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Brazilian Journal of Infectious Diseases

Print version ISSN 1413-8670On-line version ISSN 1678-4391

Braz J Infect Dis vol.7 no.6 Salvador Dec. 2003 



Troponin in Chagas disease



Roque Aras; Claudilson Bastos; Gildo Mota; Fábio Sodré; Agnaluce Moreira; Armando Tavares; José Carlos Lima

Federal University of Bahia, School of Medicine, Salvador, BA, Brazil




Chagas disease is still a major tropical disease in Latin America, affecting 16 to 18 million people. About 6 million people are infected with the causative organism, Trypanosoma cruzi, in Brazil [1]. However, it often remains for decades in its indeterminate form, symptomless, with tissue injury in about 30% of the cases, which eventually will evolve to serious arrhythmia and sudden death [1].

There is no effective clinical or laboratory technique to monitor chronic Chagas myocarditis. Several researchers have found that Troponin I and T are important biochemical markers of heart muscle damage. Increased levels of myocardial troponins have been found associated with acute myocardial ischemia, infarction, myocarditis and heart failure [2-4].

Recently, we tested sera from 60 Chagas disease patients (24 with the indeterminate form and 36 with chronic chagasic cardiomyopathy. Sera from 24 healthy volunteers (Control Group) were tested for Troponin I (Immulite 1000 Turbo DPC-Medlab). The Troponin I value was considered normal when it was below 0.15ng/dl, and high when it was above 0.30ng/dl. The upper limit was set to be at least two standard deviations above the normal value.

The mean value for Troponin I was 0.46ng/dl in the Chagas disease patients, and 0.027ng/dl in the control group. The mean age was 44.1±9.9 years of the Chagas patients, and 34 were male. When we tested We found 13 (54%) and 26 (74%) patients with high Troponin I, respectively, for chronic Chagas cardiomyopathy and the indeterminate form of Chagas disease. Twenty-one patients from the Chagas disease group were excluded due to other cardiovascular diseases, myopathy or kidney disease.

Troponin I levels were significantly higher among the Chagas disease patients with cardiomyopathy when compared to the indeterminate form and controls, mean 0.60ng/dl vs 0.25ng/dl, respectively, and controls 0.027ng/dl (P < 0.001).

All the patients with the indeterminate form of Chagas disease had normal EKGs, chest X-rays and echocardiograms. Possibly, the increased levels of Troponin I, found in our sample, are related to chronic foci of myocardial inflammation, provoked by Chagas disease.

Moreover, the utilization of a sensitive and easily measured biochemical marker should allow us to adopt different clinical cut-offs, facilitating the identification of the different degrees of myocardial damage, which now requires various diagnostic and therapeutic approaches [5].

The serum level of Troponin I is elevated in different clinical presentations of Chagas' disease and may become an important element for early detection of myocardial inflammation, to prevent further myocardial damage.



1. World Health Organization: Control of Chagas' disease, Report of a WHO. Geneva. World Health Organization Technical Series No. 811, 91p, 1991.

2. Apple F.S. Cardiac Troponin I: in Cardiac Markers, Alan Wu. Ed. Humana Press Inc 1998; New Jersey, pp. 229-43.

3. La Vecchia L., Mezzena G., Zanolla L.,et al. Cardiac Troponin I as diagnostic and prognostic marker in severe heart failure. The Journal of Heart and Lung Transplantation 2000;19(7): 644-52.

4. Missov E., Calzolari C., Pau B. Circulating cardiac Troponin I in severe congestive heart failure. Circulation 1997;96(9):2953-8.

5. Lang K., Börner A., Figulla H.R. Comparison of biochemical markers for the detection of minimal myocardial injury: superior sensitivity of cardiac Troponin- T ELISA. Journal of Internal Medicine 2000;247:119-23.



Correspondence to
Dr..Andre C Lyra, MD
Serviço de Gastro-Hepatologia do Hospital São Rafael
Salvador-BA, Brasil
Rua Socrates Guanaes Gomes, 84, room 401, Salvador — Bahia — Brazil
Zip code: 40.283.320
Phone — Fax (55)-(71)-452-9589

Received on 17 July 2002
revised 22 September 2003
This study was supported in part by the CNPq.

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