ABSTRACT
Chagas disease is among the neglected tropical diseases recognized by the World Health Organization that have received insufficient attention from governments and health agencies. Chagas disease is endemic in 21 Latin America regions. Due to globalization and increased migration, it has crossed borders and reached other regions including North America and Europe. The clinical presentation of the disease is highly variable, from general symptoms to severe cardiac involvement that can culminate in heart failure. Chagas heart disease is multifactorial, and can include dilated cardiomyopathy, thromboembolic phenomena, and arrhythmias that may lead to sudden death. Diagnosis is by methods such as enzyme-linked immunosorbent assay (ELISA) and the degree of cardiac involvement should be investigated with complementary exams including ECG, chest radiography and electrophysiological study. There have been insufficient studies on which to base specific treatment for heart failure due to Chagas disease. Treatment should therefore be derived from guidelines for heart failure that are not specific for this disease. Heart transplantation is a viable option with satisfactory success rates that has improved survival.
Subject(s)
Arrhythmias, Cardiac/complications , Chagas Cardiomyopathy/complications , Chagas Cardiomyopathy/epidemiology , Heart Failure/etiology , Thromboembolism/complications , Antiparasitic Agents/therapeutic use , Chagas Cardiomyopathy/diagnosis , Chagas Cardiomyopathy/parasitology , Death, Sudden/epidemiology , Electrocardiography/methods , Electrophysiologic Techniques, Cardiac/methods , Enzyme-Linked Immunosorbent Assay/methods , Female , Heart Failure/epidemiology , Heart Failure/therapy , Heart Transplantation/methods , Humans , Magnetic Resonance Imaging/methods , Male , Prognosis , Radiography, Thoracic/methods , Trypanosoma cruzi/genetics , Trypanosoma cruzi/isolation & purificationABSTRACT
Resumen La cardiopatía chagásica crónica se presenta en un 30% de las personas infectadas con Trypanosoma cruzi. Aunque el parásito puede ser controlado por la respuesta inmune después de la fase aguda, su detección se hace difícil en la fase crónica a pesar de la persistencia de éste en los tejidos de los individuos infectados. Dado que solo un porcentaje de estos individuos crónicamente infectados desarrolla el daño tisular, se sugiere la existencia de factores asociados que predicen la aparición de la sintomatología crónica: a) la genética del hospedero (moléculas del HLA), cuyo papel aún no se ha dilucidado, b) factores dependientes del parásito cómo la variabilidad de los genotipos (TcI a TcVI), su asociación con tropismo y daño tisular; y c) otros factores como la cantidad del inóculo, la reexposición constante a vectores infectados, las diferentes vías de infección y el estado inmunológico del hospedero. Varias teorías han sido implicadas en el compromiso cardiaco, como la persistencia del T. cruzi en los tejidos, la autoinmunidad inducida y el daño tisular producido por la respuesta inmune. En esta revisión se pretende emitir una hipótesis respecto a la disfunción celular inmune producida por la persistencia parasitaria en los tejidos y su papel en la patogénesis de la enfermedad. Se consideran aspectos como el pronóstico de los pacientes con cardiopatía chagásica llevados a trasplante de corazón por falla cardiaca avanzada comparado con otras causas de falla que conducen a trasplante y la posible organización de los infiltrados inflamatorios en el tejido cardiaco, el cual podría funcionar como un tejido linfoide terciario.
Abstract Chronic Chagas cardiomyopathy is present in 30% of people infected with Trypanosoma cruzi. Even though the parasite can be controlled by immune response after the acute phase, its detection is hard in the chronic phase despite its persistence in the tissues of infected individuals. Since only a fraction of these chronically infected individuals develop tissue damage, the existence of associated predictive factors for appearance of chronic symptoms is suggested: a) host's genetics (HLA molecules) whose role has not yet been clarified; b) parasitedependent factors such as genotype variability (TcI to TcVI), their association with tropism and tissue damage; and c) other factors like the amount of inoculum, the constant reexposure to infected vectors, the different infection routes and the host's immune status. Several theories have been put forward with regard to cardiac compromise, such as T. cruzi persistence in tissues, induce autoimmunity and tissue damage caused by immune response. This review intends to propose a hypothesis on cellular immune dysfunction produced by parasite persistence in tissues and their role in the pathogenesis of the disease. Aspects such as prognosis of patients with Chagas cardiomyopathy who undergo heart transplant due to advanced heart failure are taken into consideration and compared to other failure causes that lead to transplants, and also the possibly organisation of inflammatory infiltrates in heart tissue, which could function as a tertiary lymphoid tissue.