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Adhesion molecule expression in symptomatic and asymptomatic carotid stenosis

From the Neuroscience Program (Drs. Nuotio, Lindsberg, Carpén, and Sairanen), Biomedicum Helsinki; Departments of Neurology (Drs. Lindsberg, Soinne, and Kaste), Pathology (Dr. Carpén), Cardiothoracic Surgery (Dr. Saimanen), and Radiology (Dr. Salonen), Helsinki University Central Hospital; Department of Public Health (Dr. Sarna), University of Helsinki; and the Wihuri Research Institute (Drs. Lehtonen-Smeds, Lassila, and Kovanen), Helsinki, Finland.

Address correspondence and reprint requests to Dr. Krista Nuotio, Neuroscience Program, Biomedicum Helsinki, Room B408a1, Post Box 700, 00029 HUS, Finland; e-mail: Krista.Nuotio{at}Hus.fi

Background: Prior studies have suggested a central role for cellular adhesion molecules (CAMs) in the pathophysiology and symptoms of atherosclerotic carotid plaques (CPs).

Objective: This study examined the role of CAMs in symptom generation in patients with advanced carotid artery disease.

Methods: Ninety-two consecutive patients underwent carotid endarterectomy, six for both sides (54 symptomatic and 41 asymptomatic CPs). Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), P-selectin, and E-selectin were immunostained in fresh-frozen CP specimens and examined semiquantitatively in the endothelium and intima-media. Plasma concentrations of soluble ICAM-1 and sVCAM-1 were analyzed by ELISA.

Results: Endothelial expression of ICAM-1, VCAM-1, P-selectin, and E-selectin did not differ between symptomatic and asymptomatic CPs, but endothelial ICAM-1 was associated with serum sensitized C-reactive protein levels (p = 0.026). However, there was less ICAM-1 expression in the intima-media of the symptomatic CPs (p = 0.022), and there was a similar, but nonsignificant tendency for VCAM-1. Soluble ICAM-1 and soluble VCAM-1 were not associated with the symptom status.

Conclusions: In contrast to earlier studies, it was found that symptomatic carotid disease is not associated with increased expression of adhesion molecules in the endothelium of advanced carotid plaques or in circulation. Rather, there was less expression of adhesion molecules in the intima-media of symptomatic carotid plaques.

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