Peer-reviewed veterinary case report
Pimobendan's effect on blood clotting not changed by gene in Cavalier
By Reimann, Maria J et al.·Published in Journal of veterinary internal medicine·2023·Department of Veterinary and Animal Sciences·View original on PubMed →
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Original publication title: No impact of polymorphism in the phosphodiesterase 5A gene in Cavalier King Charles Spaniels on pimobendan-induced inhibition of platelet aggregation response.
- Species:
- dog
Plain-English summary
A study involving 52 Cavalier King Charles Spaniels found that a specific genetic variant (PDE5A:E90K) did not affect how well the medication pimobendan worked to reduce platelet clumping in their blood. Pimobendan is often used to treat heart issues like myxomatous mitral valve disease (MMVD) in dogs. The dogs were tested for their platelet function before and after receiving the medication, and the results showed that pimobendan effectively inhibited platelet aggregation regardless of the genetic variant. This means that dogs with this genetic variant can still benefit from pimobendan treatment without any concerns about altered platelet function.
People also search for: Cavalier King Charles Spaniel heart disease treatment · pimobendan for dogs · dog platelet aggregation test
Abstract
BACKGROUND: A variant in the canine phosphodiesterase (PDE) 5A gene (PDE5A:E90K) is associated with decreased concentrations of circulating cyclic guanosine monophosphate (cGMP) and response to PDE5 inhibitor treatment. Pimobendan is a PDE inhibitor recommended for medical treatment of certain stages of myxomatous mitral valve disease (MMVD) in dogs. HYPOTHESIS: PDE5A:E90K polymorphism attenuates the inhibitory effect of pimobendan on in vitro platelet aggregation and increases basal platelet aggregation in Cavalier King Charles Spaniels (CKCS). Selected clinical variables (MMVD severity, sex, age, hematocrit, platelet count in platelet-rich plasma [PRP], and echocardiographic left ventricular fractional shortening [LV FS]) will not show an association with results. ANIMALS: Fifty-two privately owned CKCS with no or preclinical MMVD. METHODS: Using blood samples, we prospectively assessed PDE5A genotype using Sanger sequencing and adenosine diphosphate-induced platelet aggregation response (area under the curve [AUC], maximal aggregation [MaxA], and velocity [Vel]) with and without pimobendan using light transmission aggregometry. Dogs also underwent echocardiography. RESULTS: Pimobendan inhibited platelet function as measured by AUC, MaxA, and Vel at a concentration of 10 μM (P < .0001) and Vel at 0.03 μM (P < .001). PDE5A:E90K polymorphism did not influence the inhibitory effect of pimobendan or basal platelet aggregation response. CONCLUSIONS AND CLINICAL IMPORTANCE: The PDE5A:E90K polymorphism did not influence in vitro basal platelet aggregation response or the inhibitory effect of pimobendan on platelet aggregation in CKCS. Dogs with the PDE5A:E90K polymorphism did not appear to have altered platelet function or response to pimobendan treatment.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/37743723/