Perspectives on Trypanosoma cruzi–Induced Heart Disease (Chagas Disease)

Abstract

Chagas disease is caused by the parasite Trypanosoma cruzi it is the most 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 percent of persons who are chronically infected with this parasite. Echocardiography and magnetic resonance imaging are important modalities in the evaluation and prognosis 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.

Chagas disease: Present status of pathogenic mechanisms and chemotherapy

“…It is characterized by the absence of clinical symptoms, but serology is positive and there is some degree of cardiac involvement evidenced by minimal, but persistent, inflammation (Dubner et al, 2008;Marin-Neto and Rassi, 2009;Punukollu et al, 2007;Tanowitz et al, 2009).…”

“…This syndrome leads to complex arrhythmias, ventricular aneurysms, heart failure, thromboembolism and sudden death. Evidence from studies in animal models and in humans supports four main pathogenic mechanisms to explain Chagas heart disease: i) parasite-dependent myocardial damage; ii) immune-mediated myocardial injury; iii) cardiac dysautonomia; and iv) microvascular abnormalities and ischemia (Marin-Neto and Rassi, 2009;Rassi et al, 2009a;Rassi and Rassi, 2009;Rassi et al, 2009c;Tanowitz et al, 2009).…”

“…It is suggested that factors, such as autoimmunity, might be involved in the development of Chagasic pathology. It is clear that antiparasite and autoreactivity responses are not mutually exclusive in Chagas disease, and that a combination of these types of immune response could be involved in the establishment of pathology (Ribeiro et al, 2009b;SathlerAvelar et al, 2009;Tanowitz et al, 2009).…”

“…There is direct interaction between platelets and inflammated endothelium when it is activated (Danese et al, 2007;Tanowitz et al, 2005) (Danese et al, 2007), for example, by T. cruzi infection. However, endothelial function may be preserved in patients without heart failure (Consolim- Colombo et al, 2004;Tanowitz et al, 2009).…”

“…In addition, trypomastigotes produce neuraminidase, an enzyme that removes sialic acid from the surface of mammalian myocardial and endothelial cells. At the endothelial surface platelet aggregation and microvascular thrombosis may occur (Sousa et al, 2008;Tanowitz et al, 2009). …”