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Thirty-four cats with primary myocardial disease were studied. The cats were divided into two groups, depending on the clinical, hemodynamic, angiocardiographic, and pathologic findings. Group A consisted of those cats with hypertrophic cardiomyopathy and Group B consisted of those cats with congestive cardiomyopathy. Similarity in the characteristics of cardiomyopathy in the human cat was found. Both Group A and Group B consisted predominantly of mature adult male cats. The most common presenting signs were dyspnea and/or thromboembolism, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (Group A) or without (Group B) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (Group A) or left ventricular dilatation (Group B). Some cats in Group A also had evidence of left ventricular outflow obstruction. The principal pathologic findings in these cats were left atrial dilatation, symmetric hypertrophy or asymmetric septal hypertrophy of the left ventricle (Group A), and dilatation of the four cardiac chambers (Group B). Aortic thromboembolism was commonly observed in both groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat is similar to the two most common forms of cardiomyopathy in the human (hypertrophic cardiomyopathy, with and without obstruction, and congestive cardiomyopathy).

Cardiology was diagnosed by means of clinical, radiographic, electrocardiographic phonocardiographic, angiocardiographic, and pathological findings in 271 or 3,745 cats necropsied from January 1962 to April 1974. The affected cats can be divided into three groups on the basis of the gross and microscopic pathological lesions: 1)endocarditis and myocarditis in 20 young cats; 2)endomyocardial fibrosis and left ventricular hypertrophy in 182 cats; and 3)myocardial degeneration and biventricular dilatation in 69 cats. Of 271 affected cats, thromboembolus was observed in the aorta, and in the carotid, femoral, iliac, renal, pulmonary, and hepatic arteries in 104 instances. The important aspects of cardiomyopathy in cats appears to be the reduced diastolic compliance of the thick left ventricle, resulting in poor fillin. Resistance to ventricular inflow raises the diastolic pressure and causes compensatory left atrial enlargement. A pathogenesis for the onset of clinical signs at any stages as the cause of the heart disease is postulated on the basis of stress causing tachycardia and poor left ventricular filling. Acute left-sided failure with pulmonary edema may be precipitated. Approximately one-fourth of the cats have enlargement of all cardiac chambers, typical of congestive cardiomyopathy. On the basis of the close similarily to cardiomyopathy in man, the cat could serve as a suitable animal model for a conservation of time and effort in the attack against this disorder. There is a need for coordinated research programs for utilizing the multiple avenues of approach such as: epidemiological, clinical, biochemical, pathological, ultrastructural, virological, and immunological.

Cardiomyopathy associated with vitamin E deficiency was diagnosed in more than 100 ruminants and primates and in 106 embryos and newly hatched chicks and ducklings. Affected bird embryos failed to pip the eggshell and died inside. Newly hatched chicks and ducklings and neonatal ruminants were weak, had difficulty standing or rising, and died within a few days. Death usually occurred without premonitory signs of disease in juvenile and adult animals. On gross examination, the hearts of the neonatal ruminants had areas of mottled, pinkish-tan myocardium. The hearts of the embryos and newly hatched birds were edematous, pinkish, and pale. In the juvenile ruminants, irregular, whitish patches or pale areas were seen in the myocardium. Histologically, there was multifocal myocytolysis in the myocardium of the neonatal and juvenile ruminants and embryos and newly hatched birds. Focal disseminated or diffuse myocardial fibrosis and myocytolysis were observed in the hearts of the adult animals. Plasma alpha tocopherol values were low enough in all species to be considered deficient. These values increased significantly after the addition of alpha tocopherol and/or vitamin E to the diets of the animals. Cardiomyopathy has not been diagnosed in any of the same groups of animals since supplementation was initiated.

In a study of 3,145 feline necropsies conducted for 11 years by the pathology department of The Animal Medical Center, 289 tumors of nonhematopoietic origin were found in 264 cats. Malignant and epithelial tumors were more common than benign or mesenchymal tumors in all ages and breeds, and in both sexes. They were also more common in female cats than in males, even after mammary neoplasms were excluded. Analysis of groups of tumors according to their tissue of origin indicated some sex and breed dispositions not observed before. Pulmonary carcinomas and osteosarcomas were more frequent in domestic short haired cats than in other breeds, whereas intestinal carcinomas occurred more often in Siamese cats. Female predominated in pulmonary carcinomas, hemangiosarcomas, osteosarcomas, and squamous cell carcinomas, but males outnumbered the females in intestinal carcinomas.

