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Platelet reactivity in response to aspirin and ticagrelor in African-Americans and European-Americans
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2 2021
Source: J Thromb Thrombolysis. 51(2):249-259 -
Alternative Title:J Thromb Thrombolysis
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Personal Author:
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Description:Background:
Platelet gene polymorphisms are associated with variable on-treatment platelet reactivity and vary by race. Whether differences in platelet reactivity and aspirin or ticagrelor exist between African-American and European-Americans remains poorly understood.
Methods:
Biological samples from three prior prospective antiplatelet challenge studies at the Duke Clinical Research Unit were used to compare platelet reactivity between African-American and European-American subjects. Platelet reactivity at baseline, on-aspirin, on-ticagrelor, and the treatment effect of aspirin or ticagrelor were compared between groups using an adjusted mixed effects model.
Results:
Compared with European-Americans (n=282; 50% female; mean±standard deviation age, 50±16), African-Americans (n=209; 67% female; age 48±12) had lower baseline platelet reactivity with platelet function analyzer-100 (PFA-100) (p<0.01) and with light transmission aggregometry (LTA) in response to arachidonic acid (AA), adenosine diphosphate (ADP), and epinephrine agonists (p<0.05). African-Americans had lower platelet reactivity on aspirin in response to ADP, epinephrine, and collagen (p<0.05) and on ticagrelor in response to AA, ADP, and collagen (p<0.05). The treatment effect of aspirin was greater in European-Americans with an AA agonist (p=0.002). Between-race differences with in vitro aspirin mirrored those seen in vivo. The treatment effect of ticagrelor was greater in European-Americans in response to ADP (p<0.05) but with collagen, the treatment effect was greater for African-Americans (p<0.05).
Conclusions:
Platelet reactivity was overall lower in African-Americans off-treatment, on aspirin, and on ticagrelor. European-Americans experienced greater platelet suppression on aspirin and on ticagrelor. The aspirin response difference in vivo and in vitro suggests a mechanism intrinsic to the platelet. Whether the absolute level of platelet reactivity or the degree of platelet suppression after treatment is more important for clinical outcomes is uncertain.
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Subjects:
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Pubmed ID:33159252
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Pubmed Central ID:PMC7889728
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