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Platelet Activation and Clopidogrel Effects on ADP-Induced Platelet Activation in Cats with or without the A31P
1Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California Davis, Davis, CA. rhli@ucdavis.edu.
Insights
Clopidogrel effectively reduces platelet activation in most cats, though some individuals may not respond. Cats with the A31P mutation exhibit higher baseline platelet activation.
Area of Science:
- Veterinary Pharmacology
- Cardiovascular Research
- Platelet Biology
Background:
- Limited data exists on clopidogrel's antiplatelet effects in cats.
- Thromboembolic events are a concern in feline cardiovascular disease.
Purpose of the Study:
- To assess clopidogrel's impact on feline platelet responsiveness.
- To investigate the influence of the MYBPC3 gene's A31P mutation on clopidogrel efficacy.
- To characterize variability in cat platelet responses to clopidogrel.
Main Methods:
- An ex vivo study involving 14 healthy cats (8 with A31P mutation, 6 wild-type).
- Cats received clopidogrel (18.75 mg PO q24h) for 14 days.
- Evaluated adenosine diphosphate (ADP)-induced P-selectin expression, platelet aggregation (optical aggregometry), pVASP, and ADP receptor response index (ARRI).
Main Results:
- Clopidogrel attenuated ADP-induced P-selectin expression and platelet aggregation.
- Cats with the A31P mutation showed significantly increased platelet activation compared to wild-type cats.
- Significantly lower ARRI was observed post-clopidogrel treatment (P = .017).
- Two of 13 cats were identified as non-responders.
Conclusions:
- Clopidogrel is effective in reducing platelet activation and aggregation in a significant portion of cats.
- The A31P mutation is associated with heightened platelet activation, contributing to variable responses.
- Further research is needed to understand non-responder variability.
Background:
Clopidogrel is commonly prescribed to cats with perceived increased risk of thromboembolic events, but little information exists regarding its antiplatelet effects.
Objective:
To 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.
Animals:
Fourteen 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.
Methods:
Ex 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.
Results:
Platelet 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 PGE1 -treated platelets had a similar level of pVASP as PGE1 -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 Importance:
Clopidogrel 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.
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