Immunophenotypic characterisation of carotid plaque: Increase amount of inflammatory cells as an independent predictor for ischaemic symptoms

Objectives: to investigate the inflammatory response within intact carotid plaques from carotid eversion endarterectomy (CEE) to determine the relationship between immunohistological plaque morphology and ischaemic cerebrovascular symptoms. Material and methods: intact CEE plaques from 71 patients with high-grade (>70%) stenosis undergoing CEE (group I, symptomatic, n=42; group II, asymptomatic, n=29) and 12 normal postmortem arteries (control group) were analysed with specific antibodies to inflammatory cells (T-Lymphocytes (CD3, CD4), cytotoxic T-cells (CD8), B-lymphocytes (CD20), natural killer cells (CD57), macrophages (CD68), endothelial adhesion molecules (ICAM-1 (CD54), P-selectin (CD62P), E-selectin (CD62E), VCAM-1 (CD106) and T-lymphocyte co-stimulatory molecule (CD40) and procoagulatory modulators (thrombomodulin (CD141), tissue factor (CD142)). Both groups were matched for gender, age, risk factors, degree of carotid artery stenosis. Plaques were measured using a semiquantitative score system in a blinded fashion by two observers. Statistical analysis of the group differences were performed by using the Kruskal-Wallis test and the Multitest Procedure with Permutation-Testing. Significance was taken as a p<0.05. Results: there were significantly more inflammatory cells, an overexpression of P-selectin and the procoagulatory markers thrombomodulin and tissue factor in symptomatic compared to both asymptomatic plaques and the ones of the control group. In both groups there was no significance for ICAM-1, VCAM-1, macrophages and co-stimulatory molecule CD40. There was also no significance for any factor between the asymptomatic and the control group. However, the differences between the symptomatic and the asymptomatic group were highly significant for all factors. Conclusion: these data suggest that structural changes and inflammatory damage within the individual plaque seems to be a critical step in promoting plaque rupture with embolic sequelae.