Selenium Treatment and Chagasic Cardiopathy (STCC)

Several induced cardiomyopathy , Mycoplasma pneumonia-induced myocarditis, heart damage investigations have shown positive effects of Se on experimental models: cardiotoxicity induced by chemotherapics, ischemic cardiopathy, CVB3 and LP-BM5 (murine AIDS, retrovirus)-in reperfused heart, and in chagasic cardiopathy. In addition, beneficial effects of Se supplementation were reported in patients with myocardial infarct, Keshan disease, and cardiac dysfunction during HPN. Our group has investigated the role and Se effect on infection by T. cruzi. By evaluating plasma Se levels in 170 chagasic patients, we discovered that the frequency of subjects with Se levels lower than normal was significantly higher in those with severe cardiopathy. Moreover, in this pioneering research, we found a positive correlation between Se levels and the LVEF, indicating that normal Se levels pave the way for efficient cardiac function. Later, we investigated if nutritional deficiency of this trace element interfered with the development of cardiopathy and the susceptibility to experimental T. cruzi infection. In that study, we found 100 % of mortality in Se deficient mice, while in the selenium adequate groups only 20% of the male and no female died even at 40 dpi. In addition, parasitemia levels of infected mice were not altered by Se deficiency, suggesting that the high susceptibility at the acute phase was not due to the parasite load. We later investigated if Se treatment could minimize the course of T. cruzi infection or the myocarditis in mice. We verified that the concentration of 4 ppm Se did not alter the resistance to infection but was able in preventing the increase of CK-MB levels in infected mice, indicating that Se helps to protect the heart from inflammatory damage driven by T. cruzi infection. Currently, experimental and clinical trials concerning Se supplementation have been performed; however, to date, there is no trial regarding the use of this micronutrient as a treatment to protect cardiac function in chagasic patients with cardiopathy. The present clinical trial aims to study the effect of Se intervention on the progression rate of the cardiopathy in patients with mild or moderate HD (LVEF between 35 % and 45 %) in order to validate this new strategy of treatment. The HD will be expressed by the progression rate and by the comparison of means of the LVEF. In this context we will test the hypothesis that Se treatment is able to interfere with the progression of cardiac dysfunction in chronic chagasic patients. We expect the impediment of the progression of ventricular dysfunction in patients with mild HD, and the improvement of cardiac function in patients with moderate HD in the group of patients receiving Se therapy. This is the first clinical trial concerning this specific group of cardiac chagasic patients with mild or moderate HD.