Chagas disease cardiomyopathy: current concepts of an old disease

Abstract

SUMMARYChagas disease continues to be a significant public health problem, as ca. 10 million people are still infected with T. cruzi in Latin America. Decades after primary infection, 30% of individuals can develop a form of chronic inflammatory cardiomyopathy known as Chagas disease cardiomyopathy (CCC). Data from both murine models and human studies support the view that an autoimmune response as well as a parasite-driven immune response involving inflammatory cytokines and chemokines may both play a role in generating the heart lesions leading to CCC. This review aims to summarize recent advances in the understanding of the immunopathogenesis of Chagas disease cardiomyopathy.

Interferon-γ and other inflammatory mediators in cardiomyocyte signaling during Chagas disease cardiomyopathy

“…Regardless of the mechanisms underlying the initiation and maintenance of the myocarditis, the bulk of the evidence indicates that the inflammatory infiltrate is a significant effector of heart tissue damage. Our group has demonstrated over the past several years that, aside from direct inflammatory damage, several cytokines and chemokines produced in the myocardium of CCC patients may also have a non-immunological pathogenic effect beyond direct inflammatory tissue damage, via modulation of gene and protein expression in cardiomyocytes and other myocardial cell types [5,7,15,16] . While IFN-γ acts as an immunological mediator during the acute stage of the disease suppressing overt parasitism, in the chronic phase of the disease it will both curtail parasitism and cause tissue damage through immunological and nonimmunological effects entertaining the gradual progression to CCC.…”

The benefits of using selenium in the treatment of Chagas disease: prevention of right ventricle chamber dilatation and reversion of Trypanosoma cruzi-induced acute and chronic cardiomyopathy in mice

“…It is caused by the intracellular parasite Trypanosoma cruzi and is most frequently associated with cardiac-related manifestations. T. cruzi initially invades myocardial cells, resulting in a diffuse and severe neutrophilic and monocytic inflammatory infiltrate in addition to myofibrillar lesions (Bilate & Cunha-Neto 2008). At the acute phase, patients can present with pericardial effusion, dyskinesis or ventricular dilatation detected by echocardiography.…”

A Patient with Erythema Nodosus Leprosum and Chagas Cardiopathy: Challenges in Patient Management and Review of the Literature

“…7 It is believed that the cardiac lesions are the result of combined damage produced by the parasitism and by the host immune response, either parasite-driven or as an autoimmune phenomenon. 8 We report a leprosy patient with repeated episodes of ENN in whom severe heart failure developed during her follow up, but whose diagnosis of Chagas disease was initially missed. We discuss the difficulties in managing a patient with both diseases, review the literature of heart failure in leprosy patients, and discuss the possible interaction between these infections and their treatments.…”