In contrast to another study where two Warmbloods were refractory
to clopidogrel (Brooks et al., 2013), all horses in the present
study exhibited ADP-induced inhibition of platelet function due to
clopidogrel (i.e., the comparison of T0 with T72 as in the previous
study, data not shown). A higher loading dose was used in our study,
and similarly superior effects in human studies have been demonstrated
with loading doses of 600 mg clopidogrel (approximately
8 mg/kg BW) compared with 300 mg (approximately 4 mg/kg BW)
(Price et al., 2006). Our loading dose of approximately 6 mg/kg BW
was chosen based on the fact that equine platelets are more susceptible
to inhibition of aggregation by P2Y12 antagonists than human
platelets. Compared with the results
of a study in which horses received 2 mg/kg BWclopidogrel (Brainard
et al., 2011) our lower maintenance dose was sufficient to retain inhibition
during therapy. Additionally, platelet function measured by
ADP-induced aggregation was inhibited for at least 6 days after the
cessation of 2 mg/kg BWclopidogrel (Brainard et al., 2011); whereas,
with our lower dose, platelet function was restored at this time.
In contrast to another study where two Warmbloods were refractoryto clopidogrel (Brooks et al., 2013), all horses in the presentstudy exhibited ADP-induced inhibition of platelet function due toclopidogrel (i.e., the comparison of T0 with T72 as in the previousstudy, data not shown). A higher loading dose was used in our study,and similarly superior effects in human studies have been demonstratedwith loading doses of 600 mg clopidogrel (approximately8 mg/kg BW) compared with 300 mg (approximately 4 mg/kg BW)(Price et al., 2006). Our loading dose of approximately 6 mg/kg BWwas chosen based on the fact that equine platelets are more susceptibleto inhibition of aggregation by P2Y12 antagonists than humanplatelets. Compared with the resultsof a study in which horses received 2 mg/kg BWclopidogrel (Brainardet al., 2011) our lower maintenance dose was sufficient to retain inhibitionduring therapy. Additionally, platelet function measured byADP-induced aggregation was inhibited for at least 6 days after thecessation of 2 mg/kg BWclopidogrel (Brainard et al., 2011); whereas,with our lower dose, platelet function was restored at this time.
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