Key result
Plaque neovasculature shows ~2-fold higher adhesion molecule expression than luminal endothelium, linked to leukocyte infiltration.
Why the study?
No previous study has evaluated the distribution of E-selectin, ICAM-1, and VCAM-1 at different sites within the arterial intima or their relation to plaque leukocyte content in human atherosclerosis.
Population
99 coronary artery segments including 34 controls and 65 with atherosclerotic plaque
Comparison
Expression of E-selectin, ICAM-1, and VCAM-1 on arterial lumen, intimal neovasculature, and intimal nonendothelial cells
Design
Cross-sectional immunohistochemical study
Authors
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May implicate neovascular endothelium in plaque inflammation; hypothesis-generating for adhesion-targeted therapies.
Cross-Sectional (n=99)
p-value: p=<.01
O’Brien et al. (1996) conducted a cross-sectional in Atherosclerosis (n=99). Atherosclerotic plaque vs. Control coronary artery segments was evaluated on Prevalence of E-selectin, ICAM-1, and VCAM-1 on plaque neovasculature and association with intimal macrophage and T-lymphocyte density (p=<.01). In atherosclerotic plaques, E-selectin, ICAM-1, and VCAM-1 expression was twofold higher on intimal neovasculature than on arterial luminal endothelium and associated with increased leukocyte density (P<0.01).
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