Background: The United States Food and Drug Administration is investigating possible diet-associated dilated cardiomyopathy (DCM) in dogs and cats. Objectives: To retrospectively review DCM cases for signalment, diet information, echocardiographic changes, and survival.

Background Recent studies have investigated dogs with presumed diet‐associated dilated cardiomyopathy (daDCM), but prospective studies of multiple breeds are needed. Hypothesis/Objectives To evaluate baseline features and serial changes in echocardiography and cardiac biomarkers in dogs with DCM eating nontraditional diets (NTDs) or traditional diets (TDs), and in dogs with subclinical cardiac abnormalities (SCA) eating NTD. Animals Sixty dogs with DCM (NTD, n = 51; TDs, n = 9) and 16 dogs with SCA eating NTDs. Methods Echocardiography, electrocardiography, and measurement of taurine, cardiac troponin I, and N‐terminal pro‐B‐type natriuretic peptide were performed in dogs with DCM or SCA. Diets were changed for all dogs, taurine was supplemented in most, and echocardiography and cardiac biomarkers were reassessed (3, 6, and 9 months). Results At enrollment, there were few differences between dogs with DCM eating NTDs or TDs; none had low plasma or whole blood taurine concentrations. Improvement in fractional shortening over time was significantly associated with previous consumption of a NTD, even after adjustment for other variables (P = .005). Median survival time for dogs with DCM was 611 days (range, 2‐940 days) for the NTD group and 161 days (range, 12‐669 days) for the TD group (P = .21). Sudden death was the most common cause of death in both diet groups. Dogs with SCA also had significant echocardiographic improvements over time. Conclusions and Clinical Importance Dogs with DCM or SCA previously eating NTDs had small, yet significant improvements in echocardiographic parameters after diet changes.

BackgroundPathophysiologic mechanisms for the development and progression of degenerative mitral valve disease (DMVD) remain elusive. Increased concentrations of circulating trimethylamine N‐oxide (TMAO) and its precursors choline and l‐carnitine are associated with the presence and severity of heart disease in people.ObjectivesTo determine if differences exist in plasma concentrations of TMAO, choline, or l‐carnitine among dogs with DMVD and congestive heart failure (CHF), dogs with asymptomatic DMVD, and healthy control dogs.AnimalsThirty client‐owned dogs: 10 dogs with CHF secondary to DMVD, 10 dogs with asymptomatic DMVD, and 10 healthy control dogs.MethodsA pilot cross‐sectional study in which echocardiography was performed and fasting plasma concentrations of TMAO, choline, and l‐carnitine (total and fractions) were measured.ResultsTMAO (P = .03), total l‐carnitine (P = .03), carnitine esters (P = .05), and carnitine esters to free carnitine ratio (E/F ratio; P = .05) were significantly higher in dogs with CHF compared to those with asymptomatic DMVD. TMAO (P = .02), choline (P = .01), total l‐carnitine (P = .01), carnitine esters (P = .02), free carnitine (P = .02), and E/F ratio (P = .009) were significantly higher in dogs with CHF compared to healthy controls.Conclusions and Clinical ImportanceDogs with CHF secondary to DMVD had higher concentrations of TMAO compared to both asymptomatic DMVD dogs and healthy controls. Larger prospective studies are warranted to determine if TMAO plays a role in the development or progression of DMVD or CHF.

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Background There is a lack of clinical data on hypertrophic cardiomyopathy (HCM) in dogs. Hypothesis/Objectives To investigate signalment, clinical signs, diagnostic findings, and survival in dogs with HCM. Animals Sixty‐eight client‐owned dogs. Methods Retrospective multicenter study. Medical records were searched between 2003 and 2015. The diagnosis of left ventricular (LV) hypertrophy was made by echocardiographic examination. Results Three hundred and forty‐five dogs with LV hypertrophy were identified, of which 277 were excluded. The remaining 68 dogs were 0.3 to 14 years old and predominantly <10 kg (85%), and without a sex predilection. Twenty‐four % were Shih Tzu and 24% terrier breeds. Most (80%) had a systolic heart murmur. Owner‐determined exercise intolerance (37%) and syncope (18%) were most commonly reported signs. The majority (84%) of dogs had symmetrical LV hypertrophy, whereas asymmetrical septal and LV free wall hypertrophy was observed in 9% and 6% of dogs, respectively. Isolated basal interventricular septal hypertrophy was not observed. Commonly recorded were systolic anterior motion of the mitral valve (60%) and LV diastolic dysfunction (89% of dogs where diastolic function was evaluated). Six dogs died unexpectedly, and 3 developed congestive heart failure. Known survival times were between 1 day and 114 months after diagnosis. Conclusions and Clinical Importance Hypertrophic cardiomyopathy in dogs should be considered as a differential diagnosis if LV hypertrophy is identified. Small breed dogs are overrepresented, and it is uncommon for dogs with HCM to develop CHF although sudden death can occur.