[Lack of correlation for anti-β1 autoantibodies and cardioelectric disorders in chagas cardiomyopathy].

*Correspondence: Justo Carbajales E-mail: cardiogenomica@gmail.com Available online: 04-04-2023 Arch Cardiol Mex. 2023;93(2):260-262 www.archivoscardiologia.com Date of reception: 21-05-2021 Date of acceptance: 26-05-2022 DOI: 10.24875/ACM.21000163 Chagas’ disease, caused by the parasite Trypanosoma cruzi, is one of the most pervasive endemic infections in Latin America, currently affecting approximately 7 million people1. Nearly 40% of patients eventually develop chronic Chagas’ cardiomyopathy (CCC), which can manifest with conduction disorders, arrhythmias, congestive heart failure, stroke, and/or sudden death1. After the initial acute phase of the disease, hosts who are incompletely treated with anti-parasitic agents enter the indeterminate phase, characterized by low levels of parasitemia and the absence of signs or symptoms. Nearly two-thirds of people in the indeterminate phase remain in this state for over 10 years. Unfortunately, the other third progress to the chronic stage, wherein patients again experience the effects of antigenic stimulation. Chronic Chagas’ disease most commonly presents as a slowly evolving inflammatory cardiomyopathy. The presence of high levels of inflammatory mediators in patients with Chagas’ disease suggests that the host’s immune response to parasitic activity could play a key role in the perpetuation of myocardial inflammation. Patients with CCC have been found to produce anti-β1 and -ß2 adrenergic autoantibodies and anti-M2 cholinergic autoantibodies in the heart2,3, through a phenomenon known molecular mimicry. The relationship between autoantibody titers and the degree of cardiac disease remains controversial. The aim of this study was to evaluate whether patients with CCC and higher levels of anti-β1 autoantibodies had a significantly higher presence of cardiac arrhythmias or conduction disorders, which are considered clinical markers of CCC. Ethics clearance was granted by the bioethics commission of Jorge Ramos Mejía Hospital in Buenos Aires, Argentina. The study population consisted of 65 patients with at least a 20-year history of positive serology for Chagas’ disease to allow adequate time for manifestations of CCC to develop (Table 1). All patients had a left ventricular ejection fraction (LVEF) of either less than or equal to 35% or greater than or equal to 50%, as evaluated by Doppler echocardiography, to eliminate subjective differences in echocardiographic data. Patients with LVEF between 36% and 49%, or who had another established cause of cardiomyopathy, were excluded from the study. The presence of arrhythmias and conduction disorders was evaluated using electrocardiograms (ECG), storage data from implantable cardioverter-defibrillators (ICD) and pacemaker interrogation, and 24-h Holter