BackgroundPimobendan 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/ObjectivesAdministration 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.Animals360 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.MethodsProspective, 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.ResultsMedian 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 ImportanceAdministration 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.

BackgroundChanges in clinical variables associated with the administration of pimobendan to dogs with preclinical myxomatous mitral valve disease (MMVD) and cardiomegaly have not been described.ObjectivesTo investigate the effect of pimobendan on clinical variables and the relationship between a change in heart size and the time to congestive heart failure (CHF) or cardiac‐related death (CRD) in dogs with MMVD and cardiomegaly. To determine whether pimobendan‐treated dogs differ from dogs receiving placebo at onset of CHF.AnimalsThree hundred and fifty‐four dogs with MMVD and cardiomegaly.Materials and MethodsProspective, blinded study with dogs randomized (ratio 1:1) to pimobendan (0.4–0.6 mg/kg/d) or placebo. Clinical, laboratory, and heart‐size variables in both groups were measured and compared at different time points (day 35 and onset of CHF) and over the study duration. Relationships between short‐term changes in echocardiographic variables and time to CHF or CRD were explored.ResultsAt day 35, heart size had reduced in the pimobendan group: median change in (Δ) LVIDDN −0.06 (IQR: −0.15 to +0.02), P < 0.0001, and LA:Ao −0.08 (IQR: −0.23 to +0.03), P < 0.0001. Reduction in heart size was associated with increased time to CHF or CRD. Hazard ratio for a 0.1 increase in ΔLVIDDN was 1.26, P = 0.0003. Hazard ratio for a 0.1 increase in ΔLA:Ao was 1.14, P = 0.0002. At onset of CHF, groups were similar.Conclusions and Clinical ImportancePimobendan treatment reduces heart size. Reduced heart size is associated with improved outcome. At the onset of CHF, dogs treated with pimobendan were indistinguishable from those receiving placebo.

Abbreviations: BPM, beats per minute; BW, body weight; CHF, congestive heart failure; EPIC, Evaluation of pimobendan in dogs with cardiomegaly caused by preclinical myxomatous mitral valve disease; HR, heart rate; IQR, inter quartile range; LA/Ao, left atrial-to-aortic root ratio; LVIDDN, left ventricular internal diameter in diastole-normalized; MMVD, myxomatous mitral valve disease; MR, mitral regurgitation; RR, respiratory rate (in clinic); RRR, resting respiratory rate (owner measured); RT, rectal temperature; VHS, vertebral heart sum. AbstractBackground: The Evaluation of pimobendan in dogs with cardiomegaly caused by preclinical myxomatous mitral valve disease (EPIC) study monitored dogs with myxomatous mitral valve disease (MMVD) as they developed congestive heart failure (CHF).Objectives: To describe the changes in clinical and radiographic variables occurring as dogs with MMVD and cardiomegaly develop CHF, compared to similar dogs that do not develop CHF.Animals: One hundred and thirty-five, and 73 dogs that did or did not develop CHF, respectively. Materials and methods:The following variables were evaluated in 2 groups of dogs (dogs that did or did not develop CHF): Heart rate (HR), clinic respiratory rate (RR), home-measured resting respiratory rate (RRR), rectal temperature (RT), body weight (BW), and vertebral heart sum (VHS). Absolute value and rate of change of each variable were calculated for each day a dog was in study. Daily means were calculated and plotted against time. The onset of CHF or last visit before leaving the study were set as reference time points.Results: The most extreme values and rate of change occurred in variables immediately before onset of CHF. Vertebral heart sum increased earliest. Heart rate, RR, and RRR also increased. Rectal temperature and BW decreased. Increases in RR and RRR were most extreme and occurred immediately before CHF.Conclusions and Clinical Importance: Dogs with MMVD and cardiomegaly experience increases in HR, RR, RRR, and VHS, and decreases in BW and RT as they develop CHF. The variables with highest absolute change and rate of change were

The VVTI is a useful index, obtained from a standard ECG recording that estimates HRV in dogs and does not require any specific equipment for its calculation. It can be useful as a diagnostic tool to assess the severity of HF and is a useful prognostic tool in dogs with DCM.

A 10-year-old male cairn terrier cross was presented with a history of myxomatous mitral valve disease diagnosed six months previously and with a four-week history of intermittent collapse. On 24 hour electrocardiograph (Holter) analysis, periods of no discernable electrical cardiac activity, which coincided with three collapsing episodes, were identified. Unfortunately, on re-presentation for removal of the Holter monitor, the dog collapsed and died. A post-mortem examination was conducted, and histology of the right and left atrium showed evidence of myocarditis. This is the first reported case, to our knowledge, of collapse because of electrical asystole in a dog with atrial myocarditis.