Chagasic Cardiomyopathy: New trends for an old burden. Epidemiology, Pathology, Diagnosis and Treatment of the American Trypanosomiasis

Abstract

The American Trypanosomiasis was first described by Carlos Chagas in 1909. Chagas´ disease is a zoonosis caused by a parasite, the Trypanosoma Cruzi. This parasite is transmitted by hematophageous bugs of the Triatominae species, in underserved rural areas of Latinamerica. Other forms of transmission include blood transfusion, intravenous drug abuse, digestive, transplacentary, breast feeding, and organ transplant. Considering these varied forms of transmission and the increasing immigration rates this disease gains importance in the United States and Europe as well. Three phases of the disease can be distinguished: 1) acute phase, with high tissue and blood parasitic involvement; 2) undetermined phase, in which the diagnosis requires further clinical investigations; 3) chronic phase (10-30 years following the infection). The diagnosis of Chagas Disease is based on epidemiology, clinical manifestations and laboratory findings. The last two factors will vary according to the phase of the disease. Given the fact that in the chronic phase there is low parasitemia, the diagnosis relies on serologic studies. Nevertheless direct studies can be used in reactivations of the disease in patients with HIV or immunosuppression states. About one fourth of infected individuals develop chronic chagasic cardiomyopathy (ChrChC), the most severe form of the disease. It can be manifested by complex ventricular arrhythmias, bradiarrhythmias, A-V blocks, apical ventricular aneurysm, thromboembolism, ventricular dysfunction with heart failure and sudden death. In our experience patients with higher mortality risk showed clinical manifestations such as third tone, right bundle branch block with left anterior hemiblock and left ventricle dilation (p<0.001). Chronic recurrent ventricular tachycardia often occurs in patients with chagasic aneurysms, and ventricular mapping indicates that these arrhythmias originate in regions adjacent to those aneurysms. ChrChC is histologically characterized by the presence of multifocal inflammatory infiltrates, composed mainly by mononuclear cells, adhered to myocytes and leading to myocytolysis, and by interstitial fibrosis with or without apical ventricular aneurysms. These lesions are thought to be mediated by immune phenomena rather than by continuing parasitic invasion of the heart The treatment of the parasite is limited to the acute phase using benznidazole or nifurtimox. Some articles support this treatment also in the undetermined phase. Heart transplantation is a useful therapy for end-stage ChrChC; however, Chagas reactivation remains a mayor complication. Given the fact that antibodies against Trypanosoma Cruzi bare great similarity with beta-1-adrenergic receptors, a new field for future treatment arises.