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PEER REVIEWED 70 JULY/AUGUST 2018 REVIEWED PEER Pimobendan is a benzimidazole-pyridazinone derivative, labeled for use in dogs to manage congestive heart failure (CHF) resulting from dilated cardiomyopathy (DCM) or degenerative mitral valve disease (DMVD) in the United States. On the basis of its positive inotropic effects combined with arteriovenous dilation, it is classified as an inodilator. 1 In this article, we provide relevant information about the pharmacology of pimobendan based on a review of the literature providing evidence to support its use for a variety of indications. As additional research is published, the indications and recommended uses for pimobendan continue to evolve. FORMULATION AND DOSING Pimobendan is available as Vetmedin ( vetmedin. com ) in oblong, half-scored chewable tablets (1.25 mg, 2.5 mg, 5 mg, or 10 mg). Because the stability and efficacy of the drug in suspension are unknown, reformulating as an oral suspension should be avoided. In some countries outside of the United States, an intravenous preparation is available. For dogs, the labeled dosage recommendation for pimobendan is 0.25 to 0.3 mg/kg PO q12h. The total daily dose can be administered in 2 unequal portions by using whole or half tablets. For initial use, especially if a more rapid onset of action is desired, the tablets should be administered on an empty stomach; however, for more chronic use, they can be administered with food. In dogs and cats, the oral preparation is rapidly absorbed; peak effect occurs within 2 to 4 hours in dogs and 0.9 hours in cats. 1,2 MECHANISMS OF ACTION Increased Cardiac Contractility The positive inotropic effects of pimobendan are mediated through a combination of 1) increased cyclic adenosine monophosphate mediated by phosphodiesterase III (PDEIII) inhibition, and 2) sensitization of the cardiac contractile apparatus to intracellular calcium. Calcium sensitization results in a positive inotropic effect without increasing myocardial oxygen demand. Vasodilation Balanced vasodilatory effects are mediated predominately through PDEIII inhibition in arterial Pimobendan and Heart Disease Ashley B. Saunders, DVM, DACVIM (Cardiology) Sonya G. Gordon, DVM, DVSc, DACVIM (Cardiology) FOCUS ON

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