Summary: | Chagas disease, caused by a <i>Trypanosona</i><i> </i><i>cruzi</i> infection, is one of the main causes of heart failure in Latin America. It was originally a health problem endemic to South America, predominantly affecting residents of poor rural areas. With globalization and increasing migratory flows from these areas to large cities, the immigration of <i>T. </i><i>cruzi</i> chronically-infected people to developed, non-endemic countries has occurred. This issue has emerged as an important consideration for heart transplant professionals. Currently, Chagas patients with end-stage heart failure may need a heart transplantation (HTx). This implies that in post-transplant immunosuppression therapy to avoid rejection in the recipient, there is the possibility of <i>T. </i><i>cruzi</i><i> </i>infection<i> </i>reactivation, increasing the morbidity and mortality rates. The management of heart transplant recipients due to Chagas disease requires awareness for early recognition and parasitic treatment of <i>T.</i><i> </i><i>cruzi</i> infection reactivation. This issue poses challenges for heart transplant professionals, especially regarding the differential diagnosis between rejection and reactivation episodes. The aim of this review is to discuss the complexity of the Chagas disease reactivation phenomenon in patients submitted to HTx for end-stage chagasic cardiomyopathy.
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