Chagas disease is caused by Trypanosoma cruzi, described by Carlos Chagas in 1909. It affects about 14 million people on the American continent, which 6 million are in Brazil. To demonstrate the clinical characteristics of the probable myocardiopathy caused by T. cruzi, a study was performed to characterize the electrocardiography, ecodopplercardiography and pathologic features in adult dogs during the acute and chronic indeterminate phase of the disease, since these animals can also be contaminated by the referred protozoan.

So, ten adult crossbreed dogs were experimentally infected with T. cruzi, Bolivian strain and submitted to electro and ecodopplercardiographic evaluation for 5 weeks (acute group, n=6) and 6 months (chronic group, n=4). Each group was compared with its respective control group.

On electrocardiography it was observed gradual increase in heart rate between 2^nd and 3^rd weeks post inoculation due to installation of sinusal tachycardia episodes as well others malignant arrhythmias. There was milivoltage suppression and electrical alternance, and reflex of myocardiac inflammatory process. Approaching the parasitemic peak it was observed junctional escape complexes in 10% of dogs, atrioventricular dissociation (10%) and sinusal tachycardia (25%). Four dogs had sudden death after R in T phenomenon that unchained episodes of sustained ventricular tachycardia and ventricular fibrillation. In chronic phase, the events was reduced to 1st degree atrioventricular blocks, ventricular premature complexes, ventricular bigeminism and electrical alternance. On echodopplercardiography was possible to observe irregular increase of myocardial echogenicity characterizing the presence of myocarditis. By M-Mode it was observed hypertrophy of left ventricle free wall and increase of biventricular diameter. By Doppler it was observed increase of A wave velocity peak of mitral flow, signalment mild diastolic dysfunction. In chronic phase was proved global increase of cardiac area, hypokinetic regions in left ventricle mainly in the apex of the heart suggesting the pathognomonic apex aneurysm of Chagas disease.

In accordance with the data obtained, it was observed acute myocarditis, ventricular arrhythmias, enlargement of right ventricle, excentric hypertrophy of the left ventricle according histopathologic features of inflammatory infiltrate and pseudocysts of T. cruzi in myocardial fibers similar to what occurs in men, which makes it an important experimental model to the comparative study of this disease during its different phases.

References

1. Acquatella , R.; et al. Value of m-model and two-dimensional echocardiography in chronic Chagas' heart disease: a clinical and pathologic study. Circulation, Baltimore, v.62, p.787-799, 1980.

2. Breniere, S. F., et al. Integrate study of a bolivian population infected by Trypanosoma cruzi, the agent of Chagas disease. Mem. Inst. Oswaldo Cruz, Rio de Janeiro, v.97, n.3, p. 289-295, 2002.

3. Meurs, K.M. et al. Chronic Trypanosoma cruzi infection in dogs: 11 cases (1887-1996). J. Am.. Vet. Med. Assoc., Schaumburg, v.213, n.4, p.497-500, 1998.