Na sociedade moderna, a deficiência de tiamina (DT) ainda é uma condição médica importante ligada à função cardíaca alterada. Há relatos contraditórios sobre o impacto da DT sobre a fisiologia do coração, especialmente no contexto da excitabilidade cardíaca. A fim de resolver essa questão em particular, nós utilizamos de um modelo de DT para investigar as propriedades elétricas de cardiomiócitos isolados das diferentes sub-regiões do miocárdio de ratos, epicárdio e endocárdio, por meio da técnica de “patch clamp”. Nenhum dos dois tipos de célula estudados apresentou diferenças significativas na morfologia do potencial de ação e corrente transitória rápida de saída de potássio. Com base em nossos resultados, podemos concluir que a DT não induz grande remodelamento elétrico em miócitos cardíacos isolados tanto nas células do endocárdio quanto nas do epicárdio.

In modern society, thiamine deficiency (TD) remains an important medical condition linked to altered cardiac function. There have been contradictory reports about the impact of TD on heart physiology, especially in the context of cardiac excitability. In order to address this particular question, we used a TD rat model and patch-clamp technique to investigate the electrical properties of isolated cardiomyocytes from epicardium and endocardium. Neither cell type showed substantial differences on the action potential waveform and transient outward potassium current. Based on our results we can conclude that TD does not induce major electrical remodeling in isolated cardiac myocytes in either endocardium or epicardium cells.

Chagas disease, which is caused by the parasite Trypanosoma cruzi, is an important cause of heart failure. We investigated modifications in the cellular electrophysiological and calcium-handling characteristics of an infected mouse heart during the chronic phase of the disease. The patch-clamp technique was used to record action potentials (APs) and L-type Ca2+ and transient outward K+ currents. [Ca2+]i changes were determined using confocal microscopy. Infected ventricular cells showed prolonged APs, reduced transient outward K+ and L-type Ca2+ currents and reduced Ca2+ release from the sarcoplasmic reticulum. Thus, the chronic phase of Chagas disease is characterised by cardiomyocyte dysfunction, which could lead to heart failure.