No impact of polymorphism in the phosphodiesterase 5A gene in Cavalier King Charles Spaniels on pimobendan‐induced inhibition of platelet aggregation response

Autor: Maria J. Reimann, Daniel N. Faisst, Mads Knold, Kathryn M. Meurs, Joshua A. Stern, Signe E. Cremer, Jacob E. Møller, Ingrid Ljungvall, Jens Häggström, Lisbeth H. Olsen
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: Journal of Veterinary Internal Medicine, Vol 37, Iss 6, Pp 2145-2156 (2023)
Druh dokumentu: article
ISSN: 1939-1676
0891-6640
DOI: 10.1111/jvim.16871
Popis: 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
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