Medical records of 12 dogs determined at necropsy as having had cardiomyopathy and of 5 live dogs with clinical, electrocardiographic and radiographic evidence of the disease were reviewed. Congestive cardiomyopathy was the most common form of the disease, affecting 15 of the 17 dogs. The dogs were primarily of large breeds and ranged in age from 2 to 8 years. Clinical findings included right and left congestive heart failure presenting as pulmonary congestion and edema, pleural effusion, hepatomegaly, and ascites. Thoracic radiographs showed moderate severe enlargement of all cardiac chambers and evidence of congestive heart failure. Atrial fibrillation was the predominant rhythmn; ventricular premature contractions and left ventricular hypertrophy were sometimes noted. At necropsy, biventricular dilation including dilation of the atrioventricular annular rings and accompanying massive atrial dilation was observed. Myocardial contractility was poor and had resulted in dilation of the heart chambers with minimal hypertrophic responses. The atrioventricular valve leaflets and chordae tendinae were usually near normal. Medical treatment included rest, digoxin, and diuretics, Medical or electrical cardioversion of atrial fibrillation to normal sinus rhythm was also attempted. Prognosis for congestive cardiomyopathy is very poor. The average survival time after onset of signs is 6-12 months; 1 dog in our study survived for 20 months. In contrast to congestive cardiomyopathy, the hypertrophic form is rare in the dog. Only two of the dogs studied had hypertrophic cardiomyopathy; one case was diagnosed at necropsy and one by angiocardiography. Both had features of idiopathic hypertrophic subaortic stenosis (IHSS) as reported in man.

Listeriosis was diagnosed in 7 bushy-tailed jirds (Sekeetamys calurus). Death in all cases was acute, and there were no clinical signs. Necropsy revealed necrotizing lesions in the liver, intestines, spleen, and hepatic and mesenteric lymph nodes. On histologic examination large numbers of gram-positive coccobacilli were seen in the lesions. Pneumonitis was seen in 6 jirds, and small numbers of bacteria were seen in the lungs in all cases except one. Diagnosis was based on bacterial culture of the liver in 2 jirds and on immunofluorescence of bacteria when tissue specimens from 2 other jirds were stained with fluorescein-labelled antiglobulins specific for Listeria monocytogenes.

Degeneration and fibrosis of the atrioventricular nodal tissue and left bundle branch, associated with cartilage of bone in the central fibrous body and fibrosis of the interventricular septal crest, were observed in 63 cats with cardiomyopathy. The cardiac lesions consisted of endocardial and myocardial fibrosis or organized endomyocarditis. Electrocardiographic, radiographic, angiocardiography, and hemodynamic changes were also observed in the cats.

Myocarditis and cardiomyopathy were diagnosed in 36 dogs from 11 litters, and myoendocarditis and restrictive cardiomyopathy were diagnosed in 51 cats. Most of the dogs and cats died unexpectedly. Spontaneous parvoviral infection in the dogs caused acute (myocytolysis with presence of intranuclear inclusion bodies in the myocytes), subacute (inflammatory reaction and myocytolysis), and chronic (fibrosis and myocytolysis) myocarditis, which led to extensive myocardial fibrosis and abnormality of the myocytes, similar to dilated cardiomyopathy in man. Spontaneous acute, subacute, and chronic myoendocarditis in the cats led to granulation, extensive fibrosis, and necrosis of the myoendocardium, i.e., like restrictive cardiomyopathy which occurs in man without eosinophilia. Thus, the dog and cat are important animal models of primary myocardial disease.

Dysplasia of the tricuspid valve in 14 dogs and 13 cats was studied. The clinical, electrocardiographic, radiographic, hemodynamic, angiocardiographic, and pathologic findings were reviewed in each species. Alterations of the tricuspid valve complex included long, thick septal leaflets adhered to the septum; absent or short, stout fused chordae tendineae; hypertrophic fused papillary muscles; insertion of papillary muscles directly into the lateral leaflets; incomplete development of the valvular tissue; and enlargement of the right atrium and ventricle. Additional intracardiac anomalies included malformation of the mitral valve complex (5 dogs and 3 cats), ventricular septal defect (3 dogs and 3 cats), pulmonary stenosis (1 dog and 1 cat), aortic stenosis (1 dog and 1 cat), and persistent left cranial vena cava (1 dog).

Papillary muscle rupture is uncommon in the dog. Two-dimensional echocardiography provides a rapid, noninvasive test in the diagnosis of acute, severe mitral regurgitation resulting from papillary muscle rupture. This report illustrates the usefulness of echocardiography to determine the cause of acute mitral regurgitation.

A benign neoplasm of smooth muscle origin was found in the tunica vaginalis testis of a 13-year-old male Miniature Poodle. The leiomyoma had caused hydrocele and atrophy of the corresponding testis. It consisted of bundles of interwoven smooth muscle cells with elongated nuclei and areas of hyalinization.

A tumor in the anterior mediastinum was found in an adult male German Shorthaired Pointer. The dog presented with hypercalcemia that varied with the removal and recurrence of the tumor. The neoplasm was characterized by an encapsulated multilobed grey-white soft mass with stroma, and the recurrent tumor infiltrated veins and the heart. The tumor consisted of groups of clear cells with well outlined cytoplasmic boundaries separated by thin vascular stroma. These cells had few organelles, scattered clumps of glycogen, clear cytosol and prominent infolding and interdigitating plasma membranes and desmosomes. The clinical, light and electron microscopic features were consistent with a functional neoplasm of parathyroid tissue origin.