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. Author manuscript; available in PMC: 2020 May 1.
Published in final edited form as: Thromb Res. 2019 Feb 13;177:59–69. doi: 10.1016/j.thromres.2019.01.017

Table 2.

Inhibitory effects of clopidorel (n = 12) and Prasugrel (n = 12) on platelet aggregation and systemic TAT levels in PCI patients.

Agonist Time (hour) Clopidogrel inhibition (% ± SE) Prasugrel inhibition (% ± SE) p-value
ADP 1 38 ± 10 84 ± 9 < 0.0001
   20 μM 2 53 ± 10 94 ± 5
4 72 ± 8 98 ± 1
16 85 ± 3 98 ± 1
SFLLRN 1 2 ± 8 62 ± 9 < 0.0001
   5 μM 2 9 ± 8 64 ± 10
4 17 ± 8 75 ± 6
16 15 ± 8 58 ± 7
AYPGKF 1 7 ± 3 39 ± 9 < 0.0001
   160 μM 2 9 ± 3 44 ± 11
4 13 ± 4 53 ± 8
16 11 ± 4 41 ± 10
Collagena 1 34 ± 11 56 ± 8 0.06
   5 μg/mL 2 39 ± 9 61 ± 6
4 58 ± 8 67 ± 4
16 48 ± 8 61 ± 8
TAT 0 258 ± 39 251 ± 27 NS
   pmol/L 1 274 ± 82 179 ± 23 NS
2 180 ± 23 226 ± 35 NS
4 284 ± 34 224 ± 15 NS
16 151 ± 10 301 ± 45 0.007

Platelets in PRP were isolated from PCI patients at baseline and after 1, 2, 4 and 16 h after bivalirudin infusion and clopidogrel and prasugrel loading dose administration, and were stimulated with 20 μM ADP, 5 μM SFLLRN, 160 μM \AYPGKF and 5 μg/L collagen. TAT levels in plasma were analyzed by ELISA as described in the methods. Data are reported as Mean ± SD and p values were determined by one-way ANOVA repeated measure test. TAT statistical analyses were performed using two-tailed student’s t-test.

a

Collagen-dependent aggregation was measured with 18 of the 24 PCI patients as shown in Fig. 4A for individual patients.