Comparison between Cardiac Troponin I and Troponin T in the Diagnosis of Acute Myocardial Infarction

Accurate measurement of cardiac troponin is important as an aid in the diagnosis of acute myocardial infarction (AMI). The Architect R new troponin I (cTnI) assays are a fully automated chemiluminescent microparticle immunoassay (CMIA). The assays, a two-step sandwich format with a highly specific monoclonal antibody, claim to provide more sensitivity than the conventional troponin T (cTnT) assay in the diagnosis of AMI patients. Moreover, the Architect R cTnI assay is suppose to be free from renal failure interferences and to provide excellent precision in the low concentration range. The aim of this study was to compare the reliability of the two cardiac specific troponin assays; namely the new Architect R cTnI and conventional cTnT assay in aiding in decision making of suspected AMI patients. We also compared the correlation of both assays in patients without AMI that have chronic kidney disease. Methods: The diagnostic study was conducted in the Emergency Department of the Ramathibodi hospital during a six month period in 2006-2007. Eligible patients had to be at least 30 years old with chest pain lasting more than 20 minutes that was suspected to be myocardial in origin with the onset occurring within 3 to 72 hours. Cardiac troponin assays were tested together with other general blood chemistries. The final diagnosis and clinical data were later obtained from their medical records. Results: Of the 87 included patients, one third (29, 33.3%) had AMI. The quantitative assays for both cTnI and cTnT were detected in 20 (68.9%) patients with AMI. In regards to the cTnI assay, the provisional cut-off point from the manufacturer (0.032 ng/ml) showed a sensitivity of 82.8% and a specificity of 79.3% (positive predictive value = 0.67, negative predictive value = 0.90). While in the cTnT assay at the cut-off point of 0.03 ng/ml, a sensitivity and specificity of 69.0% and 89.7% (PPV = 0.77, NPV = 0.85) respectively were shown. The area under the curve of troponin I was 0.87 while that of troponin T was 0.84 (p = 0.44). In patients without AMI who had chronic kidney disease (CKD) serum cTnI and cTnT concentrations were more likely to increase in association with more severe CKD. Conclusion: Although the recently developed cTnI assay claims to have more sensitivity for the diagnosis of AMI patients, our study demonstrated no significant differences between cTnI and cTnT in the diagnosis of AMI. The concern in patients with chronic kidney disease who might have false positive results from the tests, both serum cTnI and cTnT concentrations were similarly increased with increasing severity of CKD. Keywords: Acute myocardial infarction, Cardiac troponin, Chronic kidney disease