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Cardiomyopathies are a heterogeneous group of myocardial disorders of mostly unknown etiology, and they occur commonly in cats. In some cats, they are well-tolerated and are associated with normal life expectancy, but in other cats they can result in congestive heart failure, arterial thromboembolism or sudden death. Cardiomyopathy classification in cats can be challenging, and in this consensus statement we outline a classification system based on cardiac structure and function (phenotype). We also introduce a staging system for cardiomyopathy that includes subdivision of cats with subclinical cardiomyopathy into those at low risk of life-threatening complications and those at higher risk. Based on the available literature, we offer recommendations for the approach to diagnosis and staging of cardiomyopathies, as well as for management at each stage.

Background: The presence and intensity of heart murmurs are sensitive indicators of several cardiac diseases in dogs, particularly myxomatous mitral valve disease (MMVD), but accurate interpretation requires substantial clinical expertise. Objectives: Assess if a machine‐learning algorithm can be trained to accurately detect and grade heart murmurs in dogs and detect cardiac disease in electronic stethoscope recordings. Animals: Dogs (n = 756) with and without cardiac disease attending referral centers in the United Kingdom. Methods: All dogs received full physical and echocardiographic examinations by a cardiologist to grade any murmurs and identify cardiac disease. A recurrent neural network algorithm, originally trained for heart murmur detection in humans, was fine‐tuned on a subset of the dog data to predict the cardiologist's murmur grade from the audio recordings. Results: The algorithm detected murmurs of any grade with a sensitivity of 87.9% (95% confidence interval [CI], 83.8%‐92.1%) and a specificity of 81.7% (95% CI, 72.8%‐89.0%). The predicted grade exactly matched the cardiologist's grade in 57.0% of recordings (95% CI, 52.8%‐61.0%). The algorithm's prediction of loud or thrilling murmurs effectively differentiated between stage B1 and B2 preclinical MMVD (area under the curve [AUC], 0.861; 95% CI, 0.791‐0.922), with a sensitivity of 81.4% (95% CI, 68.3%‐93.3%) and a specificity of 73.9% (95% CI, 61.5%‐84.9%). Conclusion and Clinical Importance: A machine‐learning algorithm trained on humans can be successfully adapted to grade heart murmurs in dogs caused by common cardiac diseases, and assist in differentiating preclinical MMVD. The model is a promising tool to enable accurate, low‐cost screening in primary care. [ABSTRACT FROM AUTHOR]

Background: The proportion of cats with hypertrophic cardiomyopathy (HCM) that lose systolic anterior motion of the mitral valve (SAM) in the long term is unknown. Hypothesis/Objectives: Cats with HCM will lose SAM in the long term. Loss of SAM will be associated with greater age, longer scan‐interval, and altered left ventricular (LV) dimensions. Animals: Sixty unsedated cats with HCM, not receiving beta blockers or pimobendan. Methods: A retrospective cohort study from 2 referral centers. Cats were eligible if they had been diagnosed with HCM and had a repeat echocardiogram ≥1 year later. Clinical and echocardiographic data of the left heart variables were collected. Results: Thirty‐eight cats had SAM at the initial scan. After a median follow‐up time of 2.1 years (range: 1.0‐5.9), 7 cats had lost SAM (18%) and 5 cats (23%) gained SAM. On follow‐up, cats with SAM at the initial scan had a larger left atrium (P =.037), lower left atrial fractional shortening (P =.014), greater LV internal diameter in end‐systole (P =.002), and lower LV fractional shortening (P <.001). Four cats with SAM developed congestive heart failure. There were no new cases of congestive heart failure or change in left heart variables in cats without SAM at the initial scan. The gain or loss of SAM was not associated with age or time between scans. Conclusions and Clinical Importance: Similar proportions of cats gained or lost SAM. Cats with SAM at baseline had more evidence of disease progression than cats without SAM. [ABSTRACT FROM AUTHOR]

