Perspectives on Trypanosoma cruzi-induced heart disease (Chagas disease)

Abstract

Chagas disease is caused by the parasite Trypanosoma cruzi. It is a common cause of heart disease in endemic areas of Latin America. The year 2009 marks the 100th anniversary of the discovery of T cruzi infection and Chagas disease by the Brazilian physician Carlos Chagas. Chagasic cardiomyopathy develops in from 10% to 30% of persons who are chronically infected with this parasite. Echocardiography and magnetic resonance imaging (MRI) are important modalities in the evaluation and prognostication of individuals with chagasic heart disease. The etiology of chagasic heart disease likely is multifactorial. Parasite persistence, autoimmunity, and microvascular abnormalities have been studied extensively as possible pathogenic mechanisms. Experimental studies suggest that alterations in cardiac gap junctions may be etiologic in the pathogenesis of conduction abnormalities. The diagnosis of chronic Chagas disease is made by serology. The treatment of this infection has shortcomings that need to be addressed. Cardiac transplantation and bone marrow stem cell therapy for persons with Chagas disease have received increasing research attention in recent years.

Figure 1

Life cycle of Trypanosoma cruzi (CDC website)

Figure 2

The right panel is a heart obtained from an individual with chronic Chagas cardiomyopathy. There is four-chambered enlargement of the heart and an apical aneurysm. (Courtesy of Armed forces Institute of Pathology). The left panel shows the echocardiographic findings in Chagas heart disease. A. Transesophageal echocardiography demonstrating an apical aneurysm containing a large, round, and protruding thrombus (arrow); B–D. Transthoracic apical 4-chamber views of the heart showing dilated cardiac chambers (B), and functional mitral (C) and tricuspid (D) regurgitation (arrows). E. Parasternal short-axis view of the heart showing a large pericardial effusion (PE). F and G. Transmitral pulsed-Doppler (F) and lateral annulus tissue Doppler (G) demonstrating apparently normal peak early (E) and late (A) transmitral velocities, E/A ratio, and E-wave deceleration time (F) but abnormal early (E′) and late (A′) velocities (G) consistent with advanced diastolic dysfunction. LA=left atrium; LV=left ventricle; PE=pericardial effusion; RA=right atrium; RV=right ventricle.

Figure 3

A. Pseudocyst in the heart containing intracellular amastigotes (arrow). B. Infected cultured fibroblasts containing intracellular amastigotes. Some cells have ruptured and trypomastigotes are observed leaving the host cell (arrow). C. Vessel of an infected mouse demonstrating a vasculitis. D. Pseudocyst in the wall of a blood vessel. E. Acute myocarditis in the heart of a T. cruzi-infected mouse. There are many inflammatory cells and pseudocysts (arrow). F. Pseudocysts in the heart of a T. cruzi–infected mouse (arrow).