Figure 4.
TG in PRP of patients with NSTEMI treated with ticagrelor in the presence or absence of VLD rivaroxaban. (A). Representative tracings of TG in PRP of patients with NSTEMI before (baseline) and after medication with ticagrelor + ASA for 1 and 2 days (d1 and d2) in the absence (DMSO) or presence of 40 ng/mL rivaroxaban (in vitro) with resting platelets and (C) with 10 µg/ml CRP-stimulated platelets. (B) Arithmetic means ± SEM (n = 20) of lag time, TTP, peak (thrombin), and velocity of TG in PRP of patients with NSTEMI before (baseline) and after treatment with ticagrelor for 1 and 2 days (d1 and d2) in the absence (DMSO) and presence of 40 ng/mL rivaroxaban (in vitro) with resting platelets and (D) with 10 µg/mL CRP stimulated platelets. *P < .05, **P < .01, and ***P < .001 indicate statistically significant differences from solvent control at the indicated time point. #P < .05 and ###P < .001 indicate significant differences from baseline.

TG in PRP of patients with NSTEMI treated with ticagrelor in the presence or absence of VLD rivaroxaban. (A). Representative tracings of TG in PRP of patients with NSTEMI before (baseline) and after medication with ticagrelor + ASA for 1 and 2 days (d1 and d2) in the absence (DMSO) or presence of 40 ng/mL rivaroxaban (in vitro) with resting platelets and (C) with 10 µg/ml CRP-stimulated platelets. (B) Arithmetic means ± SEM (n = 20) of lag time, TTP, peak (thrombin), and velocity of TG in PRP of patients with NSTEMI before (baseline) and after treatment with ticagrelor for 1 and 2 days (d1 and d2) in the absence (DMSO) and presence of 40 ng/mL rivaroxaban (in vitro) with resting platelets and (D) with 10 µg/mL CRP stimulated platelets. *P < .05, **P < .01, and ***P < .001 indicate statistically significant differences from solvent control at the indicated time point. #P < .05 and ###P < .001 indicate significant differences from baseline.

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