IntroductionGolden retrievers are over-represented in cases of taurine-deficient dilated cardiomyopathy and recently a surge in cases has prompted further investigation.ObjectiveTo describe the clinical, dietary, and echocardiographic features in golden retrievers diagnosed with taurine deficiency and dilated cardiomyopathy, and to determine specific dietary associations. A second aim was to determine the whole blood taurine concentrations in a representative sample of healthy golden retrievers.AnimalsTwenty-four client-owned golden retrievers with documented taurine deficiency and dilated cardiomyopathy and 52 healthy client-owned golden retrievers.MethodsIn this multicenter prospective observational study, baseline and follow-up echocardiographic data, complete diet and medical histories, and whole blood, plasma, or serum taurine concentrations were obtained. Baseline and follow-up echocardiographic data were compared. Associations were evaluated between specific diets and taurine deficiency or congestive heart failure. The prevalence of low whole blood taurine concentrations in the healthy golden retrievers was calculated.ResultsTwenty-three of 24 dogs diagnosed with taurine deficiency and dilated cardiomyopathy were fed diets that were either grain-free, legume-rich, or a combination of these factors. None of these diets were feeding trial tested using Association of American Feed Control Officials (AAFCO) procedures. Twenty-three of 24 dogs had significant improvement in their echocardiographic parameters and normalization of taurine concentrations following diet change and taurine supplementation. Nine of 11 dogs diagnosed with congestive heart failure (CHF) had resolution of their congestion at follow-up with five no longer requiring diuretic therapy and four tolerating diuretic dose reduction by >50%.ConclusionsCertain diets and diet characteristics were associated with the development of taurine deficiency. Taurine deficiency and dilated cardiomyopathy in golden retrievers is likely multifactorial, including a combination of dietary, metabolic, and genetic factors.

Introduction A surge in Food and Drug Administration (FDA) consumer complaints identified concerns that legume-rich, grain-free diets were associated with nutritionally-mediated dilated cardiomyopathy (DCM). Golden retrievers represent the most reported breed affected by this condition and previous studies documented the disease is responsive to dietary change and taurine supplementation. Although dietary findings across cases are compelling, prospective studies with control groups are lacking. The role of diet in developing taurine deficiency and echocardiographic changes consistent with DCM in healthy dogs is unknown. Objectives We hypothesized that golden retrievers eating non-traditional diets are at a higher risk of having taurine deficiency and nutritionally-mediated DCM compared with those eating traditional commercial diets. We aimed to compare taurine concentrations and echocardiographic indices of systolic function between golden retrievers in each diet group and elucidate associations between diet and these variables. Additionally, we aimed to generate breed-specific reference intervals for whole blood and plasma taurine concentrations. Animals 86 golden retrievers.

No abstract

OBJECTIVE To document outcomes of thoracoscopic treatment of idiopathic chylothorax (IC) in dogs with and without constrictive pericardial physiology (CPP) and evaluate patterns of chyle flow redistribution after thoracic duct ligation (TDL). ANIMALS 26 client-owned dogs. PROCEDURES In this prospective cohort study, echocardiography and cardiac catheterization were performed to document CPP in dogs with IC. Thoracoscopic TDL with pericardiectomy was performed if CPP was present (TDL/P group). Dogs without evidence of CPP underwent thoracoscopic TDL alone (TDL group). Dogs underwent preoperative, immediate postoperative, and 3-month postoperative CT lymphangiography studies when possible. Perioperative morbidity, resolution and late recurrence rates, and long-term outcome were recorded. RESULTS 17 dogs underwent TDL, and 9 underwent TDL/P. Twenty-five of 26 (96%) survived the perioperative period. One dog died from ventricular fibrillation during pericardiectomy. Resolution rates for TDL and TDL/P were 94% and 88%, respectively (P = .55), with 1 late recurrence occurring in the TDL group in a median follow-up of 25 months (range, 4 to 60 months). On 3-month postoperative CT lymphangiography studies, ongoing chyle flow past the ligation site was demonstrated in 5 of 17 dogs, of which 1 dog developed recurrence at 13 months postoperatively. In 15 of 17 dogs, chylous redistribution after TDL was principally by retrograde flow to the lumbar lymphatic plexus. CLINICAL RELEVANCE In dogs without evidence of CPP, TDL alone was associated with a very good prognosis for treatment of IC. In the absence of CPP, the additional benefit of pericardiectomy in the treatment of IC is questionable.

