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Myocardial atrophy with fibrosis and fatty infiltration involving the cardiac conduction system is relatively unusual in horses. We herein report of such a case in a 13-year-old Arabian broodmare that had spontaneously died on a paddock. An autopsy revealed multifocal myocardial atrophy with concomitant fibrosis and fatty infiltration in both the ventricles and interventricular septum. The Purkinje fibres in the ventricles and interventricular septum were surrounded by thick fibrous or adipose tissues adjacent to atrophic myocardial cells. Myocardial fibrosis and fatty infiltration were likely secondary to myocardial atrophy, occurring as a pathological response triggered by the repair of muscular wall injury. However, there were no major vascular pathologies (e.g. atherosclerosis and arteriosclerosis); hence, the pathogenesis of myocardial atrophy was unclear. There was no evidence of myocardial atrophy ̵ induced pathologies such as infarct, ischaemic lesions, myocardial degeneration, myocarditis and endocarditis. However, such an unusual histopathological pattern may be associated with rapid clinical deterioration and death., (© 2020 The Authors. Veterinary Medicine and Science published by John Wiley & Sons Ltd.)

Cardiovascular disorders and predominantly idiopathic myocardial fibrosis are frequently associated with mortality among zoo-housed chimpanzees ( Pan troglodytes ). Formalin-fixed whole hearts of deceased chimpanzees housed in zoos ( n = 33) and an African sanctuary ( n = 2) underwent detailed macroscopic and histopathologic examination using a standardized protocol. Archived histological slides from the hearts of 23 additional African sanctuary-housed chimpanzees were also examined. Myocardial fibrosis (MF) was identified in 30 of 33 (91%) of the zoo-housed chimpanzees but none of the 25 sanctuary-housed chimpanzees. MF was shown to be characterized by both interstitial and replacement fibrosis. Immunophenotyping demonstrated that the fibrotic lesions were accompanied by the increased presence of macrophages, alpha smooth muscle actin-positive myofibroblasts, and a minimal to mild T-cell-dominant leukocyte infiltration. There was no convincing evidence of cardiotropic viral infection or suggestion that diabetes mellitus or vitamin E or selenium deficiency were associated with the presence of the lesion. However, serum vitamin D concentrations among zoo-housed chimpanzees were found to be lower in seasons of low ultraviolet light levels.

Perinatal parvoviral infection causes necrotizing myocarditis in puppies, which results in acute high mortality or progressive cardiac injury. While widespread vaccination has dramatically curtailed the epidemic of canine parvoviral myocarditis, we hypothesized that canine parvovirus 2 (CPV-2) myocardial infection is an underrecognized cause of myocarditis, cardiac damage, and/or repair by fibrosis in young dogs. In this retrospective study, DNA was extracted from formalin-fixed, paraffin-embedded tissues from 40 cases and 41 control dogs under 2 years of age from 2007 to 2015. Cases had a diagnosis of myocardial necrosis, inflammation, or fibrosis, while age-matched controls lacked myocardial lesions. Conventional polymerase chain reaction (PCR) and sequencing targeting the VP1 to VP2 region detected CPV-2 in 12 of 40 cases (30%; 95% confidence interval [CI], 18%-45%) and 2 of 41 controls (5%; 95% CI, 0.1%-16%). Detection of CPV-2 DNA in the myocardium was significantly associated with myocardial lesions ( P = .003). Reverse transcription quantitative PCR amplifying VP2 identified viral messenger RNA in 12 of 12 PCR-positive cases and 2 of 2 controls. PCR results were confirmed by in situ hybridization, which identified parvoviral DNA in cardiomyocytes and occasionally macrophages of juvenile and young adult dogs (median age 61 days). Myocardial CPV-2 was identified in juveniles with minimal myocarditis and CPV-2 enteritis, which may indicate a longer window of cardiac susceptibility to myocarditis than previously reported. CPV-2 was also detected in dogs with severe myocardial fibrosis with in situ hybridization signal localized to cardiomyocytes, suggesting prior myocardial damage by CPV-2. Despite the frequency of vaccination, these findings suggest that CPV-2 remains an important cause of myocardial damage in dogs.

