Cardiac Troponin T Measured With a Highly Sensitive Assay for Diagnosis and Monitoring of Heart Injury in Chronic Chagas Disease Silvia Gilka Mun ˜ oz Saravia, PhD; Annekathrin Haberland, PhD; Sabine Bartel, PhD; Raul Araujo, MD; Gregorio Valda, MD; Diana Duchen Reynaga, MS; Ivan Diaz Ramirez, MD; Adrian C. Borges, MD; Gerd Wallukat, PhD; Ingolf Schimke, PhD N Context.—Chronic Chagas disease (15 million patients; annual incidence, 40 000 patients; annual mortality, 12 500 patients) is the most serious parasitic disease in Latin America. Between 10 and 30 years after infection, 30% of patients with Chagas disease develop heart injury, which is the main reason for its high mortality. Conse- quently, frequent cardiac diagnostics are required for patients with Chagas disease. Objective.—To minimize time-intensive and cost-inten- sive diagnostics, such as electrocardiography, echocardi- ography, and radiologic imaging, we tested the effect of measuring serum cardiac troponin T (cTnT) with a highly sensitive assay. To indicate the pathophysiologic back- ground for cTnT release in Chagas heart injury, inflamma- tion markers, such as C-reactive protein and interleukin 6, were measured in parallel. Design.—Serum cTnT was measured in 26 healthy subjects and in 179 patients with chronic Chagas disease who were asymptomatic (indeterminate stage, n = 86), who were suffering from cardiomyopathy with or without megacolon (n = 71), or who were suffering from megacolon exclusively (n = 22). Results.—Serum cTnT was significantly higher in patients with cardiomyopathy with or without megacolon than in healthy subjects, asymptomatic subjects, and patients with megacolon, and the cTnT value was correlated with the severity of the cardiomyopathy. The lower limit of detection for the highly sensitive assay (3 ng/L) was best at distinguishing patients with, and without, heart injury. C- reactive protein and interleukin 6 were found to parallel cTnT changes in both the different Chagas groups and the cardiomyopathy groups separated by disease severity. Conclusions.—Highly sensitive cTnT measurement has the potential to contribute to diagnosis and monitoring of heart injury in patients with chronic Chagas disease. The highly sensitive assay of cTnT release seems to be related to Chagas heart disease–specific inflammation. (Arch Pathol Lab Med. 2011;135:243–248) C hronic Chagas disease (15 million patients; annual incidence, 40 000; annual mortality, 12 500 patients in 2006), caused by Trypanosoma cruzi infection, is the most serious parasitic disease in Latin America. 1 As lifelong parasite carriers, two-thirds of the patients remain clinically asymptomatic (indeterminate), whereas one- third develop clinical manifestations, with a latency of 10 to 30 years. In nearly 90% of these cases, the patient’s heart is affected. These patients present with cardiomy- opathy associated with arrhythmias, heart failure, and frequently, sudden death. The remaining 10% suffer mainly from megacolon or megaesophagus. 2–4 Conse- quently, Chagas disease places an enormous burden on the economic resources of the countries affected and dramatically influences the patients’ social and labor situation. 5,6 The cardiac troponins I and T (cTnI, cTnT) are established markers for diagnosis, risk stratification, and therapy monitoring in patients with acute coronary syndrome. 7 However, there are numerous other physio- logic heart stressors, for example, exercise, 8 general pathologies affecting the heart, 9 and cardiac diseases, such as stable angina, myocarditis, and heart failure, 10 which are accompanied by serum cardiac troponin values clearly different from those of healthy controls, although they may be less than or near the established cutoff values for acute coronary syndromes. Therefore, cardiac troponin measurement could be used as a tool for diagnosis, risk assessment, and monitoring of patients with chronic Chagas disease who develop heart injury. To date, there have been only 2 studies and a single patient observation, to our knowledge, that analyzed cardiac troponin in Chagas heart disease. 11–13 These studies—which, in our view, used assays with insufficient sensitivity, mainly in the lower range (#99th percentile of the reference population)—did not indicate a profound relationship Accepted for publication April 12, 2010. From the Department of Cardiology, Charite ´ Universita ¨tsmedizin Berlin, Berlin, Germany (Drs Mun ˜ oz Saravia, Haberland, Diaz Ramirez, and Schimke); the Department of Immunology of Cardiovascular Diseases, Max-Delbru ¨ ck–Centrum Berlin, Berlin, Germany (Drs Bartel and Wallukat); the Departments of Cardiology (Dr Araujo), Gastroen- terology (Dr Valda), and Laboratory Medicine (Dr Munoz Saravia and Ms Duchen Reynaga), Santa Ba ´ rbara Hospital Sucre, Sucre, Bolivia; and the Department of Cardiology, HELIOS Klinikum Emil von Behring, Berlin, Germany (Dr Borges). The authors have no relevant financial interest in the products or companies described in this article. Reprints: Ingolf Schimke, PhD, Department of Cardiology, Campus Charite ´ Mitte, Universita ¨tsmedizin Berlin, Charite ´platz 1, 10117 Berlin, Germany (e-mail: ingolf.schimke@charite.de). Arch Pathol Lab Med—Vol 135, February 2011 Cardiac Troponin T in Chagas Cardiomyopathy—Saravia et al 243