Abstract
The mechanisms involved in the transition from a stable to an unstable or vulnerable carotid atherosclerotic plaque are not clearly understood. We sought to test the hypothesis that pro‐inflammatory cytokines are related to carotid plaque instability and thus their modulation might be related to the prevention of stroke. Patients with at least 50% internal carotid artery stenosis undergoing carotid endarterectomy were included in this study; plaque stability was determined on the basis of clinical criteria and confirmed histologically. Intra‐plaque protein were extracted and analyzed by ELISA. Statistical testing was performed using the two‐tailed unpaired t‐test.Carotid plaques were obtained from 53 patients; 33 were considered stable and 19 unstable. Unstable carotid atherosclerotic plaques had significantly higher levels of expression of the chemokine MCP‐1 (19.8 ± 0.61 pg/ml vs. 17.3 ± 0.56 pg/ml; p=.0051) compared to stable plaques. Intra‐plaque levels of C‐reactive protein (CRP) (20.7 ± 0.64 pg/ml vs. 18.3 ± 0.53 pg/ml; p=.0056) and tumor necrosis factor‐alpha (TNF‐alpha) (450.1 ± 6.23 pg/ml vs. 326 ± 12.7 pg/ml; p<.0001) were similarly elevated in unstable compared to stable plaques. Conversely, the anti‐inflammatory cytokine interleukin‐10 (IL‐10) was decreased in unstable plaques (27.4 ± 0.40 pg/ml vs. 30.3 ± 0.52 pg/ml; p=.0002). Unstable carotid plaques exhibit a pro‐inflammatory cytokine profile. MCP‐1, which aids in the chemotaxis of monocytes, is elevated in unstable carotid atherosclerotic plaques. Small molecule inhibition of MCP‐1 may help in vulnerable plaque stabilization.
Published Version
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