Cc. Powell et al., Chronic venous insufficiency is associated with increased platelet and monocyte activation and aggregation, J VASC SURG, 30(5), 1999, pp. 844-851
Citations number
33
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Purpose: This study assessed whether the increased numbers of platelet-mono
cyte aggregates observed in patients with venous stasis ulceration (VSU) re
present a response to dermal ulceration or if it is a condition associated
with underlying chronic venous insufficiency (CVI). We also analyzed the ex
pression of CD11b in patients with CVI to determine whether leukocyte activ
ation, known to occur in VSU, is a precursor of or a response to ulceration
.
Methods: Patients with varying classes of CVI (n = 24) and healthy control
subjects (n = 15), whose status was documented by means of duplex scanning,
stood upright and stationary for 10 minutes. Two aliquots of blood, drawn
from a distal leg vein and an antecubital fossa vein, were incubated with e
ither buffer or one of three platelet agonists. After fixation, these sampl
es were further incubated with fluorescent-labeled monoclonal antibodies (f
-MoAb) specific for CD14 (monocytes) and CD61 (platelets). The activated le
ukocyte assay was performed by incubating another aliquot of the blood samp
les with f-MoAb specific for CD11b and CD14. All samples were evaluated by
means of flow cytometry.
Results: We observed significantly more platelet-monocyte aggregates throug
hout the circulation in patients with CVI than in control subjects (29% vs.
8%; P <.0002). Furthermore, patients with CVI formed significantly more of
these aggregates in response to all platelet agonists than did control sub
jects. There were no significant differences between baseline numbers of ag
gregates or response to agonists in patients who had CVI with (n = 10) or w
ithout (n = 14) ulceration. Patients with CVI had more circulating platelet
-neutrophil aggregates than control subjects (7.2% vs. 3.6%; P =.05). The a
ddition of platelet agonists to the blood of patients with CVI resulted in
more platelet-neutrophil aggregates than in control subjects. Monocyte CD11
b expression was higher in patients with CVI than in control subjects (7.5
vs. 3.7; P <.01), with no differences noted in CD11b expression between pat
ients with or without ulceration. Neutrophil CD11b expression was low and s
imilar in control subjects and patients with CVI.
Conclusion: All classes of CVI are associated with significantly increased
percentages of platelet-monocyte aggregates and increased percentages of pl
atelet-neutrophil aggregates throughout the circulation. The presence of mo
re of these aggregates and the increased propensity to form aggregates in t
he presence of platelet agonists in all classes of CVI suggests an underlyi
ng state of platelet activation and increased reactivity that is independen
t of the presence of ulceration. The increased expression of monocyte CD11b
throughout the circulation in all classes of CVI suggests that although sy
stemic monocyte activation occurs in CVI, its presence is independent of VS
U as well.