Serum interleukin-6 is elevated in symptomatic carotid bifurcation disease.
BACKGROUND
The levels of circulating proinflammatory cytokines may express the extent of the inflammatory response and their participation in plaque progression and rupture needs to be evaluated. We aimed to investigate differences in circulating levels of proinflammatory cytokines and in plaque infiltration by macrophages between patients undergoing carotid endarterectomy for symptomatic and asymptomatic carotid atherosclerotic disease.


METHODS
One hundred nineteen patients (91 men and 28 women; mean age 66 +/- 8 years; range 42-83 years) who underwent carotid endarterectomy for significant (>70%) carotid bifurcation stenosis were enrolled in this study. Patients were characterized as symptomatic (n = 62) or asymptomatic (n = 57) after neurological examination. Serum levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), IL-1beta, serum amyloid A (SAA), and high-sensitivity C-reactive protein (hs-CRP) were evaluated. Macrophage infiltration of the plaque was assessed quantitatively from endarterectomy specimens using the monoclonal antibody CD68.


RESULTS
Serum IL-6 levels were significantly higher in patients with symptomatic compared with those with asymptomatic carotid disease (3.3 [2.0-6.5] pg/ml vs 2.5 [1.9-4.1] pg/ml, P = 0.02). TNF-alpha, IL-1beta, SAA, and hs-CRP levels did not differ significantly between the two groups. Symptomatic patients had also more intense macrophage accumulation in the carotid plaque compared with asymptomatic patients (0.6 +/- 0.1% vs 0.4 +/- 0.1%, P < 0.001). Although there were correlations between the levels of the different inflammatory markers, there were no correlation between any of them and the extent of plaque macrophage infiltration.


CONCLUSIONS
Patients with symptomatic carotid atherosclerotic disease have elevated serum IL-6 levels compared with asymptomatic patients. Symptomatic patients have also more intense macrophage infiltration of the atherosclerotic plaque suggesting that inflammatory process may contribute to the destabilization of the carotid plaque.
Koutouzis
M
M
Red Cross General Hospital, Athens, Greece. koutouzismike@yahoo.gr
Rallidis
L S
LS
Peros
G
G
Nomikos
A
A
Tzavara
V
V
Barbatis
C
C
Andrikopoulos
V
V
Vassiliou
J
J
Kyriakides
Z S
ZS
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000276:immunology*; D016893:Carotid Stenosis / Q000276:immunology; D016894:Endarterectomy, Carotid; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood*; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
C508600:IL6 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein