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Abstract
Trypanosoma cruzi (T. cruzi) infection is endemic in Latin America.1 T. cruzi can be transmitted to human beings through the feces of a kissing bug, congenitally, blood transfusion, oral transmission, laboratory contamination, and organ transplantation.1 In 14–30% of patients, acute T. cruzi infection is followed by a long, clinically silent period before the clinical presentation of chronic Chagas’ disease (CD). The T. cruzi infection may result in heterogeneous heart (H) phenotypes, including bradycardia; right bundle-branch block, left anterior fascicular block; cardiomyopathy; heart failure (HF), thromboembolism; arrhythmias; sudden death; and syncope.
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