J. Graff et al., Platelet CD62 expression and PDCFAB secretion in patients undergoing PTCA and treatment with abciximab, BR J CL PH, 51(6), 2001, pp. 577-582
Aims To investigate a correlation of the platelet activation marker CD62 an
d secretion of the growth factor PDGF from platelets in coronary patients u
nder therapy with the GPIIb/IIIa-inhibitor abciximab.
Methods Flow cytometric assessment of fibrinogen binding (GPIIb/IIIa-bindin
g site) and CD62 expression, as well as PDGF release of human platelets (im
munoassay) and platelet aggregation with 20 muM ADP and 2 mug ml(-1) collag
en were evaluated in nine patients with stable coronary artery disease. Pat
ients were undergoing elective balloon angioplasty and were treated with as
pirin (100 mg day(-1)), heparin (ACT < 220 s) and abciximab (bolus and infu
sion over 12 h). Blood samples were obtained before initiation of abciximab
therapy (under aspirin and heparin) (1), 3 h after angioplasty under abcix
imab (II) and 12 h after termination of abciximab infusion (III).
Results Compared with sample I before abciximab therapy, fibrinogen binding
was reduced to 37% (+/-34 s.d., P<0.05) (II) and 55% (+/-40 s.d., P<0.05)
(III). Reduced fibrinogen binding also led to a significant reduction of th
e aggregation response to ADP (down to 37% +/- 20) and collagen (down to 0%
,). Mean fluorescence intensity of CD62-expression was 78 units (+/-20 s.d.
) (I), 72 units (+/-14 s.d.) (II) and 64 units (+/-12 s.d., P<0.05) (III).
PDGF release from isolated, washed platelets was 99 (+/-33 s.d.) ng/10(9) p
latelets at (I), 82 (+/-31 s.d.) ng/10(9) platelets and 96 (+/-30 s.d.) ng/
10(9) platelets.
Conclusions The results indicate that despite a strong reduction of GPIIb/I
IIa-binding and platelet aggregation, CD62 as a marker of platelet secretio
n and the secretion product PDGF were only slightly reduced under abciximab
treatment. No direct correlation between CD62 expression and PDGF release
could be demonstrated.