Background Pimobendan is effective in treatment of dogs with congestive heart failure (CHF) secondary to myxomatous mitral valve disease (MMVD). Its effect on dogs before the onset of CHF is unknown. Hypothesis/Objectives Administration of pimobendan (0.4–0.6 mg/kg/d in divided doses) to dogs with increased heart size secondary to preclinical MMVD, not receiving other cardiovascular medications, will delay the onset of signs of CHF, cardiac‐related death, or euthanasia. Animals 360 client‐owned dogs with MMVD with left atrial‐to‐aortic ratio ≥1.6, normalized left ventricular internal diameter in diastole ≥1.7, and vertebral heart sum >10.5. Methods Prospective, randomized, placebo‐controlled, blinded, multicenter clinical trial. Primary outcome variable was time to a composite of the onset of CHF, cardiac‐related death, or euthanasia. Results Median time to primary endpoint was 1228 days (95% CI: 856–NA) in the pimobendan group and 766 days (95% CI: 667–875) in the placebo group (P = .0038). Hazard ratio for the pimobendan group was 0.64 (95% CI: 0.47–0.87) compared with the placebo group. The benefit persisted after adjustment for other variables. Adverse events were not different between treatment groups. Dogs in the pimobendan group lived longer (median survival time was 1059 days (95% CI: 952–NA) in the pimobendan group and 902 days (95% CI: 747–1061) in the placebo group) (P = .012). Conclusions and Clinical Importance Administration of pimobendan to dogs with MMVD and echocardiographic and radiographic evidence of cardiomegaly results in prolongation of preclinical period and is safe and well tolerated. Prolongation of preclinical period by approximately 15 months represents substantial clinical benefit.

Background: Published information regarding survival and long-term cardiac remodeling after patent ductus arteriosus (PDA) closure in dogs is limited. Objectives: To report outcome and identify prognostic variables in dogs with PDA, and to identify risk factors for persistent remodeling in dogs with a minimum of 12 months of follow-up after closure. Animals: Five hundred and twenty client-owned dogs. Methods: Retrospective review of medical records of 520 dogs with PDA. Outcome was determined by contacting owners and veterinarians. Dogs with PDA closure and ≥ 12 months of follow-up were asked to return for a re-evaluation. Results: In multivariable analysis of 506 dogs not euthanized at the time of diagnosis, not having a PDA closure procedure negatively affected survival (HzR = 16.9, P < .001). In 444 dogs undergoing successful PDA closure, clinical signs at presentation (HzR = 17, P = .02), concurrent congenital heart disease (HD) (HzR = 4.8, P = .038), and severe mitral regurgitation (MR) documented within 24 hours of closure (HzR = 4.5, P = .028) negatively affected survival. Seventy-one dogs with ≥ 12 months follow-up demonstrated a significant reduction in radiographic and echocardiographic measures of heart size (P = 0) and increased incidence of acquired HD (P = .001) at re-evaluation. Dogs with increased left ventricular size and low fractional shortening at baseline were more likely to have persistent remodeling at re-evaluation. Conclusions and Clinical Importance: Patent ductus arteriosus closure confers important survival benefits and results in long-term reverse remodeling in most dogs. Clinical signs at presentation, concurrent congenital HD, and severe MR negatively affect survival. Increased left ventricular systolic dimensions and systolic dysfunction at baseline correlated significantly with persistent remodeling.

Background: Transarterial ductal occlusion with the Amplatzer vascular plug was first reported in dogs by Hogan et al in 2005. Hypothesis: Use of the Amplatzer vascular plug is a safe, efficacious method of patent ductus arteriosus (PDA) occlusion. Animals: Thirty-one client-owned dogs with PDA. Methods: Records of 31 dogs in which transarterial occlusion of PDA with an Amplatzer vascular plug was attempted were reviewed. Results: All dogs had a type II PDA, with 27 dogs having type IIA morphology and 4 dogs having type IIB morphology. Appropriate device deployment was achieved in 29 of 31 dogs. Postdeployment angiography in 21 dogs documented complete occlusion in 10 dogs, trivial residual flow in 5 dogs, mild residual flow in 2 dogs, moderate residual flow in 3 dogs, and severe residual flow in 1 dog. Transthoracic color Doppler echocardiography documented complete occlusion in 22 dogs, whereas 2 dogs had trivial residual flow, 2 dogs had mild residual flow, 2 dogs had mild to moderate residual flow, and 1 dog had severe residual flow. Of the 7 dogs with residual flow, 2 had complete occlusion 2–4 months postoperatively, 1 had moderate residual flow 1 month postoperatively, and 4 were lost to follow-up. One dog required a larger device than was able to be deployed through the largest sheath placed in the femoral artery. Pulmonary embolization of the device occurred in 1 dog. Conclusion: We conclude that ductal occlusion with an Amplatzer vascular plug is a safe and efficacious therapy for PDA in dogs.