Editorials |
From the Department of Pathology and Biochemistry, University of Vermont College of Medicine, Colchester.
Address correspondence to Dr Russell P. Tracy, Professor of Pathology and Biochemistry, University of Vermont College of Medicine, 208 South Park Dr, Ste 2, Colchester, VT 05446. E-mail Russell.tracy@uvm.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
"We know that the tail must wag the dog, for the horse is drawn by the cart; but the Devil whoops, as he whooped of old: Its clever, but is it Art?"1 (Rudyard Kipling, 18651936)
In 1998, I wrote an editorial that attempted to make two points.2 The first point was biological: there existed at that time an active debate over whether inflammation was a cause or a result of cardiovascular disease (CVD), and I suggested that this debate was in fact based on a false distinction, and that both positions where likely to be correct. While atherothrombotic disease is inflammatory, inflammation mediators actually participate in the disease process. The second point was clinical: the routine use of a marker of inflammation in cardiovascular risk prediction was likely in the near future, since this dimension of vascular disease was important and relatively easy to capture with a blood test. C-reactive protein (CRP) seemed to be a good candidate for reasons that were not so much biological as technical and logistic.
See page 1668
Since that time, much of the debate over cause and effect has subsided and, to my reading at least, most articles addressing inflammation and CVD risk these days either directly or tacitly acknowledge both positions. In addition, CRP has become, if not an accepted component of CVD risk assessment, at least a commonly measured CVD risk factor.3 While this has been excellent progress, however, many questions remain both on the scientific front and on the clinical
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