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Am. J. Trop. Med. Hyg., 70(2), 2004, pp. 210-220
Copyright © 2004 by The American Society of Tropical Medicine and Hygiene

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TRYPANOSOMA CRUZI DNA IN CARDIAC LESIONS OF ARGENTINEAN PATIENTS WITH END-STAGE CHRONIC CHAGAS HEART DISEASE

ALEJANDRO G. SCHIJMAN, CARLOS A. VIGLIANO, RODOLFO J VIOTTI, JUAN M. BURGOS, SILVIA BRANDARIZ, BRUNO E. LOCOCO, MARIA I. LEZE, HECTOR A. ARMENTI, AND MARIANO J. LEVIN
Laboratorio de Biología Molecular de la Enfermedad de Chagas, INGEBI, Consejo Nacional de Ciencia y Tecnologia, Department of Fisiology, Celular and Molecular Biology, F.CEyN, University of Buenos Aires, Buenos Aires, Argentina; Department of Cardiology, Eva Perón Hospital, San Martin, Buenos Aires, Argentina; Division of Pathology, Instituto de Cardiología y Cirugía Cardiovascular, Fundación Favaloro, Buenos Aires, Argentina

The extent of inflammation, fibrosis, and progression of chronic Chagas heart disease (cChHD) was associated with persistence of parasite DNA in cardiac lesions of necropsies or explants from Argentinean cChHD patients. A Trypanosoma cruzi-based polymerase chain reaction showed a positive result in 1) 15% of cardiac sections with less than 10 mononuclear inflammatory cells/high-power field (440x) (MNC/HPF), 89% with 10–19 MNC/HPF, and 100% with more than 20 MNC/HPF (P < 0.0001); 2) 33% with less than 10% fibrosis, 79% with 10–19% fibrosis, and 100% with more than 20% fibrosis (P < 0.01); 3) 25% of specimens from patients classified in Kuschnir groups 0 and I, 70% in group II and 90% in group III (P < .001); and 4) 45% and 90% of the specimens from cChHD patients without or with heart failure, respectively (P < 0.01). These findings stress the role of the parasite in pathogenesis and disease progression of cChHD.


Received August 1, 2003. Accepted for publication October 22, 2003.

Acknowledgments: We are grateful to Dr. Rubén Laguens (Division de Anatomía Patológica, Instituto de Cardiología y Cirugía Cardiovascular, Fundación Favaloro, Buenos Aires, Argentina) and Dr. Felipe Kierszenbaum (Department of Microbiology, Michigan State University, East Lansing, MI) for their helpful comments on the manuscript, and to Sonia Lafon and Julia Ferrando for their skillful technical assistance.

Financial support: This work was supported by grants from the World Health Organization-Tropical Diseases Research projects, the Regional Technical Cooperation project RLA 6-0-26 and Coordinated Research Project of the International Atomic Energy Agency, Consejo Nacional de Ciencia y Tecnologia (PEI 107/97), the University of Buenos Aires, FONCyT BID 802/OC-AR PICT 01421 and PI CT 02030, the Alberto Roemmers and Bunge and Born Foundations, and Ramon Carrillo-Arturo Oñativia of the Secretary of Health of Argentina. The work of Matiano J. Levin was partially supported by an International Research Scholar grant from the Howard Hughes Medical Institute (Chevy Chase, MD).

Authors’ addresses: Alejandro G. Schijman, Juan M. Burgos, Silvia Brandariz, and Mariano J. Levin, Vuelta de Obligado 2490, Second Floor, (CP 1428), Buenos Aires, Argentina, Telephone: 54-11-4783-2871, Fax: 54-11-4786-8578, E-mail: MLevin{at}dna.uba.ar. Carlos A. Vigliano, División Patología. Instituto de Cardiología y Cirugía Cardiovascular, Fundación Favaloro, Belgrano 1746 (CP 1093), Buenos Aires, Argentina, Telephone and fax : 54-11-4378-1315 and Departamento de Cardiología, Hospital Eva Perón, Ruta 8 y Diego Pombo, San Martín, Provincia de Buenos Aires, Buenos Aires, Argentina 005411-3781315. Rodofo J. Viotti, Bruno E. Lococo, María I. Leze, and Héctor A. Armenti, Departamento de Cardiología, Hospital Eva Perón, Ruta 8 y Diego Pombo, San Martín, Provincia de Buenos Aires, Buenos Aires, Argentina 005411-3781315.




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