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.

Background: Pimobendan has been shown to impart a significant survival benefit in cardiomyopathic cats who receive it as part of heart failure therapy. However, use of pimobendan remains controversial in cats with hypertrophic cardiomyopathy (HCM) due to lack of pharmacodynamic data for pimobendan in cats with HCM and due to theoretical concerns for exacerbating left ventricular outflow tract obstructions.Hypothesis/Objectives: Our objective was to investigate the cardiac effects of pimobendan in cats with HCM. We hypothesized that pimobendan would not exacerbate left ventricular outflow tract obstructions and that it would improve echocardiographic measures of diastolic function.Animals: Thirteen purpose-bred cats were studied from a research colony with naturally-occurring HCM due to a variant in myosin binding protein C.Methods: Cats underwent two examinations 24 h apart with complete standard echocardiography. On their first day of evaluation, they were randomized to receive oral placebo or 1.25 mg pimobendan 1 h prior to exam. On their second examination, they were crossed over and received the remaining treatment. Investigators were blinded to all treatments.Results: The pimobendan group had a significant increase in left atrial fractional shortening (pimobendan group 41.7% ± 5.9; placebo group 36.1% ± 6.0; p = 0.04). There was no significant difference in left ventricular outflow tract (LVOT) velocities between the groups (pimobendan group 2.8 m/s ± 0.8; placebo group 2.6 m/s ± 1.0). There were no significant differences between the number of cats with LVOT obstructions between groups (12 in pimobendan group; 11 in placebo group; p = 1.00). There were no detectable differences in any systolic measures, including left ventricular fractional shortening, mitral annular plane systolic excursion, and tricuspid annular plane systolic excursion. Doppler-based diastolic function assessment was precluded by persistent tachycardia.Conclusions: Improved left atrial function in the pimobendan group could explain some of the reported survival benefit for HCM cats in CHF. Pimobendan did not exacerbate LVOT obstructions and thus may not be contraindicated in HCM cats with LVOT obstructions. Future studies are needed to better characterize other physiologic effects, particularly regarding diastolic function assessment, and to better assess safety of pimobendan over a longer time-course.

Subvalvular aortic stenosis (SAS) and valvular pulmonic stenosis (PS) are two of the most common congenital heart diseases of dogs. The aim of this study was to determine the prevalence and mode of inheritance of these congenital heart diseases in a large veterinary teaching hospital population. Case records of dogs presented to the University of California Davis, Veterinary Medical Teaching Hospital (UCD VMTH) between January 2008 to December 2017 were reviewed retrospectively and pedigree information was obtained when available. There were 259 unique SAS and 336 unique PS cases diagnosed during the study period. The prevalence of SAS was 0.3% of overall hospital admissions and 4.7% for all dogs seen by the cardiology service. The prevalence for PS was 0.41% of overall hospital admissions and 6.1% of dogs seen by the cardiology service. Bullmastiffs and Newfoundlands had the greatest prevalence (6.59 and 4.46%, respectively) and odds ratio (52.43 and 34.73, respectively) for SAS. Bulldogs and French Bulldogs had the greatest prevalence (4.8 and 2.7%, respectively) and odds ratio (13.32 and 7.52, respectively) for PS. The identified prevalence of SAS and PS is higher than previously reported. Pedigree analysis in SAS affected Bullmastiffs, Golden Retrievers, and Rottweilers suggested an autosomal recessive pattern of inheritance. The mode of inheritance for PS in Bulldogs, also appears to be autosomal recessive. The results of this study can be used to inform future selection of breeding pairs and genetic studies aimed at reducing the prevalence of these common congenital heart diseases.

Coronary artery anomalies have been reported in Bulldogs and present an increased risk when performing balloon valvuloplasty. Identification of coronary anomalies has been reported using multidetector‐row computed tomographic (MDCT) angiography with electrocardiographic gating. However, the utility of non‐electrocardiographic‐gated 16‐row computed tomographic for MDCT for the identification of coronary artery anatomy or anomalies to the authors’ knowledge has not been fully investigated. The purpose of this study was to evaluate the feasibility of non‐electrocardiographic‐gated computed tomographic (CT) angiography to identify coronary anomalies in Bulldogs with pulmonary valve stenosis. In this prospective, observational study, Bulldogs with echocardiographically diagnosed pulmonary valve stenosis, an echocardiographically derived transpulmonic pressure gradient >70 mm Hg, and a clinician recommendation for balloon valvuloplasty were included. Anesthetized dogs underwent a 16‐row MDCT non‐electrocardiographic‐gated CT angiography. A board‐certified veterinary radiologist and board‐certified veterinary cardiologist reviewed the CT angiography studies and identified the coronary artery anatomy. When normal coronary artery anatomy was detected on CT angiography, a right ventricular outflow tract fluoroscopic angiogram was performed and evaluated during levophase to confirm normal coronary anatomy prior to balloon valvuloplasty. Dogs with coronary anomalies noted on CT angiography were recovered from anesthesia and balloon valvuloplasty was not performed. All dogs (10/10; 100%) had interpretable images from the non‐electrocardiographic‐gated CT angiography. Coronary anomalies were identified in six dogs based on non‐electrocardiographic‐gated CT angiography, five with type R2A anomaly and one had a single left coronary ostium. Four dogs had normal coronary anatomy based on non‐electrocardiographic‐gated CT angiography. Balloon valvuloplasty was performed without incident in these four dogs. We conclude that non‐electrocardiographic‐gated CT angiography represents a noninvasive method for diagnosing coronary anomalies in Bulldogs with pulmonary valve stenosis.

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