%0 Journal Article
%T Chronic ChagasĄŻ heart disease ¨C From pathogenesis to treatment regimes
%A Silvia Gilkas Munoz-Saravia
%A Annekathrin Haberland
%A Gerd Wallukat
%A Ingolf Schimke
%J Applied Cardiopulmonary Pathophysiology
%D 2012
%I Pabst Science Publishers
%X Chronic ChagasĄŻ heart disease ¨C From pathogenesis to treatment regimes Silvia Gilka Munoz-Saravia, Annekathrin Haberland, Gerd Wallukat, Ingolf SchimkeCharit¨Ś - Universit tsmedizin Berlin, Berlin, Germany [Applied Cardiopulmonary Pathophysiology 16: 55-81, 2012] AbstractChagasĄŻ disease, caused by Trypanosoma cruzi infection, was discovered nearly 100 years ago (1909) by the Brazilian physician Carlos Chagas. Chronic ChagasĄŻ disease is still ranked as the most serious parasitic disease in Latin America. Infected patients remain lifelong parasite carriers. With a latency of 10 to 30 years, nearly one third of parasite carriers develop life-threatening complications: the majority develop ChagasĄŻ heart disease (90%). Gastrointestinal disorders (megaesophagus, megacolon) and neuronal afflictions mainly affecting the parasympathetic nerve system were found in the others. ChagasĄŻ heart disease presenting with sudden death, heart failure, malign cardiac arrhythmia, and thromboembolism is currently the major cause of morbidity and mortality in Latin America, enormously burdening economic resources and dramatically affecting patientsĄŻ social and employment situations. ChagasĄŻ disease is starting to become a worldwide problem due to migration, international tourism and parasite transfer by blood contact, intrauterine transfer and organ transplantation. In this review, we reflect on the epidemiology and etiopathology of ChagasĄŻ heart disease. We summarize the mechanisms that have been suggested to drive ChagasĄŻ heart disease, mainly those based on autoimmunity phenomena. In this context, we focus on autoantibodies directed to G-protein coupled receptors. Following the autoimmunity story in chronic ChagasĄŻ heart disease ¨C and in addition to antiparasitic therapy, the treatment of heart failure, arrhythmia and thromboembolism and under study strategies such as heart transplantation and cell therapy ¨C we describe regimes that use peptides and aptamers for autoantibody removal or neutralization. At present, such regimes are mostly proposed for beta-1-receptor autoantibodies in patients with dilated cardiomyopathy but, in principle, they can be adapted for patients with chronic ChagasĄŻ heart disease who are positive for comparable autoantibodies.
%K autoantibodies
%K ChagasĄŻ heart disease
%K epidemiology
%K G-protein coupled receptors
%K pathogenesis
%K treatment
%K Trypanosoma cruzi
%U http://www.applied-cardiopulmonary-pathophysiology.com/fileadmin/downloads/acp-2012-1_20120301/05_munoz-saravia.pdf