Evidence accumulated over the last decade gives adequate proof for the existence of circulating antibodies in Chagas' disease which bind to beta adrenergic and muscarinic cholinergic receptors of myocardium. The interaction of antibodies with cardiac neurotransmitter receptors behaving as an agonist, triggers intracellular signal transductions in the cells that alter the physiological behaviour of the heart. These events convert the normal to pathologically active cells. The interaction of antibodies against heart beta adrenergic and cholinergic receptors triggers physiologic, morphologic, enzymatic and molecular alterations, leading to cardiac damage. The analysis of the prevalence and distribution of these antibodies shows a strong association with seropositive asymptomatic patients with autonomic dysfunction in comparison with those asymptomatic without alteration of the heart autonomic disorders. The presence of these antibodies may thus partially explain the cardiomyoneuropathy of Chagas' disease, in which the sympathetic and parasympathetic systems are affected. The deposit of autoantibodies on the myocardial neurotransmitter receptors, behaving like an agonist, induced desensitization and/or down regulation of the receptors. This in turn, could lead to a progressive blockade of myocardium neurotransmitter receptors, with sympathetic and parasympathetic dennervation, a phenomenon that has been described in the course of Chagas cardioneuropathy.