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      Chagas’ heart disease: gender differences in myocardial damage assessed by cardiovascular magnetic resonance

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          Abstract

          Background

          Since a male-related higher cardiovascular morbidity and mortality in patients with Chagas’ heart disease has been reported, we aimed to investigate gender differences in myocardial damage assessed by cardiovascular magnetic resonance (CMR).

          Methods and results

          Retrospectively, 62 seropositive Chagas’ heart disease patients referred to CMR (1.5 T) and with low probability of having significant coronary artery disease were included in this analysis. Amongst both sexes, there was a strong negative correlation between LV ejection fraction and myocardial fibrosis (male r = 0.64, female r = 0.73, both P < 0.001), with males showing significantly greater myocardial fibrosis ( P = 0.002) and lower LV ejection fraction ( P < 0.001) than females. After adjustment for potential confounders, gender remained associated with myocardial dysfunction, and 53% of the effect was mediated by myocardial fibrosis ( P for mediation = 0.004). Also, the transmural pattern was more prevalent among male patients (23.7 vs. 9.9%, P < 0.001) as well as the myocardial heterogeneity or gray zone (2.2 vs. 1.3 g, P = 0.003).

          Conclusions

          We observed gender-related differences in myocardial damage assessed by CMR in patients with Chagas’ heart disease. As myocardial fibrosis and myocardial dysfunction are associated to cardiovascular outcomes, our findings might help to understand the poorer prognosis observed in males in Chagas’ disease.

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          Most cited references26

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          Pathogenesis of chronic Chagas heart disease.

          Chagas disease remains a significant public health issue and a major cause of morbidity and mortality in Latin America. Despite nearly 1 century of research, the pathogenesis of chronic Chagas cardiomyopathy is incompletely understood, the most intriguing challenge of which is the complex host-parasite interaction. A systematic review of the literature found in MEDLINE, EMBASE, BIREME, LILACS, and SCIELO was performed to search for relevant references on pathogenesis and pathophysiology of Chagas disease. Evidence from studies in animal models and in anima nobile points to 4 main pathogenetic mechanisms to explain the development of chronic Chagas heart disease: autonomic nervous system derangements, microvascular disturbances, parasite-dependent myocardial aggression, and immune-mediated myocardial injury. Despite its prominent peculiarities, the role of autonomic derangements and microcirculatory disturbances is probably ancillary among causes of chronic myocardial damage. The pathogenesis of chronic Chagas heart disease is dependent on a low-grade but incessant systemic infection with documented immune-adverse reaction. Parasite persistence and immunological mechanisms are inextricably related in the myocardial aggression in the chronic phase of Chagas heart disease. Most clinical studies have been performed in very small number of patients. Future research should explore the clinical potential implications and therapeutic opportunities of these 2 fundamental underlying pathogenetic mechanisms.
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            Development and validation of a risk score for predicting death in Chagas' heart disease.

            Chagas' disease is an important health problem in Latin America, and cardiac involvement is associated with substantial morbidity and mortality. We developed a model to predict the risk of death in patients with Chagas' heart disease. We retrospectively evaluated 424 outpatients from a regional Brazilian cohort. The association of potential risk factors with death was tested by Cox proportional-hazards analysis, and a risk score was created. The model was validated in 153 patients from a separate community hospital. During a mean follow-up of 7.9 years, 130 patients in the development cohort died. Six independent prognostic factors were identified, and each was assigned a number of points proportional to its regression coefficient: New York Heart Association class III or IV (5 points), evidence of cardiomegaly on radiography (5 points), left ventricular systolic dysfunction on echocardiography (3 points), nonsustained ventricular tachycardia on 24-hour Holter monitoring (3 points), low QRS voltage on electrocardiography (2 points), and male sex (2 points). We calculated risk scores for each patient and defined three risk groups: low risk (0 to 6 points), intermediate risk (7 to 11 points), and high risk (12 to 20 points). In the development cohort, the 10-year mortality rates for these three groups were 10 percent, 44 percent, and 84 percent, respectively. In the validation cohort, the corresponding mortality rates were 9 percent, 37 percent, and 85 percent. The C statistic for the point system was 0.84 in the development cohort and 0.81 in the validation cohort. A simple risk score was developed to predict death in Chagas' heart disease and was validated in an independent cohort. Copyright 2006 Massachusetts Medical Society.
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              Oral transmission of Chagas disease.

              Chagas disease is now an active disease in the urban centers of countries of nonendemicity and endemicity because of congenital and blood and/or organ transplantation transmissions and the reactivation of the chronic disease in smaller scale than vectorial transmission, reported as controlled in countries of endemicity. Oral transmission of Chagas disease has emerged in unpredictable situations in the Amazon region and, more rarely, in areas of nonendemicity where the domiciliary triatomine cycle was under control because of exposition of the food to infected triatomine and contaminated secretions of reservoir hosts. Oral transmission of Chagas disease is considered when >1 acute case of febrile disease without other causes is linked to a suspected food and should be confirmed by the presence of the parasite after direct microscopic examination of the blood or other biological fluid sample from the patient.
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                Author and article information

                Contributors
                antonildes@usp.br
                mjerosch-herold@partners.org
                rodrigojlm07@hotmail.com
                alvima88@hotmail.com
                lilianerocha@yahoo.com.br
                jatorreao@hotmail.com
                fabio.fernandes@incor.usp.br
                barbara.ianni@incor.usp.br
                charles.mady@incor.usp.br
                jose.ramires@incor.usp.br
                roberto.kalil@incor.usp.br
                + 55 11 2661-5587 , rochitte@incor.usp.br
                Journal
                J Cardiovasc Magn Reson
                J Cardiovasc Magn Reson
                Journal of Cardiovascular Magnetic Resonance
                BioMed Central (London )
                1097-6647
                1532-429X
                28 November 2016
                28 November 2016
                2017
                : 18
                : 88
                Affiliations
                [1 ]Heart Institute, InCor, University of Sao Paulo Medical School, Cardiovascular Magnetic Resonance and Computed Tomography Sector, Av. Dr. Enéas de Carvalho Aguiar, 44, Andar AB, Cerqueira César, São Paulo, SP 05403-000 Brazil
                [2 ]Department of Radiology, Brigham and Women’s Hospital, Boston, MA USA
                Article
                307
                10.1186/s12968-016-0307-5
                5125033
                27890014
                f2f65dbb-7318-4778-8608-0d74fe7ed4e7
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 29 July 2016
                : 12 November 2016
                Funding
                Funded by: São Paulo Research Foundation (FAPESP)
                Award ID: 2010/51900-3
                Award Recipient :
                Funded by: Zerbini Foundation
                Categories
                Research
                Custom metadata
                © The Author(s) 2016

                Cardiovascular Medicine
                chagas’ heart disease,gender differences,myocardial fibrosis,myocardial dysfunction

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