Physiopathology of Chagas' heart disease: correlations between clinical and experimental findings.

In penetrating the heart and developing in it, Trypanosoma cruzi produces an immunoallergic reaction that leads to changes in the histological structure of the myocardium; these changes alter the fundamental properties of the heart, causing fundamental dynamic disorders and morphological changes in the organ.In Chagas' cardiomyopathy, the velocity of impulse propagation diminishes in the auricular and ventricular musculature, altering the activation mechanism, this being shown by changes in the P-wave and in ventricular focal blocks.The functional refractory period (FRP) is shortened in the auricular and ventricular tissue and constitutes, together with changes in conductivity, the physiopathological basis that explains the circus movement-the fundamental factor of the arrhythmias of this stage of the disease. Localization of the inflammation in the A-V conduction system increases the duration of the FRP, producing all types of A-V block.The oedema and the cellular interstitial infiltration seen during this acute phase reduce the distensibility of the fibres; this, in turn, limits their contractility, producing a decrease in systolic volume and an increase in the final diastolic pressure in the chambers of the heart-fundamental factors in reducing kinesia and in increasing the heart's volume.In the chronic phase, destruction of the contractile tissue and fibroblastic proliferation bring into play compensatory mechanisms that maintain the strength of cardiac contractions; the elongation of the fibres and the nature of the dynamic pressure-volume curves explain the dilatation of the chambers of the heart and the dynamic changes seen in this phase of the disease.