A 7.5-year-old male Persian cat with a history of asymptomatic hypertrophic cardiomyopathy was examined for severe lethargy and dyspnoea. Physical examination revealed bradycardia (60 beats/ minute), and ECG investigation revealed persistent atrial standstill that was most likely caused by atrial fibrosis. Persistent atrial standstill is a very rare cardiac condition in cats and is characterized by a complete lack of mechanical, electrical, and possibly endocrine function of the atria. Several pathophysiological mechanisms can cause atrial standstill and include hyperkalaemia, intoxication, and atrialfibrosis. On the basis of the clinical findings, atrial fibrosis was the most likely cause of atrial standstill in this cat. Treatment depends on the underlying cause, but pacemaker implantation can be considered if there are structural abnormalities. The prognosis is guarded in such cases. In this particular case, the cat was euthanized at the owner's request.

The pathology of 33 moustached tamarins (Saguinus mystax) previously used in hepatitis A and GB virus studies is reported. Chronic lesions in colon, heart, and kidney were common in the monkeys and appeared not to be due to the experimental exposures. Colitis cystica profunda (CCP), a disease that affects humans and is characterized by the presence of mucin-filled epithelial downgrowths and cysts in the colonic submucosa, was found in 24 of the 33 (72.7%) tamarins. Interstitial myocardial fibrosis was present in 22 (66.6%) animals, and various degrees of membranoproliferative glomerulonephritis occurred in 28 (84.8%) monkeys. In addition, 28 (84.8%) tamarins demonstrated diffuse hepatocellular vacuolation with mild lymphoplasmacytic infiltrates, possibly as a result of the experimental infections, and peliosis hepatis occurred in 7 (21.2%) animals. The etiology of CCP is unknown, and no reliable animal models are available because most cases in animals are reported only sporadically. Myocardial fibrosis in tamarins has not been reported previously, and all current animal models require experimental manipulation of the animal to mimic the human disease. The results from this study suggest that captive S. mystax has high incidence of spontaneous CCP, myocardial fibrosis, and membranoproliferative glomerulonephritis. This species may be a spontaneous animal model for pathogenesis and experimental therapy studies of the analogous human diseases.

From 1994 to 1999, 16 captive African hedgehogs (Atelerix albiventris), from among 42 necropsy cases, were diagnosed with cardiomyopathy. The incidence of cardiomyopathy in this study population was 38%. Fourteen of 16 hedgehogs with cardiomyopathy were males and all hedgehogs were adult (>1 year old). Nine hedgehogs exhibited 1 or more of the following clinical signs before death: heart murmur, lethargy, icterus, moist rales, anorexia, dyspnea, dehydration, and weight loss. The remaining 7 hedgehogs died without premonitory clinical signs. Gross findings were cardiomegaly (6 cases), hepatomegaly (5 cases), pulmonary edema (5 cases), pulmonary congestion (4 cases), hydrothorax (3 cases), pulmonary infarct (1 case), renal infarcts (1 case), ascites (1 case), and 5 cases showed no changes. Histologic lesions were found mainly within the left ventricular myocardium and consisted primarily of myodegeneration, myonecrosis, atrophy, hypertrophy, and disarray of myofibers. All hedgehogs with cardiomyopathy had myocardial fibrosis, myocardial edema, or both. Other common histopathologic findings were acute and chronic passive congestion of the lungs, acute passive congestion of the liver, renal tubular necrosis, vascular thrombosis, splenic extramedullary hematopoiesis, and hepatic lipidosis. This is the first report of cardiomyopathy in African hedgehogs.

A study was designed to determine whether phenytoin (PHE) prevents the myocardial necrosis and subsequent fibrosis produced by isoproterenol (ISO). Seven groups of female rats of the Wistar strain were used. Rats in groups 1 and 5 served as controls. Rats in group 3 were injected SC with 85 mg of ISO/kg of body weight for 2 consecutive days. Rats in groups 2 and 6 received 100 mg of PHE/kg orally. Rats in groups 4 and 7 received both PHE and ISO. There were 6 to 9 rats/group. Effects of ISO and PHE were evaluated gravimetrically, histologically, and electrocardiographically. Heart weight/body weight ratios for each group receiving ISO, with or without PHE, were greater than for groups not receiving ISO (P less than 0.05). Light microscopic examination of heart sections of rats given ISO alone or ISO + PHE revealed multiple and diffuse areas of fibrosis. Fibrosis in hearts from rats receiving PHE + ISO was less severe than that in hearts from rats receiving ISO alone, but the difference was not statistically significant. Electrocardiographic changes of statistical significance were not observed in rats receiving any compound (alone or in combination), when compared with the control groups of equal age.