M. Jeziorska et De. Woolley, Neovascularization in early atherosclerotic lesions of human carotid arteries: Its potential contribution to plaque development, HUMAN PATH, 30(8), 1999, pp. 919-925
Citations number
36
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Neovascularization is a prominent feature of late-stage atherosclerotic les
ions and their complications but is generally regarded as an insignificant,
undetectable component of the earliest stages of plaque development, proba
bly because of relatively poor histological techniques. Using an improved v
ascular staining procedure, we have examined the extent of neovascularizati
on in the earliest plaque lesions. Combined monoclonal antibodies to CD31,
CD34, and von Willebrand factor have provided an ultrasensitive technique w
ith which to visualize blood vessels in early atherosclerotic lesions (n =
55) of human carotid arteries obtained through surgical procedures. Capilla
ry-like microvessels were shown in very early atherosclerotic lesions (type
II), where they were associated with the distribution of macrophages and a
few immature mast cells. Neovascularization was more prominent in type III
lesions with vessels of variable size, often providing a focus around whic
h local accumulations of macrophages and apolipoproteins A-I and B were vis
ualized. Thickened type III lesions usually showed an intricate network of
microvessels, together with numerous mast cells. These studies have shown n
eovascularization as a prominent feature of early stages of atherosclerotic
plaque development, Whereas distribution of apolipoproteins A-I and B were
observed in the very earliest stages of the plaque intima, these lipids, t
ogether with macrophages, foam cells, and mast cells, were observed as peri
vascular accumulations in a proportion of type II and III lesions. Such fin
dings indicate that neovascularization is an important feature of early pla
que development and may provide an additional or alternative source of leuk
ocyte and lipid accumulations relative to the arterial lumen. (C) 1999 by W
.B. Saunders Company.