Background: The natural history of hypertrophic cardiomyopathy (HCM) in cats has been mainly studied in cats referred for suspected heart disease, which can skew the results towards cats with clinical signs. Few data are available on factors associated with development of HCM in cats. Hypotheses: (1) Clinical variables can predict which cats will develop HCM; (2) HCM in cats not referred for suspected heart disease is associated with a low rate of cardiovascular events. Animals: One hundred seven cats from rehoming centers without a history of clinical signs of cardiac or systemic disease at the time of adoption. Methods: Prospective longitudinal study. After rehoming, shelter cats were reexamined for serial echocardiograms. Cox regression analysis was used to identify predictors of development of HCM in cats that were normal at baseline. Adverse cardiovascular events including heart failure, thromboembolism, or sudden death were recorded. Results: Cats were monitored for a median of 5.6 [1.2-9.2] years. At baseline, 68/107 cats were normal, 18/107 were equivocal and 21/107 had HCM. Nineteen cats developed HCM during the study period. The factors at baseline associated with increased hazard of developing HCM were lower left atrial fractional shortening, higher left ventricular fractional shortening, and higher body weight. Cardiovascular events were observed in 21% of cats with HCM. Conclusions and Clinical Importance: Cardiovascular events were common in cats with HCM from a rehoming center study sample. Lower left atrial systolic function appears to precede overt HCM.

Background Atrial fibrillation (AF) is associated with increased risk of sudden cardiac death (SCD) in humans, independent of secondary risk factors such as thrombogenic disorders. In dogs, SCD is described in a number of heart diseases, but an association between AF and SCD is unreported. Hypothesis (a) A higher proportion of dogs with AF will experience SCD, and (b) SCD will be associated with complex ventricular arrhythmias. Animals One-hundred forty-two dogs with AF, and 127 dogs without AF. Methods Retrospective, multicenter, case-control study. Dogs included in the AF group were compared to a control group of dogs in sinus rhythm, matched for echocardiographic diagnosis. Descriptive statistics were used to identify proportions of each group suffering SCD, compared using chi-squared testing. Risk factors for SCD in dogs with AF were evaluated at the univariable and multivariable level using binary logistic regression. Significance was P < .05. Results A significantly higher proportion of dogs with AF suffered SCD than dogs in the control group (14.8% vs 5.5%; P = .01). Younger age at diagnosis, larger left atrial size, and a history of syncope all were independent predictors of SCD in dogs with AF (χ², 16.3; P = .04). Conclusions and Clinical Importance Atrial fibrillation was associated with a higher prevalence of SCD in dogs. A history of syncope may be a useful predictor of SCD risk.

Background N‐terminal pro B‐type natriuretic peptide (NT‐proBNP) and cardiac troponin‐I (cTnI) are biomarkers commonly evaluated in cats with suspected heart disease. Many cats with hypertrophic cardiomyopathy (HCM) have systolic anterior motion of the mitral valve (SAM), but its influence on circulating NT‐proBNP or cTnI concentrations is currently unknown. Hypothesis/Objectives Cats with HCM and SAM (HCM^SAM+) have higher NT‐proBNP and cTnI concentrations than do cats with HCM but without SAM (HCM^SAM−). Animals One hundred forty cats with HCM: 70 with SAM and 70 without SAM. Methods Retrospective case‐to‐case study. Cats were recruited if diagnosed with HCM by echocardiography and results were available for NT‐proBNP or cTnI concentrations or both. Cats with SAM were matched to those without SAM for clinical presentation, left atrial (LA) size and left ventricular (LV) fractional shortening. Results A total of 119 NT‐proBNP and 123 cTnI results were available. The HCM^SAM+ cats had higher median concentrations than did HCM^SAM− cats for NT‐proBNP (729 pmoL/L; interquartile range [IQR], 275‐1467 versus 65 pmoL/L; IQR, 25‐271; P < .001) and cTnI (0.27 ng/mL; IQR, 0.10‐0.81 versus 0.07 ng/mL; IQR, 0.01‐0.43; P = .002). In general linear models for both NT‐proBNP and cTnI, the independent explanatory variables were SAM, congestive heart failure, maximal LV wall thickness, and LA size. Conclusions and Clinical Importance For cats with HCM and equivalent LA size and LV systolic function, those with SAM had higher NT‐proBNP and cTnI concentrations than did those without SAM. Presence of SAM should be considered when interpreting biomarker concentrations in cats with HCM.

Compromised gut health and dysbiosis in people with heart failure has received a great deal of attention over the last decade. Whether dogs with heart failure have a similar dysbiosis pattern to what is described in people is currently unknown. We hypothesised that dogs with congestive heart failure have quantifiable dysbiosis compared to healthy dogs that are similar in sex and age. A total of 50 dogs (15 healthy dogs and 35 dogs with congestive heart failure) were prospectively recruited, and their faecal gut microbiome was assessed using 16S rRNA sequencing (Illumina MiSeq platform). There was no significant change in the microbial diversity and richness in dogs with congestive heart failure. However, there was an increase in abundance of Proteobacteria in the congestive heart failure group (p = 0.014), particularly due to an increase in the familyEnterobacteriaceae(p = 0.002) andEscherichia coli(p = 0.033). We conclude that dogs with congestive heart failure have dysbiosis, and we show additional trends in our data suggesting that dogs may have a similar pattern to that described in people. The results of this study provide useful preliminary information and raise the possibility that dogs represent a clinically relevant animal model of dysbiosis in people with heart failure.