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Peer-reviewed veterinary case report

Heart muscle noncompaction found in adult Maine Coon cross cat

By Kittleson, M D et al.·Published in Journal of veterinary internal medicine·2017·Department of Medicine & Epidemiology, United States·View original on PubMed

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Original publication title: Naturally Occurring Biventricular Noncompaction in an Adult Domestic Cat.

Species:
cat

Plain-English summary

A Maine Coon cross cat was found to have a heart condition called left ventricular noncompaction (LVNC), which was diagnosed through ultrasound and confirmed after the cat passed away from an unrelated issue. This condition involves an unusual structure in the heart muscle, making it look "moth-eaten" and leading to abnormal heart function. The cat had regular heart check-ups starting at age two, and while it showed signs of LVNC, it lived until six years old without any heart-related symptoms. Unfortunately, there is no specific treatment mentioned for this condition, but the cat's heart was monitored closely throughout its life.

People also search for: cat heart problems · Maine Coon heart disease · left ventricular noncompaction in cats

Abstract

A definitively diagnosed case of left ventricular noncompaction (LVNC) has not been previously reported in a non-human species. We describe a Maine Coon cross cat with echocardiographically and pathologically documented LVNC. The cat was from a research colony and was heterozygous for the cardiac myosin binding protein C mutation associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats (A31P). The cat had had echocardiographic examinations performed every 6 months until 6 years of age at which time the cat died of an unrelated cause. Echocardiographic findings consistent with LVNC (moth-eaten appearance to the inner wall of the mid- to apical region of the left ventricle (LV) in cross section and trabeculations of the inner LV wall that communicated with the LV chamber) first were identified at 2 years of age. At necropsy, pathologic findings of LVNC were verified and included the presence of noncompacted myocardium that consisted of endothelial-lined trabeculations and sinusoids that constituted more than half of the inner part of the LV wall. The right ventricular (RV) wall also was affected. Histopathology identified myofiber disarray, which is characteristic of HCM, although heart weight was normal and LV wall thickness was not increased.

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Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/28158907/