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Platelet Activation and Clopidogrel Effects on ADP-Induced Platelet Activation in Cats with or without the A31P Mutation in MYBPC3

Background: Clopidogrel is commonly prescribed to cats with perceived increased risk of thromboembolic events, but little information exists regarding its antiplatelet effects. ObjectiveTo determine effects of clopidogrel on platelet responsiveness in cats with or without the A31P mutation in the MYBPC3 gene. A secondary aim was to characterize variability in feline platelet responses to clopidogrel. AnimalsFourteen healthy cats from a Maine Coon/outbred mixed Domestic cat colony: 8 cats homozygous for A31P mutation in the MYPBC3 gene and 6 wild-type cats without the A31P mutation. MethodsEx vivo study. All cats received clopidogrel (18.75 mg PO q24h) for 14 days. Before and after clopidogrel treatment, adenosine diphosphate (ADP)-induced P-selectin expression was evaluated. ADP- and thrombin-induced platelet aggregation was measured by optical aggregometry (OA). Platelet pVASP and ADP receptor response index (ARRI) were measured by Western blot analysis. ResultsPlatelet activation from cats with the A31P mutation was significantly (P = .0095) increased [35.55% (18.58-48.55) to 58.90% (24.85-69.90)], in response to ADP. Clopidogrel treatment attenuated ADP-induced P-selectin expression and platelet aggregation. ADP- and PGE(1)-treated platelets had a similar level of pVASP as PGE(1)-treated platelets after clopidogrel treatment. Clopidogrel administration resulted in significantly lower ARRI [24.13% (12.46-35.50) to 11.30% (-7.383 to 23.27)] (P = .017). Two of 13 cats were nonresponders based on OA and flow cytometry. Conclusion and Clinical ImportanceClopidogrel is effective at attenuating platelet activation and aggregation in some cats. Cats with A31P mutation had increased platelet activation relative to the variable response seen in wild-type cats.

Identiferoai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/622355
Date09 1900
CreatorsLi, R.H.L., Stern, J.A., Ho, V., Tablin, F., Harris, S.P.
ContributorsUniv Arizona, Coll Med, Dept Cellular & Mol Med, Department of Anatomy, Physiology and Cell Biology; School of Veterinary Medicine; University of California Davis; Davis CA, Department of Medicine and Epidemiology; School of Veterinary Medicine; University of California Davis; Davis CA, Department of Anatomy, Physiology and Cell Biology; School of Veterinary Medicine; University of California Davis; Davis CA, Department of Anatomy, Physiology and Cell Biology; School of Veterinary Medicine; University of California Davis; Davis CA, Department of Cellular and Molecular Medicine; College of Medicine; University of Arizona; Tucson AZ
PublisherWILEY-BLACKWELL
Source SetsUniversity of Arizona
LanguageEnglish
Detected LanguageEnglish
TypeArticle
RightsCopyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License
Relationhttp://doi.wiley.com/10.1111/jvim.14568

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