title: Increased endothelial expression of intercellular adhesion molecule-1 in symptomatic versus asymptomatic human carotid atherosclerotic plaque.
abstract: OBJECTIVE
  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.
authors.affiliation: National Institutes of Neurological Disorders and Stroke/Stroke Branch, National Institutes of Health, Bethesda, MD 20892-4128, USA. tjd@helix.nih.gov
authors.forename: T J
authors.initials: TJ
authors.lastname: DeGraba
authors.forename: A L
authors.initials: AL
authors.lastname: Sirén
authors.forename: L
authors.initials: L
authors.lastname: Penix
authors.forename: R M
authors.initials: RM
authors.lastname: McCarron
authors.forename: R
authors.initials: R
authors.lastname: Hargraves
authors.forename: S
authors.initials: S
authors.lastname: Sood
authors.forename: K D
authors.initials: KD
authors.lastname: Pettigrew
authors.forename: J M
authors.initials: JM
authors.lastname: Hallenbeck
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D001161:Arteriosclerosis / Q000378:metabolism* / Q000601:surgery; D002340:Carotid Artery Diseases / Q000378:metabolism* / Q000601:surgery; D004691:Endarterectomy; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011184:Postoperative Period; D012016:Reference Values; D012995:Solubility
chemical_list: D018799:Intercellular Adhesion Molecule-1