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Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats
Y Kimura1, S Karakama1, A Hirakawa2
1Laboratory of Veterinary Clinical Oncology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu, Tokyo, Japan.
Insights
This study reveals feline restrictive cardiomyopathy (RCM) involves endocardial thickening due to mesenchymal cell proliferation, not inflammation. Findings suggest RCM in cats is not virus-induced.
Area of Science:
- Veterinary Pathology
- Cardiovascular Research
- Feline Medicine
Background:
- Feline restrictive cardiomyopathy (RCM) is a significant cardiac disease in cats.
- The underlying pathological mechanisms of feline RCM require further elucidation.
Purpose of the Study:
- To investigate the pathological and molecular features of feline RCM.
- To determine the cellular origins and potential causes of endocardial lesions in feline RCM.
Main Methods:
- Gross and microscopic examination of 41 feline hearts with RCM.
- Immunohistochemical analysis of endocardial tissues.
- Molecular analysis (DNA/RNA) for viral genomes in a subset of cases.
Main Results:
- Consistent endocardial thickening of the left ventricle, characterized by fibrous tissue and mesenchymal cells.
- Mesenchymal cells showed smooth muscle differentiation and contributed to lesion formation.
- Absence of endocarditis, endomyocarditis, and detectable viral genomes in examined cases.
Conclusions:
- Feline RCM is characterized by mesenchymal cell proliferation and fibrosis, not inflammatory processes.
- The findings suggest that viral infections are unlikely to be the cause of feline RCM.
- Left ventricular false tendons play a role in the structural framework of RCM lesions.
Abstract:
This study reports pathological and molecular features in 41 cases of feline restrictive cardiomyopathy (RCM). Grossly, there were patchy or diffuse areas of endocardial thickening affecting the left ventricle. The more common patchy endocardial lesions occurred as large trabecular or irregular broad bands of fibrous tissue bridging the left ventricular free wall and ventricular septum. Microscopically, regardless of the gross pattern, the thickened endocardium contained various numbers of stellate, spindle-shaped or elongated mesenchymal cells surrounded by fibrous connective tissue. Immunohistochemical findings were indicative of smooth muscle differentiation in mesenchymal cells. These cells proliferated vigorously and produced alcian blue-positive ground substance and collagen fibres; it was considered that the mesenchymal cells contributed to the formation of the endocardial lesions. In addition, multiple left ventricular 'false tendons' were invariably included within the trabecular or broad fibrous bands, providing a framework for formation of those bands. Evidence of endocarditis or endomyocarditis was lacking in all 41 cases, and no viral genomes were detected in any of the DNA or RNA samples obtained from 14 of the hearts. These observations suggest that any relationship between feline RCM and a virus-induced inflammatory response seems unlikely.
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