Simple Summary: A variation in the Alström syndrome protein 1 (ALMS1) gene was recently identified as a possible cause of hypertrophic cardiomyopathy (HCM) in Sphynx cats. The primary aims of this study were to describe the prevalence of HCM in Sphynx cats in New Zealand, and to assess the association between HCM and ALMS1 gene. In this prospective study, 55 apparently healthy Sphynx cats from registered Sphynx breeders and pet owners in New Zealand were screened by a cardiologist. A total of 42 of these cats had a repeat cardiac examination after median 1.8 years (range: 1.6–2.2). The frequency of ALMS1 variant was 70.9%. At the median age of 5.8 years (range: 2.4–13.1), the prevalence of HCM was 40% (20 out of 55 cats). Three cats with HCM died during the study with congestive heart failure. Necropsy revealed that all three cats suffered a heart attack (myocardial ischemia or infarction). The ALMS1 gene was not associated with the HCM diagnosis. In summary, HCM is commonly diagnosed in this population, suggesting Sphynx cats are predisposed to this disease. The ALMS1 variant was also frequently detected; however, it was not associated with the HCM diagnosis in the studied population. Recently, hypertrophic cardiomyopathy (HCM) in Sphynx cats has been associated with a variant in the gene encoding Alström syndrome protein 1 (ALMS1). The primary aims of this study were to describe the prevalence of HCM in Sphynx cats in New Zealand, and to assess the association between HCM and the ALMS1 variant in this population. In this prospective study, 55 apparently healthy Sphynx cats from registered Sphynx breeders and pet owners in New Zealand were screened by a cardiologist. A total of 42 of these cats had a repeat cardiac examination after median 1.8 years (range: 1.6–2.2). The frequency of the ALMS1 variant was 70.9% (11 homozygous and 28 heterozygous). At the median age of 5.8 years (range: 2.4–13.1), the prevalence of HCM was 40% (20 out of 55 cats). Three cats with HCM died during the study with congestive heart failure. All three cats had focal but extensive myocardial ischemia or infarction at necropsy. The ALMS1 variant was not associated with the HCM diagnosis. In summary, HCM was common in the studied cohort, suggesting Sphynx cats are predisposed to this disease. While the ALMS1 variant was also frequently detected, it was not associated with HCM in this population. [ABSTRACT FROM AUTHOR]

Mitral valve degeneration (MVD) is the most common form of heart disease in dogs, frequently leading to left-sided congestive heart failure and cardiac mortality. Although breed-specific disease characteristics and overrepresentation point towards a genetic origin for MVD, a causative mutation and complete molecular pathogenesis are unknown. Whippet dogs are overrepresented in incidence of MVD, suggesting an inherited component in this breed. Expressivity of this condition is variable with some dogs showing evidence of more severe disease at earlier ages than other dogs. This phenomenon makes a traditional case versus control genetic study prone to phenotyping error. This study sought to avoid these common pitfalls by identifying genetic loci associated with severity of MVD in Whippets through a genome-wide association study (GWAS). 138 Whippet dogs were characterized for MVD by echocardiographic examination and a novel disease severity score was developed and adjusted for age in each subject. Single nucleotide polymorphism (SNP) genotype data (170k Illumina CanineHD SnpChip) was obtained for DNA isolated from blood of each study subject. Continuous variable genome wide association was performed after correction for population stratification by efficient mixed model association expedited (EMMAX) in 130 dogs. A genome wide significant association was identified on chromosome 15 (peak locus 57,770,326; Padj = 0.049) and secondary loci of suggestive association were identified on chromosome 2 (peak locus 37,628,875; Padj = 0.079). Positional candidate genes were identified within the primary and secondary loci including follistatin-related protein 5 precursor (FSTL5) and Rho GTPase-activating protein 26 (ARHGAP26). These results support the hypothesis that severity of MVD in whippets has a genetic basis and warrants further study by either candidate gene sequencing or next-generation techniques.

