Hypertrophic cardiomyopathy (HCM) is the most prevalent acquired heart disease in cats and shares many clinical, phenotypical and pathological features with human HCM. Despite its relevance, knowledge on the pathomechanisms underlying the disease is limited. The present study aimed to characterize the molecular phenotypic changes in cardiomyocytes in feline HCM (fHCM) to better understand their contribution to the pathogenesis. To achieve this, the myocardium of the left ventricular free wall of 15 cats with confirmed fHCM and 30 control cats (two age groups: 16 cats 18-month-old, and 14 older adult cats without cardiac disease) were subjected to RT-qPCRs for markers representative of cardiomyocyte function. Overall, all markers were expressed at the highest level in young control cats, and increasing age correlated with decreased expression, regardless of sex. The comparison between the older adult control cats and those with HCM showed increased transcription levels for most markers associated with the disease, and higher expression of all markers in affected male cats compared to females. The constitutive transcription of all markers provides evidence of continuous myocardial adaptation throughout cats’ life. The high transcription values in the myocardium of young healthy cats and male cats affected by HCM suggest a particularly high myocardial responsiveness early in life and with HCM and reveal sex as relevant factor in the disease process. These results support the relevance of age and sex in the cardiac response to HCM in feline hearts.

Feline valvular mitral stenosis (VMS) is uncommonly reported. The aim of this study was to describe diagnostic and clinicopathological characteristics of VMS in adult cats. Eighteen client-owned cats were included in this study. A retrospective observational study. Clinical records were searched based on echocardiography. Data regarding clinical, laboratory, echocardiographic findings, outcome, and, in four cats, gross postmortem images of the heart were reviewed, and histological examinations performed. Most cats were non-pedigree (11/18), with a median age of 13.2 years. Congestive heart failure was common (15/18). Three cats had hypertrophic cardiomyopathy phenotype, including one with transient myocardial thickening. Concomitant hyperthyroidism (9/18) was frequent. In one cat, echocardiography performed one year earlier did not show any changes. Upon echocardiography, all 18 cats had characteristic hockey-stick appearance of the anterior leaflet and narrow turbulent diastolic flow across the mitral valve. Twelve cats had fused diastolic transmitral waves, with a median velocity of 0.54 m/s (0.71-3.24 m/s). The remaining six had a median peak velocity of the early and late-diastolic transmitral waves of 1.3 m/s (0.95-2.8 m/s) and 0.99 m/s (0.65-2.05 m/s), respectively. Eleven cats had died, 10 of cardiac death (median survival time: 366 days). Macroscopically, the mitral valve leaflets appeared thickened and distorted, and the surrounded ventricular endocardium thickened. Histology revealed marked endocardial fibrosis of the mitral valve and surrounding ventricular endocardium, dominated by type I collagen. The most striking finding is the documented acquirement of VMS in one cat, while the acquired nature of the lesion could not be confirmed in the other cases. The pathological findings are compatible with a chronic remodeling process that results in marked endocardial fibrosis in four cats.