Myocardial scars correlate with eletrocardiographic changes in chronic Trypanosoma cruzi infection for dogs treated with Benznidazole

Abstract

Objectives The cardiac form of Chagas disease is evidenced by a progressive cardiac inflammation that leads to myocarditis, fibrosis and electrocardiographic (ECG) conduction abnormalities. Considering these characteristics, the aim of this study was to prospectively evaluate the early ECG changes in dogs that were experimentally inoculated with Benznidazole (Bz)-susceptibly (Berenice-78) and Bz-resistant (VL-10, and AAS) Trypanosoma cruzi strains and, later, evaluate the efficacy of Bz treatment for preventing these ECG alterations. Methods Electrocardiographic changes of treated and untreated animals were prospectively evaluated for up to 270days after infection, at which point collagen (right atrium) quantification was performed. Results All infected dogs had a high intensity of heart fibrosis (4616.00±1715.82 collagen/74931μm2 in dogs infected with Berenice-78 strain, 5839.2±1423.49 collagen/74931μm2 in infected by AAS and 6294.40±896.04 collagen/74931μm2 in animals infected with VL-10 strain), while 78.57% of all infected dogs showed ECG alterations. Bz Therapy reduced or prevented fibrosis in Bz-susceptible Berenice-78 (2813.00±607.13 collagen/74931μm2) and Bz-resistant AAS strains (4024±1272.44 collagen/74931μm2), coincident with only 10% de ECG alterations at 270days. However, in those animals infected with a Bz-resistant VL-10 strain, specific treatment did not alter collagen deposition (6749.5±1596.35 collagen/74931μm2) and there was first atrioventricular block and chamber overload at 120 and 270days after infection, with 75% abnormal ECG exams. Conclusions These findings indicate that an effective antiparasitic treatment in the early stage of Chagas disease can lead to a significant reduction in the frequency and severity of the parasite-induced cardiac disease, even if parasites are not completely eliminated. © 2012 Blackwell Publishing Ltd.