Objective Characterize the inhibition of platelet P2Y12 receptor and COX-1 pathway after clopidogrel adding to aspirin intake.
Methods 32 inpatients with coronary atherosclerosis were enrolled; 600 mg clopidogrel was given in consecutive two days, 100 mg/d Aspirin intake simultaneously. Inhibition of platelet aggregation induced by ADP/AA on Thrombelastography, platelet aggregation activated by ADP/AA, CD62p and vasodilator stimulated phosphoprotein (VASP) were measured at no clopidogrel, 10th hour and 36th hour after the first 300mg loading dose of clopidogrel.
Results (1) Inhibition ADP increases to (42.5±29.1)% statistically (p=0.034) at 10 h but not continues to the 36th hour (p=0.106), Inhibition AA increases from (56.6±36.6)% to (85.4±20.8)% statistically (p=0.101) at 36 h, indicates COX-1 pathway is inhibited stronger than single aspirin intake. (2) Aggregation ADP decreases statistically (p=0.036) until 36 h, Aggregation AA decrease statistically (p=0.021) at 10 h and stabled to 36 h (p=0.045). Platelet response described by aggregation is different from inhibition percentage on TEG. (3) Change of Platelet Reactivity Index (PRI) in VASP assay is similar to Aggregation ADP, CD62p fluctuates from (7.5±1.4)% to (4.2±1.1)% (p=0.035) and (4.3±0.2)% (p=0.211) in a different way.
Conclusion No correlation could be found between results of platelet inhibition and aggregation, induced by whether ADP or AA. VASP helps to identify platelet responses to Clopidogrel specific. Absence of standard on platelet function measurement results in variety of clopidogrel resistance study.