[Flow-cytometric analysis of platelet activation during rotablation]

Acute occlusion and subacute restenosis of the coronary artery are still the limiting factors of the otherwise successful interventional cardiology. Platelets and especially activated platelet populations play a key role concerning these typical and sometimes fatal complications. In this study we used flow-cytometry to determine the influence of the modern interventional technique 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 PTCA and rotablation (PTCA: CD41a p=0.8 and 0.9; CD42b p=0.5 and 0.2; rotablation: CD41a p=0.2 and 0.2; CD42b p=0.4 and 0.1). But platelet activation could be detected directly after PTCA and rotablation measuring the mean channel fluorescence intensity (MCFI) of CD62p, CD63 and fibrinogen binding (all p<0.05). Thirty minutes after finishing the procedures there were again significant changes in MCFI in PTCA (CD62p, CD63, fibrinogen binding; all p<0.05), but not in rotablation (CD62p p=0.1; CD63 p=0. 9; fibrinogen binding p=0.5). But MCFI for CD62p and fibrinogen binding in rotablation was higher than in PTCA. The results of our study show that rotablation also induces significant platelet activation that is higher than in PTCA alone. Flow cytometry is a sensitive and specific, multiparametric tool in establishing platelet activation. The individual platelet activation process is part of a complex cascade of events happening in the rotablated coronary segment leading to a vascular-molecular inflammatory process and consecutive clinical problems in some patients.