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Editor's Correspondence |

The Arterial Inflammation Hypothesis

Deepak L. Bhatt, MD; Eric J. Topol, MD
Arch Intern Med. 2002;162(19):2249-2251. doi:.
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We read with interest the recent commentary by Kushner and Sehgal1 regarding the use of high-sensitivity C-reactive protein (hs-CRP) as a screening test for cardiovascular risk. Interestingly, many of the arguments lodged against the use of hs-CRP are the same as the ones initially used against measurement of cholesterol levels. Numerous studies in diverse populations have shown the value of hs-CRP in predicting risk, independent of other established markers.2 Even an incremental ability to prognosticate risk above and beyond stress testing and coronary angiography has been demonstrated.35 High-sensitivity CRP has now been proven to predict the risk of sudden cardiac death, a major cause of mortality that lacks effective preventive therapies.6 Furthermore, it appears that CRP is not just an innocent bystander in atherosclerosis, but actually has a direct pathogenic role in arterial disease.7 Studies have documented the ability of CRP to activate complement, to increase the uptake of low-density lipoprotein by macrophages, and to enhance T-cell–mediated endothelial cell destruction.810 In fact, patients with elevated levels of hs-CRP have more CRP in their plaque.6



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