Histopathology of the heart conducting system in experimental Chagas disease in mice

Although mice infected with Trypanosoma cruzi develop a wide variety of electrocardiographic (ECG) alterations, the typical isolated right bundle branch block or its association with the left anterior hemiblock patterns are not found in this model. This has been explained as related to topographic differences in the anatomy of the murine conducting system. However, there is no conclusive evidence that the murine conducting system differs from the human system. In this study, the anatomy of the murine conducting system is described, as well as its involvement in the chronic stages of experimental infection. 24 three-month-old C3H mice were infected with 50 bloodstream forms of T. cruzi, Tulahuén strain. Animals were killed after 3, 8 and 12 months. Whole frontal sections of the heart, including the conducting system, were serially studied. The sinoatrial node was located in the right atrial appendage, or in the junction between the superior vena cava and the right atrium, or “riding” on the interatrial septum. The atrioventricular (A-V) node and the His bundle showed a similar anatomic course to that in man. Therefore, there was no important anatomical difference that might have explained the lack of the ECG patterns observed in human chagasic myocardiopathy. The inflammatory involvement and the lesions of the conducting system were diverse and rarely severe. No significant difference was observed in animals killed at different times. The lesions in the working myocardium were similar to those observed in humans (chronic inflammatory infiltrates). Nevertheless, the topography of lesions was different: there was a selective involvement in the neighbourhood of the A-V groove. The experimental chronic chagasic infection thus obtained did not reproduce the distribution nor the large extension of the “panmyocarditis” observed in man. The lack of comparability in the ECG of the human disease and this model might be due to 3 factors: (a) little damage to the conducting system; (b) insufficient “cardiomyopathy” to generate complete bundle branch blocks and arrhythmias, and (c), less probably, short time course of infection.