Análise quantitativa das lesões cardíacas na cardiomiopatia chagásica crônica canina

Lesions observed in chronic chagasic cardiopathy frequently produce electrocardiographic alterations and affect cardiac function. Through a computerized morphometrical analysis we quantified the areas occupied by cardiac muscle, connective and adipose tissues in the right atrium of dogs experimentally infected with Trypanosoma cruzi. All of the infected dogs showed chronic myocarditis with variable reduction levels of cardiac muscle, fibrosis and adipose tissue replacement. In the atrial myocardium of dogs infected with Be78 and Be62 cardiac muscle represented 34 and 50%, fibrosis 28 and 32% and adipose tissue 38 and 18%, respectively. The fibrosis observed was both diffuse and focal and mostly intrafascicular, either partially or completely interrupting the path of muscle bundles. Such histological alterations probably contributed to the appearance of electrocardiographic disturbances verified in 10 out 11 dogs which are also common in human chronic chagasic cardiopathy. Fibrosis was the most important microscopic occurrence found since it produces rearrangements of collagen fibers in relation to myocardiocytes which causes changes in anatomical physiognomy and mechanical behavior of the myocardium. These abnormalities can contribute to the appearance of cardiac malfunction, arrythmias and congestive cardiac insufficiency as observed in two of the analyzed dogs. Strain Be78 caused destruction of atrial cardiac muscle higher than that induced by strain Be62.As lesões observadas na cardiopatia chagásica crônica frequentemente produzem alterações eletrocardiográficas e afetam a função cardíaca. Através de uma análise morfométrica computadorizada nós quantificamos as áreas ocupadas por músculo cardíaco, tecido conjuntivo fibroso e tecido adiposo no átrio direito de cães experimentalmente infectados pelo Trypanosoma cruzi. Todos os cães infectados apresentaram miocardite crônica fibrosante com graus variáveis de redução de músculo cardíaco, fibrose e substituição por tecido adiposo. No miocárdio atrial dos cães infectados pelas cepas Be78 e Be62 foram observados 34 e 50% de músculo cardíaco, 28 e 32% de fibrose e, 38 e 18% de tecido adiposo, respectivamente. A fibrose observada era tanto difusa quanto focal e, principalmente intrafascicular interrompendo total ou parcialmente o percurso dos feixes musculares. Tais alterações histológicas provavelmente contribuiram para o surgimento dos distúrbios eletrocardiográficos verificados em 10 dos 11 cães estudados e que são comuns na cardiopatia chagásica crônica humana. De todos os achados microscópicos encontrados, a fibrose foi a mais importante por produzir rearranjos na fibras colágenas em relação aos miocardiócitos, modificando a fisionomia anatômica e o comportamento mecânico do miocárdio. Tais anormalidades estruturais podem contribuir para o surgimento à disfunção cardíaca, arritmias e à insuficiência cardíaca congestiva como verificado em dois cães analisados. A cepa Be78 produziu uma destruição de músculo cardíaco atrial estatisticamente superior à induzida pela cepa Be62

Immunohistochemical studies in acute and chronic canine chagasic cardiomyopathy.

A major characteristic of Chagas’ disease is a myocarditis constituted primarily of mononuclear cells, both during the acute and chronic phases of the disease. Using monoclonal antibodies and image analyses we have quantified canine CD8+ T cells (caCD8+ T cells), canine CD4+ T cells (caCD4+ T cells) and neutrophils in canine chagasic myocardiopathy induced by two strains isolated from the first human clinical case of Chagas’ disease. We also evaluated the influence of tissue parasitism in the genesis of chronic myocarditis through immunohistochemistry. As in human myocarditis, there was a predominance of T lymphocytes in the inflammatory infiltrate in all animals studied. In the dogs inoculated with strain Berenice 78 (Be78) and necropsied during the acute phase of infection, we found 58% caCD8+ and 42% caCD4+ T cells. In chronically infected animals, 53% of T cells were represented by caCD8+ and 47% were caCD4+ T cells. Since normal canine lymphoid organs are constituted by 70–80% caCD4+ T cells and 20–30% caCD8+ T cells our results indicate a higher proliferation of caCD8+ T cells in dogs inoculated with the Be78 strain. In chronic myocarditis induced by the Berenice 62 (Be62) strain, caCD8+ cells constituted 33% of the T cells and 67% were caCD4+ T cells, a proportion similar to that found in normal canine lymphoid organs. Since the Be78 strain induces greater loss of myocardiocytes than strain Be62, we believe that the caCD8+ T cells, among other factors, can be important in the genesis of these lesions. Amastigote nests and immunohistochemically labelled Trypanosoma cruzi antigen were not found in dogs necropsied during the chronic phase. The absence of the parasite in the myocardium suggests the involvement of othe