C-reactive protein and carotid intimal medial thickness in a community population

C-reactive protein (CRP) has been linked to cardiovascular disease and atherosclerosis. Large-scale epidemiological studies have shown a correlation of CRP level with risk of stroke, myocardial infarction and peripheral arterial disease. Nevertheless, the question whether serum CRP itself is an inde...

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Published inJournal of cardiovascular risk Vol. 9; no. 2; p. 97
Main Authors Sitzer, Matthias, Markus, Hugh S, Mendall, Michael A, Liehr, Rüdiger, Knorr, Uwe, Steinmetz, Helmuth
Format Journal Article
LanguageEnglish
Published England 01.04.2002
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Summary:C-reactive protein (CRP) has been linked to cardiovascular disease and atherosclerosis. Large-scale epidemiological studies have shown a correlation of CRP level with risk of stroke, myocardial infarction and peripheral arterial disease. Nevertheless, the question whether serum CRP itself is an independent indicator of the atherosclerotic process remains unanswered. In a community-based sample free of advanced atherosclerotic disease (n = 1018; mean age +/- SD, 54.1 +/- 12.0 years; 49.7% women) we examined the relationship between carotid intimal medial thickness (IMT), conventional vascular risk factors (that is, smoking, obesity, elevated blood pressure, diabetes mellitus, hypercholesterolaemia) and serum CRP. We found an association between increasing IMT values with increasing CRP values for all sites within the carotid system (for example, common carotid artery [CCA-] IMT, beta = 0.174, P < 0.001). The relationship was weakened after accounting for the above-mentioned conventional risk factors (linear regression), particularly body mass index, but remained significant (for example, mean CCA-IMT beta = 0.02, P = 0.042). Including fibrinogen in the regression made the relationship no longer significant (mean CCA-IMT beta = 0.01, P = 0.277). It is unlikely that CRP per se is a major independent cause of early arteriosclerosis. Elevations of CRP, or less specifically chronic inflammation, may mediate the effect of certain conventional risk factors on promoting atherogenesis, especially obesity.
ISSN:1350-6277
DOI:10.1097/00043798-200204000-00005