Left-dominant arrhythmogenic cardiomyopathy in a Fila Brasileiro dog.

Background: In human medicine, arrhythmogenic left ventricular cardiomyopathy was described as a primary disease of the heart characterized by fibroadipose replacement of the myocardium.. Case Description: We report the case of a dog, with history of syncope and irregular cardiac rhythm. Electrocardiogram, echocardiography, and a 24-hour Holter monitoring showed, respectively, the presence of premature ventricular complexes with right bundle branch block morphology, an increase of the left ventricle end-diastolic diameter with preserved fractional shortening and ejection fraction, and a sinus arrhythmia as baseline rhythm with supraventricular tachycardia episodes and ventricular complexes with left bundle branch block morphology. After the death of the canine, a postmortem examination showed cardiomegaly. Fibroadipose replacement of the septum and both ventricles, with left ventricle myocardial fibrosis, suggestive of previous necrosis, was observed. Conclusion: These findings are suggestive of left-dominant arrhythmogenic cardiomyopathy which, to the best of our knowledge, has not been described in veterinary medicine.

Findings suggestive of coronary microvascular dysfunction in cats with myocardial ischemia.

Background: Myocardial infarction (MI) is an important cause of death and disability among humans worldwide. Few studies have reported the occurrence of MI in small animals as well. Reports in human medicine indicate that up to 30% of patients with clinical signs compatible with myocardial ischemia suggestive of coronary disease exhibit normal epicardial arteries at angiography. These symptoms have been associated with a syndrome characterized by alterations in cardiac microvasculature, known as coronary microvascular dysfunction (CMD). Aim: This study aimed to describe the necropsy findings and clinical-pathological characterization (when available) of cats with histopathological findings suggesting CMD. Methods: Necropsy records of cats presenting histopathological diagnosis compatible with acute and/or chronic MI, with normal epicardial arteries and microvascular disorders were evaluated. Results: Twenty animals met the inclusion criteria. Eight cats (40%) exhibited findings compatible with mild hypertrophic cardiomyopathy (HCM) without left atrial enlargement, one (5%) presented restrictive cardiomyopathy, and another one (5%) had lesions consistent with histiocytoid cardiomyopathy. The remaining cats (50%) showed alterations compatible with severe HCM with left atrial enlargement. In all cases, epicardial arteries were normal (without obstruction). All the evaluated hearts exhibited myocardial multifocal fibrosis along with replacement of cardiomyocytes by adipose tissue and blood vessels with hyperplasia and hypertrophy of the muscular layer with protrusion of the nuclei of the endothelial cells. Conclusion: These findings suggest the presence of microvascular dysplasia of the coronary arteries. Further studies are necessary to confirm and clinically characterize these results.

Biochemical and Morphological Alterations in Hearts of Copper-Deficient Bovines.

Copper deficiency is an important disease of cattle that produces several clinical signs and lesions, due to alterations in copper-dependent enzymes. One of the organs affected by this deficiency is the heart (falling disease), but nevertheless, these cardiac lesions have not been extensively studied in bovines. The aim of this work was to propose a possible pathogenic mechanism for cardiac lesions in cattle affected by copper deficiency. Because of the possible existence of oxidative distress caused by low levels of copper-zinc-superoxide dismutase and cytochrome oxidase, ultrastructural and histological lesions have been evaluated in the heart of bovines in which a Cu deficiency had been induced using high molybdenum and sulfur levels in the diet. Our results indicated that copper deficiency produces significant damage in myocardium with high levels of lipid oxidation and a significant reduction in copper-zinc-superoxide dismutase activity leading to an oxidative distress situation. However, cytochrome oxidase activity was not significantly reduced. Histological observation revealed a significant increase in the amount of connective tissue, enlarged basement membranes of myocytes, and numerous Anichkov cells, in the hearts of deficient animals. Ultrastructural observation showed a significant enhancement in the mitochondrial volume density, with presence of lesions such as swelling and cristae disruption. We conclude that copper deficiency in bovines causes morphological lesions in the heart due to an oxidative damage produced by copper-dependent enzyme alterations.