From the National Institutes of Neurological Disorders and Stroke/Stroke
Branch (T.J.D., L.P., R.M.M., S.S., J.M.H.), National Institutes of Health,
Bethesda, Md; the Uniform Services University of the Health Sciences (T.J.D.,
A.-L.S.), Bethesda; the National Naval Medical Center, Department of
Neurosurgery (T.J.D., L.P., R.H.), Bethesda; and the National Institute of
Mental Health (K.D.P.), National Institutes of Health, Bethesda, Md.
Correspondence to Thomas J. DeGraba, MD, Stroke Branch, NINDS, NIH, 36 Convent Dr MSC 4128, Bldg 36 Room 4A03, Bethesda, MD 20892-4128. E-mail tjd{at}helix.nih.gov
Background and Purpose—The
mechanisms that cause carotid atherosclerotic plaque to become
symptomatic remain unclear. Evidence suggests that
mediators of inflammation are not only instrumental in the formation of
plaque but may also be involved in the rapid progression of
atheromatous lesions leading to plaque fissuring,
endothelial injury, and intraluminal thrombosis. Our
goal is to determine whether intercellular adhesion molecule-1
(ICAM-1), a known component of the inflammatory pathway, is
preferentially expressed on symptomatic versus
asymptomatic carotid plaques.
Methods—Carotid plaques from symptomatic (n=25) and
asymptomatic (n=17) patients undergoing carotid
endarterectomy with lesions involving >60%
stenosis were snap-frozen at the time of surgery.
Immunofluorescence studies were performed to
measure the percentage of luminal endothelial surface
that expressed ICAM-1. The relationships of stroke risk factors, white
blood cell count, percent stenosis, and soluble ICAM-1
(sICAM-1) plasma levels to endothelial ICAM-1
expression were investigated.
Results—An increased expression of ICAM-1 was found in the
high-grade regions of symptomatic (29.5%±2.4%,
mean±SEM) versus asymptomatic (15.7%±2.7%, mean±SEM)
plaques (P=0.002) and in the high-grade versus the
low-grade region of symptomatic plaques (29.5±2.4,
mean±SEM, versus 8.9±1.6; P<0.001). Plasma sICAM-1
levels were not predictive of symptomatic disease, and no
significant correlation between risk factor exposure and
endothelial ICAM-1 expression was found.
Conclusions—An elevation in ICAM-1 expression in
symptomatic versus asymptomatic plaque suggests
that mediators of inflammation are involved in the conversion of
carotid plaque to a symptomatic state. The data also
suggest a differential expression of ICAM-1, with a greater expression
found in the high-grade region than in the low-grade region of the
plaque specimen.
© 1998 American Heart Association, Inc.
Original Contributions
Increased Endothelial Expression of Intercellular Adhesion Molecule-1 in Symptomatic Versus Asymptomatic Human Carotid Atherosclerotic Plaque
Key Words: atherosclerosis • carotid endarterectomy • endothelium • intercellular adhesion molecule-1 • inflammation
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