, demonstrated the deposition of rabbit CRP in experimental myocardial infarction lesions. The association between CRP and cardiovascular disease thus has a very long history. In 1979 Kushner reported the kinetics of the acute phase CRP response to human acute myocardial infarction, and soon afterward we first investigated critically the behavior of CRP in clinical coronary artery disease and myocardial infarction.² We observed that persistently elevated circulating CRP concentrations after an infarct were associated with a poor prognosis, although at that time we were focusing mainly on CRP as a sensitive nonspecific marker of all the various complications of coronary occlusion and their treatment.

The current phase of interest in CRP . . . [Full Text of this Article]

Related Article:

C-Reactive Protein–Induced In Vitro Endothelial Cell Activation Is an Artefact Caused by Azide and Lipopolysaccharide

Karolina E. Taylor, John C. Giddings, and Carmen W. van den Berg
Arterioscler Thromb Vasc Biol 2005 25: 1225-1230. [Abstract] [Full Text] [PDF]

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