Association between the elevation of biomarkers and incipient alterations in ventricular function in patients with Chagas disease without evidence of specific organ damage

Abstract

Abstract Background Chagas disease (ChD) has a long asymptomatic period, where there is no evidence of myocardial damage. However, incipient alterations in ventricular systo-diastolic function have been described using echocardiography with Tissue Doppler and Strain. On the other hand, the presence of elevated higth-sensitivity T troponin (HS-TnT) and N-terminal pro B-type natriuretic peptide (NT-pro BNP) has been documented in the early stages of the ChD. The association between the elevation of both markers and incipient alterations in ventricular function in patients with ChD without evidence of heart damage has been poorly studied. Purpose The aim of this study is to evaluate the prevalence of elevation of both biomarkers (HS-TnT and NT-proBNP) and their association with insipients alterations in systo-diastolic function in patients with ChD without evidence of structural heart affection. Materials and methods Outpatients with stage 0 of ChD (positive serology, with normal electrocardiogram, holter and chest teleradiography) were included prospectively. They were divided in three groups according to the dosage of HS-TnT and NT-proBNP. Group 1: patients with both markers within normal values; group 2: patients with elevation of one of the markers (HS-TnT>13 ng/L OR NT-proBNP>125 pg/ml) and group 3: patients with elevation of both markers (HS-TnT>13 ng/L AND NT-proBNP>125 pg/ml). All of them underwent Doppler echocardiography with tissue Doppler. Results Two hundred and sixty-one patients were included, with 47±9 years old of age, 44% woman, 86.6% (n=226) in group 1, 9.6% (n=25) in group 2 and 3.8% (n=10) in group 3. Table 1 shows the main results. Conclusions Elevation of both markers was found in almost 4% of patients. This elevation was associated with a higher E/e' ratio, E/A ratio, Letf Atrial Area and a lower S'-wave lateral. Funding Acknowledgement Type of funding source: None