Objective: To describe arrhythmias associated with administration of lidocaine in dogs treated for supraventricular tachyarrhythmias. Case summaries: Four dogs with recent‐onset supraventricular tachyarrhythmias: 3 dogs had atrial fibrillation (AF), and 1 had focal atrial tachycardia (FAT), which was thought to be AF at the time of assessment. The substrate of the supraventricular tachyarrhythmia was considered to be due to primary cardiomyopathy in 1 dog, high vagal tone in 2 dogs, and the change in hemodynamics from heavy sedation in 1 dog. Pharmacological cardioversion using lidocaine was only successful in the 2 dogs with vagally mediated AF. In these 2 cases, lidocaine administration resulted in a paroxysmal atrial flutter that was self‐limiting and quickly led to sinus rhythm within 10 seconds in 1 dog but did not change over a 5‐minute interval and required additional boluses in another dog. In the latter case, the dog showed severe bradycardia for 17.5 seconds prior to achieving sinus rhythm. The 2 unsuccessful cases both developed ventricular arrhythmias shortly after the lidocaine administration, with 1 case degenerating into ventricular fibrillation and cardiac arrest. New or unique information provided: Arrhythmias associated with lidocaine should be considered when treating dogs with supraventricular tachyarrhythmia. [ABSTRACT FROM AUTHOR]

Norwegian Forest cats (NFCs) are often listed as a breed predisposed to cardiomyopathy, but the characteristics of cardiomyopathy in this breed have not been described. The aim of this preliminary study was to report the features of NFC cardiomyopathy based on prospective echocardiographic screening of affected family groups; necropsy findings; and open-source breed screening databases. Prospective examination of 53 NFCs revealed no murmur or left ventricular (LV) outflow tract obstruction in any screened cat, though mild LV hypertrophy (defined as diastolic LV wall thickness ≥5.5mm) was present in 13/53 cats (25%). Gross pathology results and histopathological sections were analysed in eight NFCs, six of which had died of a cardiac cause. Myocyte hypertrophy, myofibre disarray and interstitial fibrosis typical of hypertrophic cardiomyopathy were present in 7/8 cats, but endomyocardial fibrosis suggestive of restrictive cardiomyopathy was also present in the same cats. Pedigree data analysis from 871 NFCs was supportive of a familial cardiomyopathy in this breed. [ABSTRACT FROM AUTHOR]

Recently, hypertrophic cardiomyopathy (HCM) in Sphynx cats has been associated with a variant in the gene encoding Alström syndrome protein 1 (ALMS1). The primary aims of this study were to describe the prevalence of HCM in Sphynx cats in New Zealand, and to assess the association between HCM and the ALMS1 variant in this population. In this prospective study, 55 apparently healthy Sphynx cats from registered Sphynx breeders and pet owners in New Zealand were screened by a cardiologist. A total of 42 of these cats had a repeat cardiac examination after median 1.8 years (range: 1.6-2.2). The frequency of the ALMS1 variant was 70.9% (11 homozygous and 28 heterozygous). At the median age of 5.8 years (range: 2.4-13.1), the prevalence of HCM was 40% (20 out of 55 cats). Three cats with HCM died during the study with congestive heart failure. All three cats had focal but extensive myocardial ischemia or infarction at necropsy. The ALMS1 variant was not associated with the HCM diagnosis. In summary, HCM was common in the studied cohort, suggesting Sphynx cats are predisposed to this disease. While the ALMS1 variant was also frequently detected, it was not associated with HCM in this population.

Extracellular vesicles (EV) are sub-micron circulating vesicles found in all bodily fluids and in all species so far tested. They have also recently been identified in seawater and it has further been shown that they are released from microorganisms and may participate in interspecies communication in the gut. EV are typically composed of a lipid bilayer formed from the plasma membrane and which encases a cargo that can include genetic material, proteins, and lipids. At least two different processes of formation and release have been described in mammalian cells. The exosome population (50 to 150nm size) are produced via a lyso-endosomal pathway, while microvesicles (100 to 1000nm) are formed by budding of the plasma membrane in a calcium dependent process. Both pathways are highly regulated and appear to be conserved amongst different species. EV release has been shown to be upregulated in a number of human chronic diseases including cardiovascular disease, metabolic disorders, obesity, and cancer; evaluation of their presence in veterinary samples may aid diagnosis in the future. This review will provide insight into the formation of EV and their detection in bodily fluids from different veterinary species and how they may provide a novel addition to the veterinary toolkit of the future.