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The Arterial Inflammation Hypothesis
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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.3-5 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 . . . [Full Text of this Article]
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RELATED ARTICLE
Is High-Sensitivity C-Reactive Protein an Effective Screening Test for Cardiovascular Risk?
Irving Kushner and Ashwini R. Sehgal
Arch Intern Med. 2002;162(8):867-869.
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