Abstract
Objective To study the characteristic of inhibition on platelet P2Y12 and short-term change after clopidogrel intake in patients with cardiovascular disease. Methods Thirty-two patients with cardiovascular disease were enrolled. Samples at baseline, 10 h and 36 h after 300 mg loading dose and 75 mg/d maintenance dose of clopidogrel with 100 mg/d Aspirin intake were measured respectively. Platelet aggregation (PAgT) was measured on thromboelastograph(TEG) induced by ADP/AA. INH was detected and calculated activated by Kaolin, AA, ADP and Activator((R)) in the TEG reagent. CD62p and VASP phosphorylation (PRI), platelet activation markers were tested with FACSCalibur Flow Cytometry, and platelet secretion activity and suppression of P2Y12 receptor were detected respectively. The changes of indicators were compared before and after clopidogrel intake, and evaluate their function in platelet receptor activation. Results INHADP at baseline was (11.5 ±9.3)%, and increased to (42.5 ±29.1)% statistically (t =3.155, P 0. 05) , INHAA increases from baseline level (56. 6 ± 36. 6) % to (83.0 ±27. 3)% at 10h(t=2.086,P>0.05) and (85. 4 ±20. 8)% at 36 h (t= 1. 888, P>0.05), no statistical defferences were found. Inhibition on platelet activativation induced by ADP function well till 36 h after 300 mg loading dose. PAgTADP decrease from (53. 7 ± 14. 1)% at baseline to (49. 2 ±22. 8)% at 10 h non-statistically (t=0.656, P>0.05), and (40.7±12.8)% at 36 h statistically (t=2.418, P 0.05) and (59.6 ±28.0)% at 36 h (t=1.930,P 0. 05 ). Inhibition of secretion activity reflected by CD62p was significant. In contrast, it was more obvious inhibition in COX-1 passway, while the inhibition of P2Y12 receptor varied due to assay difference. Conclusions AA-induced platelet activation is significantly decreased in the inhibition of clopidogrel and aspirin, while ADP receptor is significantly inhibited until 36 h after the loading dose of clopidogrel. Platelet function in whole blood reflects total activity of platelet interaction with other components, in which no significant inhibition could be witnessed within 10 h. Key words: Coronary disease; Ticlopidine; Platelet aggregation inhibitors; Flow cytometry
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