Iván Mendoza, Federico Moleiro,
Juan Marques, Julio Guerrero, Alvaro Matheus, Freddy Rodriguez, Ana Rodriguez, Iván
Mendoza Britto, Antonio Bayés de Luna*, Agustin Castellanos**.
Section of Cardiology, Tropical Medicine Institute, Central University of
Venezuela, Caracas, Venezuela, *Hospital Sant Pau, Barcelona, Spain, **Jackson Memorial
Hospital, University of Miami, Miami, USA
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American trypanosomiasis or Chagas' disease, first
described in 1909 by the brazilian physician Carlos Chagas who also discovered its
aetiological agent and mode of transmission, is a disabling and potentially lethal disease1. It is caused by the flagellate parasite Trypanosoma
cruzi, a protozoan harbores by a variety of domestic and wild animals1.
The insect vectors of the disease are present throughout most South and Central America,
and their zone of distribution extend across the southern United States, where at least
some of these vectors are infected with Trypanosoma2,3.
In Latin America, 20 million people are thought to have Chagas' disease and 90 million are
considered to be at risk of infection2. It is the most
common cause of dilated cardiomyopathy in countries where the disease is endemic and is
responsible for over 30 percent of deaths from any cause and nearly all deaths from
cardiovascular causes in areas where the disease is endemic4,5
Chagas' disease commonly presents with symptomatic ventricular arrhythmias, symptomatic
bradyarrhythmias, sudden deaths, heart failure, embolic events, chest pain and high
susceptibility to proarrhythmia5. The clinical picture
mimics that of coronary artery disease as well as idiopathic dilated cardiomyopathy. The
prognosis is poor for patients with malignant ventricular arrhythmias, heart failure, left
ventricular aneurysm or global systolic dysfunction6,9.
The infection is characterized by an acute symptomatic phase with high parasitemia and
is followed by a lifelong intermediate phase in which low numbers of parasites are
sequestered in tissues; however the acute phase often is clinically silent5. Chronic progressive Chagas' heart disease develops in
approximately 20 to 40 percent of infected persons6,9.
This chronic phase is usually manifested by a cardiomyopathy due to progressive multifocal
damage in both the myocardium and the conduction system6,9.
It has long been observed that loss of cardiac innervation is frequently found
pathologically in Chagas' disease. This abnormality often precedes other evidence of
cardiac involvement and is associated with clinically dectable abnormalities of autonomic
function. Such a strong propensity for autonomic dysfunction is a unique feature of
Chagas' disease that distinguishes it from other cardiomyopathic disorders and has led
some to hypothesize that it may contribute to the pathogenesis of cardiac damage10.
Within the group of patients with Chagas' disease, atypical chest pain occurred in 53
percent. Whether the ischemic like syndrome of the chagasic patients was due to coronary
vasospasm because an autonomic imbalance or because of abnormalities of endothelium -
derives relaxing factors has to be determined. In a group of chagasic patients with left
ventricular apical aneurysm, the intracoronary infusion of acetylcholine or adenosine
elicited a paradoxical coronary vasoconstrictive response, suggesting that an abnormality
of the endothelium-dependent coronary vasomotion may have a role in both the chest pain
and the development of segmental-wall-motion abnormalities11.
The pathogenesis of the cardiomyopathic in chronic Chagas' disease is incompletely
understood. A dynamic hypothesis begins with direct parasite-related tissue damage,
followed by progressive damage perpetuated by autoimmune and microvascular abnormalities.
Studies in animals suggest involvement of cellular mechanisms particulary CD4 + T
lymphocytes, along with macrophage activation and inflammatory cytokine mediators.
Autonomic dysfunction probably has a secundary role, and the contribution of persistent
occult infection remains unclear. Further understanding of the pathogenetic mechanisms is
paramount to devising potential strategies for treatment and vaccination12.
In its usual mode of transmission, the disease is spread by the insect vectors,
usually members of the reduviidee family (Kissing bug). These insects puncture the skin of
the host to suck blood. They carry Trypanosoma cruzi in their gastrointestinal tract; they
defecate as they suck blood, and the excreted Trypanosoma cruzi then penetrates into the
host through the punctured skin. Blood transfusion are the second most frequent mode of
transmission of Chagas' disease. The congenital form, transmitted through the placenta, is
also relatively frequent. The risk of infection is directly related to socio-economic
factors, since the triatomine bugs preferred habitat is in crevices in the wall of
poor-quality houses in rural areas and periurban slums.
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