Soluble P-selectin - A marker of platelet activation and vessel wall injury. Increase of soluble P-selectin in the blood plasma of patients with myocardial infarction, massive atherosclerosis and primary pulmonary hypertension
Av. Semenov et al., Soluble P-selectin - A marker of platelet activation and vessel wall injury. Increase of soluble P-selectin in the blood plasma of patients with myocardial infarction, massive atherosclerosis and primary pulmonary hypertension, TERAPEVT AR, 72(4), 2000, pp. 15-20
Aim. A comparative analysis of the content of the soluble form of cell adhe
sion protein P-selectin in the blood plasma of patients with acute myocardi
al infarction (AMI), massive atherosclerosis (MA) and primary pulmonary hyp
ertension (PPH), investigation of the relationship between plasma content o
f P-selectin and known markers of platelets and endothelial cells activatio
n, preliminary assessment of the prognostic value of P-selectin determinati
on.
Materials and methods. This study included 16 patients with AMI, 20 patient
s with MA, 21 patients with PPH and 18 healthy donors. The follow-up was 1-
5 years. End-points in the group of patients with AMI were recurrent acute
coronary syndrome and coronary artery by-pass operation, in the group with
MA - thrombotic complications (acute coronary syndrome, ischemic stroke) an
d in the group with PPH - death. P-selectin tons measured by ELISA and plat
elet factor 4 (PF4), thromboxane B2 (TXB2), endothelin-1 and stable prostac
yclin metabolite 6-keto-prostaglandin F1 alpha(6-keto-PGF1 alpha) by means
of commercial ELISA kits.
Results. Mean level of P-selectin in blood plasma of patients with AMI (1 d
ay) (361+/-18 ng/ml), MA (410+/-31 ng/ml) and PPH (627+/-83 ng/ml) was incr
eased in comparison with the group of healthy donors (269+/-12 ng/ml) (ever
ywhere p<0.001). In AMI, P-selectin was increased on day 1 only, on days 2,
3 and 10-14 of the disease the level of P-selectin was significantly lower
than on day 1 and did not differ from the control level in the group of do
nors. In patients with MA a significant correlation was detected between pl
asma content of P-selectin and platelet activation marker PF4 (r=0.606, P=0
.007) and in patients with PPH between the content of P-selectin and anothe
r platelet activation marker TXB2 (r=0.622, p=0.013). However, no correlati
on was found in PPH patients between the content of P-selectin and markers
of endothelial activation and/or damage (endothelin-1 and 6-keto-PGF1 alpha
). Difference in the concentration of P-selectin in patients with or withou
t end-points during the follow-up period was detected in patients with AMI
(353+/-14 ng/ml and 451+/-24 ng/ml, p=0.009) and PPH (477+/-58 ng/ml and 92
7+/-184 ng/ml, p=0.017) but not with MA (426+/-37 ng/ml and 361+/-24 ng/ml,
p=0.295).
Conclusion. The level of P-selectin in plasma was increased in patients wit
h acute thrombosis (AMI, 1 day) as wed as in patients without clinical sign
s of thrombosis but with a massive injury of the vasculature (MA and PPH).
The increase of P-selectin was, presumably, caused by its secretion from ac
tivated platelets since its concentration in plasma correlated with platele
t concentration but not endothelial activation markers. Preliminary data in
dicate that blood plasma soluble P-selectin may be considered as a potentia
l prognostic marker in AMI and PPH.