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Low-grade Inflammation and Coronary Heart Disease

John Danesh, MBChB, MSc, DPhil

JAMA. 1999;282:2169-2171.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

C-reactive protein (CRP) is the classic "acute-phase reactant," the plasma levels of which can increase as much as 10,000-fold in response to tissue injury and infection.¹ C-reactive protein was discovered in the plasma of patients with acute pneumococcal pneumonia 70 years ago and was so named for its capacity to bind pneumococcal C-polysaccharide. Plasma CRP level has long been a widely measured marker of disease activity in inflammatory conditions, but recently, there has been increased interest in the possible relevance of low-grade inflammatory processes to cardiovascular disease and vascular risk factors.^2-3

A number of favorable biological characteristics make CRP a useful marker of such subtle inflammation: its plasma levels are determined mainly by the synthesis rate in the liver and closely reflect inflammatory activity; the protein is stable in frozen blood samples, allowing measurements in banked serum samples; and, despite sharp increases that occur during . . . [Full Text of this Article]

Author Affiliation: Clinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, England.

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