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Circulation. 2002;106:e9064-e9065
doi: 10.1161/01.CIR.0000050660.54263.69
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(Circulation. 2002;106:e9064.)
© 2002 American Heart Association, Inc.

Cardiovascular News

Robin Fox, FRCP

Circulation Newswriter


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

C-Reactive Protein—Cause or Effect?

During the past month, C-reactive protein (CRP) has been much in the news. CRP has been likened to a Cinderella, dwelling in obscurity for many years, then being magically uplifted and taken in a coach to the ball. The supporter in this instance is Paul M. Ridker, MD, from Brigham and Women’s Hospital in Boston, Mass, whose study on 27 939 women generated astonishment by showing CRP to be a stronger predictor of cardiovascular events than LDL cholesterol. One message of his report was that CRP might be a useful means of screening people who are at excess risk of vascular disease despite normal LDL cholesterol; 46% of first cardiovascular events were in women with an LDL <130 mg/dL (3.36 mmol/L). Providing a foil for Dr Ridker, the part of critical commentator was played by Lori Mosca, MD, of Columbia University in New York, who was skeptical about this proposal. Where, she asked, is the evidence that CRP improves usefully on conventional markers? Statistical significance is not clinical significance. Until better data emerge, "It is prudent to focus effort and resources on screening for and treatment of major conventional risk factors."

This scene, played out originally in the November 14, 2002, issue of the New England Journal of Medicine (N Engl J Med. 2002;347:1557–1565, 1615–1616), was reenacted with an additional cast at the American Heart Association’s (AHA) 2002 Scientific Sessions in Chicago, Ill. Moderating the debate, Sidney C. Smith Jr, MD, from the University of North Carolina in Chapel . . . [Full Text of this Article]