Joonbum Seo

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.

To evaluate the prevalence of subclinical cardiomyopathy and cardiac mortality in a research colony of non-purebred cats, established as a model of the wider cat population in New Zealand. All apparently healthy, compliant, non-pregnant, non-neonatal cats in the colony at the Centre for Feline Nutrition (Massey University, Palmerston North, NZ) underwent physical examination and echocardiography using a 4.4-6.2-MHz probe by a board-certified veterinary cardiologist. Cardiac phenotype was classified following current guidelines. Hypertrophic cardiomyopathy (HCM) phenotype was defined as an end-diastolic left ventricular wall thickness ≥ 6 mm. Colony mortality data from February 2012 to February 2022 was reviewed to determine cardiac mortality. Cats (n = 132; 65 females and 67 males) included in the study had a median age of 4.1 (IQR 3.0-8.0) years. Thirty-two (24%) cats had a heart murmur, and three (2%) cats had an arrhythmia. Echocardiography revealed heart disease in 24 (18.2%) cats, including 23 with an HCM phenotype and one with a restrictive cardiomyopathy phenotype. Of the cats with the HCM phenotype, 3/23 had systemic hypertension or hyperthyroidism or both, and these cats were excluded from the final diagnosis of HCM (20/132; 15.2 (95% CI = 9.5-22.4)%).Between 2012 and 2022, 168 colony cats died, with 132 undergoing post-mortem examination. Heart disease was considered the cause of death in 7/132 (5.3%; 95% CI = 2.2-10.6%) cats; five had HCM, one a congenital heart defect, and one myocarditis. The overall prevalence of death related to HCM in the colony during this period was 3.8% (95% CI = 1.2-8.6%). Three cats with HCM and the cat with a congenital heart defect died unexpectedly without prior clinical signs, while congestive heart failure was observed prior to death in two cats with HCM and the cat with myocarditis. Additionally, 30/132 (22.7%) cats had cardiac abnormalities but died for non-cardiac reasons. Subclinical cardiomyopathy, specifically HCM, was common in cats in the colony. Given that the colony originated as a convenience selection of non-purebred cats in New Zealand, the true prevalence of HCM in the wider New Zealand population is likely to fall within the 95% CI (9.5-22%). The proportion of deaths of colony cats due to HCM was lower (3.8%) supporting the conclusion that subclinical cardiomyopathy may not progress to clinical disease causing death. Veterinarians should be aware of the high prevalence of subclinical HCM when treating cats. CAM: Systolic anterior motion of the chordae tendineae; CFN: Centre for Feline Nutrition; HCM: Hypertrophic cardiomyopathy; LA/Ao: Left atrial to aortic ratio; LV FS: Left ventricular fractional shortening; LVIDd: Left ventricular internal diameters in end-diastole; LVIDs: Left ventricular internal diameter in end-systole; LVWT: Max Maximum left ventricular wall thickness; SAM: Systolic anterior motion of the mitral valve; 2D: Two-dimensional.

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.

Background: Impairment of left ventricular (LV) longitudinal function is an early marker of systolic dysfunction in hypertrophic cardiomyopathy (HCM). Aortic annular plane systolic excursion (AAPSE) is a measure of LV longitudinal function in people that has not been evaluated in cats. Hypothesis: Aortic annular plane systolic excursion is lower in cats with HCM compared to control cats, and cats in stage C have the lowest AAPSE. Animals: One hundred seventy-five cats: 60 normal, 61 HCM stage B and 54 HCM stage C cats. Materials: Multicenter retrospective case-control study. Electronic medical records from 4 referral hospitals were reviewed for cats diagnosed with HCM and normal cats. HCM was defined as LV wall thickness ≥6 mm and normal cats ≤5 mm. M-mode bisecting the aorta in right parasternal short-axis view was used to measure AAPSE. Results: Aortic annular plane systolic excursion was lower in HCM cats compared to normal cats (3.9 ± 0.9 mm versus 4.6 ± 0.9 mm, P < .001) and was lowest in HCM stage C (2.4 ± 0.6 mm, P < .001). An AAPSE <2.9 mm gave a sensitivity of 83% (95% CI 71%-91%) and specificity of 92% (95% CI 82%-97%) to differentiate HCM stage C from stage B. AAPSE correlated with mitral annular plane systolic excursion (r = .6 [.4-.7], P < .001), and atrial fractional shortening (r = .6 [.5-.7], P < .001), but showed no correlation with LV fractional shortening. Conclusions and Clinical Importance: Aortic annular plane systolic excursion is an easily acquired echocardiographic variable and might be a new measurement of LV systolic performance in cats with HCM.

Case summary: We describe two cats that had episodic tachypnoea and increased respiratory effort during periods of paroxysmal supraventricular tachycardia (SVT). Thoracic radiographs at the time of clinical signs were consistent with cardiogenic pulmonary oedema. Echocardiography following stabilisation revealed a hypertrophic cardiomyopathy phenotype with normal left atrial size in both cats. The first cat was initially treated with diltiazem, but this did not reduce the frequency of the clinical episodes. Diltiazem was switched to atenolol and the cat remained well without further recurrence. At the time of writing, the cat was reported to be well, 3 years after the initial diagnosis of SVT. The second cat was first managed with diltiazem and was then transitioned to atenolol due to recurrent clinical episodes. The episodes were less frequent with atenolol but still present. Therefore, atenolol was changed to sotalol. The cat remained well on sotalol for 2 years with only one recurrent episode during a painful event. The patient then suffered a sudden cardiac death, 5 years after the initial diagnosis of SVT. Relevance and novel information: To our knowledge, this is the first report that describes flash pulmonary oedema developing secondary to episodic paroxysmal SVT in cats. Despite the severity and speed of respiratory compromise, prognosis may be good with an adequate arrhythmia control.

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.