Prospective analysis of myocardial strain through the evolution of Chagas disease in the hamster animal model

Fernando Fonseca França Ribeiro,Henrique Turin Moreira,Benedito C Maciel,Cibele M Prado,André Schmidt,Marcus V Simões,Luciano F L Oliveira,Camila G Fabricio,Minna Moreira Dias Romano,Denise M Tanaka,Antônio Carlos Leite De Barros-Filho,José A Marin-Neto

doi:10.1007/s10554-021-02379-w

Abstract

Speckle tracking echocardiography (STE) enables early diagnosis of myocardial damage by evaluating myocardial strain. We aimed to study sequential changes in structural and ventricular functional parameters during Chagas disease (CD) natural history in an animal model. 37 Syrian hamsters were inoculated intraperitoneally with Trypanosoma cruzi (Chagas) and 20 with saline (Control). Echocardiography was performed before the infection (baseline), at 1 month (acute phase), 4, 6, and 8 months (chronic phase) using Vevo 2100 (Fujifilm Inc.) ultrasound system. Left ventricular end-diastolic diameter, Left ventricular end-systolic diameter (LVESD), Left ventricular ejection fraction (LVEF), Global longitudinal (GLS), circumferential (GCS) and radial (GRS) strain were evaluated. Tricuspid annular plane systolic excursion (TAPSE) was used to assess right ventricular function. At 8 months, animals were euthanized and LV myocardial samples were analyzed for quantitation of inflammation and fibrosis. LVEF decreased over time in Chagas group and a difference from Control was detected at 6 months (p-value of groups#time interaction = 0.005). There was a pronounced decrease in GLS, GCS and TAPSE in Chagas group (p-value of groups#time interaction = 0.003 for GLS, < 0.001 for GCS and < 0.009 for TAPSE vs Control) since the first month. LVESD, LVEF and GLS were significantly correlated to the number of inflammatory cells (r = 0.41, p = 0.046; r = − 0.42, p = 0.042; r = 0.41, p = 0.047) but not to fibrosis. In the Syrian hamster model of CD STE parameters (GLS and GCS) showed an early decrease. Changes in LVEF, LVESD, and GLS were correlated to myocardial inflammation but not to fibrosis.

Highlights

Chagas disease (CD) remains one of the most prevalent infectious diseases in Latin America, where more than six million people are infected by the protozoan Trypanosoma cruzi [1, 2]
Changes in Left ventricular ejection fraction (LVEF), Left ventricular end-systolic diameter (LVESD), and Global longitudinal strain (GLS) were correlated to myocardial inflammation but not to fibrosis
The pathogenesis of Chronic Chagas cardiomyopathy (CCC) is pleomorphic and involves various mechanisms related to parasite persistence causing low grade but incessant inflammation and myocardial injury mediated by the immune system

Summary

Introduction

Chagas disease (CD) remains one of the most prevalent infectious diseases in Latin America, where more than six million people are infected by the protozoan Trypanosoma cruzi [1, 2]. The World Health Organization (WHO) recognizes CD as one of the thirteen most neglected tropical diseases in the world, with 25 million people at risk of infection [3, 4]. The pathogenesis of CCC is pleomorphic and involves various mechanisms related to parasite persistence causing low grade but incessant inflammation and myocardial injury mediated by the immune system. A particular aspect of the pathogenesis of CCC is delayed myocardial damage, which is related to a persistently low intensity but incessant parasitism and myocardial injury mediated by the immune system [11]. Most patients require specialized care, anticoagulation, pacemaker, cardioverterdefibrillator implantation and heart transplantation, with a high overall medical and social burden [12, 13]

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