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Dilated Cardiomyopathy Phenotype With Global (Four‐Chamber) Involvement in a Cat: Echocardiographic, Pathological, Histopathological, and Immunohistochemical Findings
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Dilated Cardiomyopathy Phenotype With Global (Four‐Chamber) Involvement in a Cat: Echocardiographic, Pathological, Histopathological, and Immunohistochemical Findings
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Journal Article
Dilated Cardiomyopathy Phenotype With Global (Four‐Chamber) Involvement in a Cat: Echocardiographic, Pathological, Histopathological, and Immunohistochemical Findings
2026
Overview
An 8‐year‐old castrated male Exotic Shorthair cat was referred due to the onset of abdominal effusion. Echocardiography revealed a dilated cardiomyopathy phenotype affecting both ventricles, associated with biatrial dilatation, left atrial dysfunction with spontaneous echocontrast, and right‐sided congestive heart failure. Additional diagnostic tests (thoracic radiographs, complete blood cell count, serum biochemistry, assessment of thyroid status, cardiac troponin I and plasma taurine concentrations, and urinalysis) ruled out secondary conditions able to cause a similar echocardiographic phenotype. Despite prompt initiation of cardiac therapy (furosemide, pimobendan, clopidogrel, and rivaroxaban) and subsequent hospitalization for further medical support, the cat′s clinical condition deteriorated, ultimately leading to euthanasia. Postmortem examination revealed extensive areas of myofiber thinning with a wavy appearance in both ventricles, closely resembling the attenuated wavy fiber pattern described in dogs affected by dilated cardiomyopathy. Additionally, multifocal replacement of myofibers by adipose tissue was found in both atria. Immunohistochemical analysis showed abnormal expression patterns of desmin, vimentin, and connexin 43, similar to those previously reported in humans and dogs with dilated cardiomyopathy. Given the thorough antemortem and postmortem investigations and the associated findings, a rare case of feline dilated cardiomyopathy with biventricular and biatrial involvement was diagnosed.
Publisher
John Wiley & Sons, Inc,Wiley
Subject
