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Pathologic alterations in hypertrophic and congestive cardiomyopathy of cats
Insights
Feline hypertrophic cardiomyopathy shares many similarities with human disease, showing myocardial hypertrophy and fibrosis. Congestive cardiomyopathy in cats also mirrors human forms, making feline models valuable for studying these cardiac conditions.
Area of Science:
- Veterinary Pathology
- Comparative Cardiology
- Animal Models of Human Disease
Background:
- Cardiomyopathy is a significant cardiac disease in both humans and felines.
- Understanding feline cardiomyopathy aids in comparative pathology and developing animal models.
Purpose of the Study:
- To characterize the pathologic alterations in cats with cardiomyopathy.
- To compare feline cardiomyopathy with human forms for potential use as disease models.
Main Methods:
- Histopathologic and ultrastructural examination of cardiac tissues from 15 cats with cardiomyopathy.
- Classification of cardiomyopathy into hypertrophic and congestive types based on gross and microscopic findings.
Main Results:
- Hypertrophic cardiomyopathy in cats presented with myocardial hypertrophy, fibrosis, and coronary artery changes, similar to human hypertrophic cardiomyopathy.
- Congestive cardiomyopathy in cats showed chamber dilatation with mild interstitial edema and fibrosis, comparable to human congestive cardiomyopathy.
- Cats with cardiomyopathy exhibited features that closely resemble human cardiac disease spectrums.
Conclusions:
- Feline hypertrophic and congestive cardiomyopathies serve as valuable models for studying human cardiac diseases.
- The morphologic similarities support the use of cats in translational cardiovascular research.
Abstract:
Pathologic alterations were studied in 15 cats with cardiomyopathy. Ten of these had hypertrophic cardiomyopathy, characterized by cardiomegaly, diffuse myocardial hypertrophy, small left ventricular cavities, and dilated left atria; the ventricular septum and left ventricular free walls were thick, but asymmetric septal hypertrophy was not present. Aortic thromboembolism, renal infarction, and pulmonary congestion and edema were frequent. Histopathologic and ultrastructural study revealed hypertrophy and disarray of cardiac muscle cells (most severe in left ventricle and ventricular septum), interstitial fibrosis, and fibromuscular hyperplasia of small intramural coronary arteries. The hypertrophied fibers had large nuclei, prominent Golgi complexes, and numerous polysomes; some fibers had crisscrossing myofibrils. Degenerative alterations in hypertrophied myocytes were: perinuclear distension of elements of sarcoplasmic reticulum, focal myofibrillar lysis, numerous thick clumps of Z-band material, and abundant lipofuscin granules. The interstitium showed accumulations of collagen fibrils, increased numbers of fibroblasts, and scattered remnants of external lamina. One cat had dilated chambers, but also had typical histologic and ultrastructural alterations of hypertrophic cardiomyopathy and was considered to have a late stage of this disorder. Four cats had congestive cardiomyopathy, with cardiomegaly and dilatation of all chambers. Hydrothorax and pulmonary congestion and edema were generally present. Cardiac histopathologic and ultrastructural alterations consisted only of mild interstitital edema and fibrosis. Detailed comparisons reveal many similarities in the spectrum of morphologic features of hypertrophic cardiomyopathy in human beings and cats; there are not marked differences in the morphologic features of congestive cardiomyopathy in human beings and cats. Thus, cardiomyopathies in the cat constitute useful models for the study of these diseases in human beings.