Arrhythmogenic Manifestations of Chagas Disease: Perspectives From the Bench to Bedside

Author:

Roman-Campos Danilo1ORCID,Marin-Neto José Antonio2ORCID,Santos-Miranda Artur3,Kong NathanORCID,D’Avila AndréORCID,Rassi Anis4ORCID

Affiliation:

1. Departamento de Biofísica, Escola Paulsita de Medicina, Laboratório de Cardiobiologia, Universidade Federal de São Paulo, São Paulo, SP, Brazil (D.R-C).

2. Unidade de Hemodinâmica e Cardiologia Intervencionista, Escola de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil (J.A.M-N.).

3. Departamento de Fisiologia, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil (A.S.-M).

4. Hospital do Coração Anis Rassi, Goiânia, GO, Brazil (A.R.J.).

Abstract

Chagas cardiomyopathy caused by infection with the intracellular parasite Trypanosoma cruzi is the most common and severe expression of human Chagas disease. Heart failure, systemic and pulmonary thromboembolism, arrhythmia, and sudden cardiac death are the principal clinical manifestations of Chagas cardiomyopathy. Ventricular arrhythmias contribute significantly to morbidity and mortality and are the major cause of sudden cardiac death. Significant gaps still exist in the understanding of the pathogenesis mechanisms underlying the arrhythmogenic manifestations of Chagas cardiomyopathy. This article will review the data from experimental studies and translate those findings to draw hypotheses about clinical observations. Human- and animal-based studies at molecular, cellular, tissue, and organ levels suggest 5 main pillars of remodeling caused by the interaction of host and parasite: immunologic, electrical, autonomic, microvascular, and contractile. Integrating these 5 remodeling processes will bring insights into the current knowledge in the field, highlighting some key features for future management of this arrhythmogenic disease.

Publisher

Ovid Technologies (Wolters Kluwer Health)

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