IJCS | Volume 31, Nº2, March / April 2018

174 asymptomatic or have only the mild and non-specific symptoms of an infectious syndrome, and rarely present myocarditis or symptomatic meningoencephalitis. As soon as the acute phase collapses, generally after 4 to 8 weeks, the patient evolves to a chronic phase, which includes two forms of the disease: an indeterminate (latent or preclinical) form, and a determined form, with clinical expression, which subdivides into cardiac, digestive or cardiodigestive. There may also be a direct evolution from the acute phase to the chronic phase, without the occurrence of the indeterminate form, in 5 to 10% of cases. 7 Reactivation of the chronic disease can also occur, presenting as an acute (exacerbated) disease, in individuals with natural immunosuppression, due to diseases such as AIDS, or iatrogenically (e.g. in solid‑organ-transplanted patients). Figure 1 represents the natural evolution of the disease. The indeterminate form includes patients with evidence of T. cruzi infection (positive serological tests, based on the presence of antiparasite circulating antibodies), but without clinical manifestations of cardiac or digestive tract disease. About 30 to 50% of patients with the indeterminate form, whichmay usually last from 10 to 30 years, will develop CCC throughout their lives. 8 CCC not only is the most commonmanifestation, but it is also the most severe, withmorbidity rates of up to 30%. 9,10 Also, considering that late evolution of CCC involves the appearance of a clinical picture of dilated cardiomyopathy, with global LV dysfunction, and heart failure syndrome, the Latin American guidelines for the diagnosis and treatment of Chagas cardiomyopathy have proposed a clinical classification of LV dysfunction in Chagas' disease which reflects the progression of evolutionary stages of heart failure adopted in the international guidelines for this syndrome. Thus, the chronic phase of CCC can be classified into 5 evolutionary stages (A, B1, B2, C and D) of LV dysfunction (Chart 1). Etiopathogeny In the acute phase, organic damage is clearly associated with parasitic infestation and multiplication in the myocardium, in addition to other commonly impaired tissues, such as the nervous system and the digestive tract. Lymphadenopathy and enlargement of the spleen and liver are a result of the systemic immune reaction and correlate with the high parasitemia. Human exposure to T cruzi (vectorial, via transfusion, congenital, oral, via organ transplant, accidental) No infection Cure (50–80% of cases) Cure (20–60% of cases) Antiparasitic drug Antiparasitic drug Antiparasitic drug < 5–10% of symptomatic cases Acute Chagas infection (asymptomatic or symptomatic) Death from myocarditis or meningoencephallitis Chronic phase in indeterminate form Chronic phase in determinate form 10–30 years later Cure (lower proportion of cases than for the indeterminate form) Permanent indeterminate form Immunosuppression Reactivation Cardiac Cardiodigestive Digestive Figure 1 – Natural History of Chagas Disease. Reprinted from Rassi A.Jr et alii. Lancet. 2010:1388-402. Simões et. al. Chagas Disease Cardiomyopathy Int J Cardiovasc Sci. 2018;31(2)173-189 Review Article