BackgroundThe teratogenic effects of immunomodulatory and certain antimicrobial therapies are described in small rodents and humans. While the described teratogenic effects in small rodents have been extrapolated to make conclusions about its use in the pregnant dam, teratogenic effects of prednisone and doxycycline have not yet been reported in the dog. Here we report and describe midline defects observed in a litter of golden retriever puppies exposed to mid-gestational immunosuppressive and antimicrobial therapy.Case presentationTwenty-one days into gestation, the dam of a litter of eight golden retriever puppies was administered prednisone, doxycycline, and tramadol as treatment for immune-mediated polyarthritis. The individuals in the litter were subsequently diagnosed with a variety of midline defects and congenital cardiac defects. This case series describes the variety of identified defects and presents a descriptive account of complex congenital abnormalities that are likely secondary to teratogenic effects of one or more drugs administered during gestation. The available puppies, dam, and grand dam underwent thorough physical examination, complete echocardiogram, and where indicated, advanced imaging with various surgical corrections when possible.Numerous midline congenital defects and congenital heart disease were identified in the puppies evaluated. Ultimately 5 of 8 puppies born to the dam were presented for thorough evaluation. The midline defects include: gastroschisis (1), peritoneopericardial diaphragmatic hernias (4, PPDH), umbilical hernia (4), unilateral cryptorchidism (1 of 4 males), cleft palate (1), renal agenesis (1), renal abnormalities (1), sternal and vertebral abnormalities (3), remnant liver lobe (1) and malformations consistent with ductal plate malformations with congenital hepatic fibrosis (1). The congenital cardiac defects include: ventricular septal defect (4, VSD) and subaortic stenosis (4, SAS). The presence of greater than one congenital defect was noted in all 5 of the dogs evaluated. Surgical correction was necessary for PPDH in 4 puppies. Medical intervention was recommended for congenital cardiac disease in 1 puppy.ConclusionThis case report is the first to describe midline defects in dogs that have been exposed to immunomodulatory therapy during gestation. A causative relationship between mid-gestational immunomodulatory exposure and midline defects cannot be proven, however, this case supports a clear association and provides case-based evidence to support its avoidance when possible.

We sought to establish a large animal model of inherited hypertrophic cardiomyopathy (HCM) with sufficient disease severity and early penetrance for identification of novel therapeutic strategies. HCM is the most common inherited cardiac disorder affecting 1 in 250–500 people, yet few therapies for its treatment or prevention are available. A research colony of purpose-bred cats carrying the A31P mutation in MYBPC3 was founded using sperm from a single heterozygous male cat. Cardiac function in four generations was assessed by periodic echocardiography and measurement of blood biomarkers. Results showed that HCM penetrance was age-dependent, and that penetrance occurred earlier and was more severe in successive generations, especially in homozygotes. Homozygosity was also associated with progression from preclinical to clinical disease. A31P homozygous cats represent a heritable model of HCM with early disease penetrance and a severe phenotype necessary for interventional studies aimed at altering disease progression. The occurrence of a more severe phenotype in later generations of cats, and the occasional occurrence of HCM in wildtype cats suggests the presence of at least one gene modifier or a second causal variant in this research colony that exacerbates the HCM phenotype when inherited in combination with the A31P mutation.

No abstract

BackgroundSotalol is a commonly used antiarrhythmic drug that may alter ventricular function.ObjectiveTo determine the effect of sotalol on echocardiographic indices of ventricular systolic function in dogs with ventricular arrhythmias.AnimalsThirty‐five client‐owned dogs with ventricular arrhythmias.MethodsDogs with ventricular arrhythmias (n = 27) had an echocardiogram and 5‐minute ECG performed at baseline and 2‐4 hours post‐sotalol (2‐2.5 mg/kg PO once). Eight additional dogs underwent the same protocol but did not receive sotalol (within‐day variability controls). Left ventricular (LV) internal dimension at end‐systole normalized to bodyweight (LVIDs_N), LV ejection fraction (LV EF), LV shortening area, LV fractional shortening, tricuspid annular plane systolic excursion (TAPSE), and right ventricular systolic myocardial velocity were evaluated as indices of systolic function.ResultsAll indices except TAPSE had mild decreases in systolic function post‐sotalol (all P ≤ .0007) compared with baseline but only the percent change in LVIDs_N and LV EF were significantly (P ≤ .0079) different from the percent change of the same indices in control dogs. Sinus heart rate, ventricular premature complexes/5‐minutes, and arrhythmia grade also were decreased post‐sotalol (all P ≤ .01) compared with baseline when assessed by a 5‐minutes ECG. No dog experienced an adverse event post‐sotalol, including dogs with systolic dysfunction or atrial enlargement.Conclusions and Clinical ImportanceA single dose of sotalol may cause a mild decrease in LV systolic function in dogs with ventricular arrhythmias. Sotalol appears to be well tolerated, even in dogs with atrial enlargement or systolic dysfunction.