title: Myocardial scars correlate with eletrocardiographic changes in chronic Trypanosoma cruzi infection for dogs treated with Benznidazole.
abstract: OBJECTIVE
  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 270 days 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/74931 μm(2) in dogs infected with Berenice-78 strain, 5839.2 ± 1423.49 collagen/74931 μm(2) in infected by AAS and 6294.40 ± 896.04 collagen/74931 μm(2) 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/74931 μm(2) ) and Bz-resistant AAS strains (4024 ± 1272.44 collagen/74931 μm(2) ), coincident with only 10% de ECG alterations at 270 days. However, in those animals infected with a Bz-resistant VL-10 strain, specific treatment did not alter collagen deposition (6749.5 ± 1596.35 collagen/74931 μm(2) ) and there was first atrioventricular block and chamber overload at 120 and 270 days 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.
authors.affiliation: Núcleo de Pesquisas em Ciências Biológicas, Universidade Federal de Ouro Preto, Minas Gerais, Brazil.
authors.forename: Ivo Santana
authors.initials: IS
authors.lastname: Caldas
authors.forename: Paulo Marcos
authors.initials: PM
authors.lastname: da Matta Guedes
authors.forename: Fabiane Matos
authors.initials: FM
authors.lastname: dos Santos
authors.forename: Lívia
authors.initials: L
authors.lastname: de Figueiredo Diniz
authors.forename: Tassiane Assíria Fontes
authors.initials: TA
authors.lastname: Martins
authors.forename: Alvaro Fernando
authors.initials: AF
authors.lastname: da Silva do Nascimento
authors.forename: Maira Araújo
authors.initials: MA
authors.lastname: Azevedo
authors.forename: Wanderson Geraldo
authors.initials: WG
authors.lastname: de Lima
authors.forename: Raimundo Marques Nascimento
authors.initials: RM
authors.lastname: Neto
authors.forename: Rosália Morais
authors.initials: RM
authors.lastname: Torres
authors.forename: André
authors.initials: A
authors.lastname: Talvani
authors.forename: Maria Terezinha
authors.initials: MT
authors.lastname: Bahia
mesh_terms: D000818:Animals; D054537:Atrioventricular Block; D014355:Chagas Disease / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology / Q000662:veterinary; D002908:Chronic Disease; D002921:Cicatrix / Q000517:prevention & control*; D003094:Collagen / Q000378:metabolism*; D004285:Dogs; D004351:Drug Resistance / Q000187:drug effects; D004562:Electrocardiography; D005355:Fibrosis / Q000517:prevention & control; D006325:Heart Atria / Q000187:drug effects* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*; D009593:Nitroimidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D011446:Prospective Studies; D016896:Treatment Outcome; D014344:Trypanocidal Agents / Q000494:pharmacology / Q000627:therapeutic use; D014349:Trypanosoma cruzi
chemical_list: D009593:Nitroimidazoles; D014344:Trypanocidal Agents; D003094:Collagen; C009999:benzonidazole