Premium
Plasma levels of high‐sensitive C ‐reactive protein do not correlate with inflammatory activity in carotid atherosclerotic plaques
Author(s) -
Grufman H.,
Gonçalves I.,
Edsfeldt A.,
Nitulescu M.,
Persson A.,
Nilsson M.,
Nilsson J.
Publication year - 2014
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/joim.12133
Subject(s) - inflammation , medicine , c reactive protein , carotid endarterectomy , tumor necrosis factor alpha , monocyte , subclinical infection , cytokine , macrophage , pathology , immunology , carotid arteries , biology , biochemistry , in vitro
Background It is well established that subjects with moderately elevated plasma levels of C‐reactive protein ( CRP ) have an increased risk of development of cardiovascular events. As atherosclerosis is a disease characterized by chronic arterial inflammation, it is possible that moderate increases in CRP level reflect the presence of plaque inflammation. To investigate this possibility, we compared plasma levels of hs CRP the day before carotid endarterectomy with the degree of inflammation in the excised plaque tissue. Methods Luminex immunoassays were used to determine the levels of IL ‐6, IL ‐10, monocyte chemoattractant protein‐1 and tumour necrosis factor‐α ( TNF ‐α) in plasma and in homogenized plaque tissue from 160 endarterectomy specimens. Plaque sections were stained with antibodies against CD 68 to determine the plaque macrophage content. Results Plasma high‐sensitivity (hs) CRP levels were significantly correlated with plasma IL ‐6 and TNF ‐α. However, there were no significant associations between plasma hs CRP concentration and plaque cytokine levels or macrophage contents. Conclusions The present findings strongly argue against hs CRP as a marker of plaque inflammation. Hence, it is more likely that elevated hs CRP is a sign of a subclinical systemic inflammation and this in turn may contribute to progression of cardiovascular disease.