Acute occlusion and subacute restenosis of the coronary artery are still th
e limiting factors of the otherwise successful interventional cardiology. P
latelets and especially activated platelet populations play a key role conc
erning these typical and sometimes fatal complications. In this study we us
ed flow-cytometry to determine the influence of the modern interventional t
echnique of rotablation on platelet antigens and their possible alteration.
A PTCA control group was included. We analyzed the fluorescence expression
of structural antigens CD41a (GPII-IIIa) and CD42b (GPIb-V-IX), and of the
activation-dependent antigens CD62p (P-selectin, PADGEM, GMP-140) and CD63
(GP53). Furthermore we analyzed the binding of fibrinogen to the platelet
flow-cytometrically. CD41a and CD42b did not show significant alternations
in fluorescence before, directly after and thirty minutes after finishing P
TCA and rotablation (PTCA: CD41a p = 0.8 and 0.9; CD 42b p = 0.5 and 0.2; r
otablation: CD41a p = 0.2 and 0.2; CD42b p = 0.4 and 0.1). But platelet act
ivation could be detected directly after PTCA and rotablation measuring the
mean channel fluorescence intensity (MCFI) of CD62p, CD63 and fibrinogen b
inding (all p < 0.05). Thirty minutes after finishing the procedures there
were again significant changes in MCFI in PTCA (CD62p, CD63, fibrinogen bin
ding; all p < 0.05), but not in rotablation (CD62p p = 0.1; CD63 p = 0.9; f
ibrinogen binding p = 0.5). But MCFI for CD62p and fibrinogen binding in ro
tablation was higher than in PTCA. The results of our study show that rotab
lation also induces significant platelet activation that is higher than in
PTCA alone. Flow cytometry is a sensitive and specific, multiparametric too
l in establishing platelet activation. The individual platelet activation p
rocess is part of a complex cascade of events happening in the rotablated c
oronary segment leading to a vascular-molecular inflammatory process and co
nsecutive clinical problems in some patients.