Flow-cytometric analysis comparing platelet activation during percutaneoustransluminal coronary angioplasty, stent placement and rotablation

Background: Acute occlusion and subacute restenosis of the coronary artery remain the limiting factors of the otherwise successful techniques of inter ventional cardiology. Platelets and especially activated platelet subpopula tions play a key role in these sometimes fatal complications. In this study , we used flow cytometry to compare the influences of percutaneous translum inal coronary angioplasty (PTCA, n = 12 patients), stenting (n = 8) and rot ablation in = 10) on platelet antigens and their possible alteration, indic ating platelet activation. Material and Methods: Samples for flow cytometry were taken directly from the arterial sheath in free flow before the proce dures, directly after the procedures, and 30 min after finishing either PTC A, stenting or rotablation. One aliquot of the sample was immediately fixed and then stabilized. Aliquots were labeled with saturating amounts of anti bodies against CD41a (GPIIb-IIIa), CD42b (GPIb-V-IX), CD62p (P-selectin), C D63 (GP53), and antihuman fibrinogen, and measured within 2 h. For flow-cyt ometric analyses we used a FACScan cytometer. Results: CD41a and CD42b did not show significant alterations in mean channel fluorescence intensity (MC FI) before, directly after, and 30 min after finishing PTCA, stenting, or r otablation (PTCA: CD41a p = 0.8 directly after and p = 0.9 30 min after fin ishing; CD42b p = 0.5 and p = 0.2; stenting: CD41a p = 0.3 and p = 0.2, CD4 2b p = 0.5 and p = 0.7; rotablation: CD41a p = 0.2 and p = 0.2; CD42b p = 0 .4 and p = 0.1). However, measuring the MCFI of CD62p, CD63, and fibrinogen binding tall p < 0.05), platelet activation could be detected directly aft er PTCA, stenting, or rotablation. Compared with values obtained directly a fter the procedures, there were further significant changes 30 min after fi nishing the procedures in MCFI after PTCA and stenting (CD62p, CD63, fibrin ogen binding, all p < 0.05), but not after rotablation (CD62p p = 0.1; CD63 p = 0.9; fibrinogen binding p = 0.5). Conclusions: The results of our stud y show that all three techniques induce significant platelet activation. Ac tivation differs between the procedures. Detecting platelet activation may help to determine patients at risk for thrombophilic adverse effects.