[Cell therapy in dilated cardiomyopathy]. / Terapia celular na cardiomiopatia dilatada.

A forty-one-year-old male with systolic heart failure, FC-III NYHA, clinical stage C due to dilated cardiomyopathy was submitted to an autologous transplant of the mononuclear fraction of bone marrow via coronary artery system through heart catheterism. Two months after the procedure, there was a decrease in plasma BNP and cardiac area reduction at the thorax X-ray and nuclear magnetic resonance. The echocardiogram showed decrease of the secondary regurgitation and mitral ring dilatation. There was a better performance at the ergospirometry, with increase of the maximum oxygen consumption and consequent reduction in drug therapy. The absence of adverse events characterized by clinical/hemodynamic instability, enzymatic alteration or electrocardiogram demonstrate the safety and feasibility of this procedure carried out and described with pioneering spirit in dilated cardiomyopathy.

Terapia celular na cardiomiopatia dilatada / Cell therapy in dilated cardiomyopathy

Homem de 41 anos em insuficiência cardíaca sistólica, CF III NYHA, estágio clínico C, por cardiomiopatia dilatada, foi submetido ao transplante autólogo da fração mononuclear da medula óssea, via sistema arterial coronariano, através de cateterismo cardíaco. Dois meses após o procedimento, houve diminuição do BNP plasmático, diminuição da área cardíaca ao estudo radiológico do tórax e à ressonância nuclear magnética. O ecocardiograma demonstrou diminuição do fluxo regurgitante secundário a dilatação do anel mitral. Na ergoespirometria houve melhor desempenho, com aumento do consumo máximo de oxigênio, sendo possível redução da terapêutica medicamentosa. A ausência de eventos adversos caracterizados por: instabilidade clínica/hemodinâmica, alteração enzimática ou eletrocardiográfica apontam para segurança e exeqüibilidade deste procedimento realizado e descrito com pioneirismo na cardiomiopatia dilatada.

Sera from patients with idiopathic dilated cardiomyopathy decrease ICa in cardiomyocytes isolated from rabbits.

Autoantibodies against muscarinic and adrenergic receptors have been found in the sera of patients with idiopathic dilated cardiomyopathy (IDC) and Chagas disease, but it is still unclear whether they can functionally interact with their respective receptors to modulate cardiac functions. In this study, our goal was to detect the presence of those antibodies in the sera of patients with IDC and characterize their electrophysiological effects on cardiomyocytes from rabbits. By using ELISA immunoassays, we detected high titers of antibodies against muscarinic M2 receptors in the sera of all IDC patients, whereas the detection of antibodies against the beta1-receptor occurred in 50% of them. Electrophysiological experiments using the whole cell configuration of the patch-clamp technique showed that sera from 43% of IDC patients induced a significant decrease (approximately 26%) in isoproterenol-stimulated L-type Ca2+ currents in rabbit ventricular myocytes, whereas the sera from healthy blood donors failed to do so. As expected, IDC sera also decreased the action potential duration (by 10.5%) due to a shortening of the plateau phase. Sera that reduced isoproterenol-stimulated L-type Ca2+ currents did not cause any effect on K+ currents. We conclude that sera from IDC patients have autoantibodies, which interact with muscarinic M2 receptors of rabbit cardiomyocytes, acting in an agonist-like fashion. This action results in changes in electrogenesis, which, as often observed in patients with IDC, could initiate ventricular arrhythmias that lead to sudden death.