Clinical efficacy of three assays for cardiac troponin I for risk stratification in acute coronary syndromes: A thrombolysis in myocardial infarction(TIMI) 11B substudy

Background: Significant analytic variability exists between the multiple as says for cardiac troponin I (cTnI) approved for clinical use. Until adequat e cTnI standardization is possible, an evidence-based approach evaluating e ach assay at specific thresholds appears warranted. Methods: We examined the efficacy of three cTnI assays for predicting death , myocardial infarction (MI), or the composite of death, MI, or urgent reva scularization at 43 days among patients with non-ST-elevation acute coronar y syndromes enrolled in the Thrombolysis In Myocardial Infarction (TIMI) 11 B study. Results: Six hundred eighty-one patients with serum samples obtained at bas eline and/or 12-24 h had cTnI determined using all three assays. Baseline c TnI was greater than or equal to 0.1 mu g/L for 368, 395, and 418 patients with the Bayer Immune 1(TM), ACS:180(R), and Dimension(R) RxL assays, respe ctively. Correlation coefficients for the RxL with the ACS:180 and Bayer Im mune 1 results were 0.89 (P = 0.0001) and 0.87 (P = 0.0001), with a coeffic ient of 0.92 (P = 0.0001) for the ACS:180 and Bayer Immuno 1 assays. Patien ts with cTnI greater than or equal to 0.1 mu g/L were at increased risk for death or MI by 43 days (relative risk, 2.2-3.0; P < 0.0006), regardless of the assay used. This prognostic capacity persisted among those with creati ne kinase MB isoenzyme concentrations within the reference interval. Moreov er, cTnI was the strongest multivariate predictor of death, MI, or urgent r evascularization with adjusted odds ratios of 2.1-2.9 (P < 0.0006). Conclusion: This study demonstrates the prognostic efficacy of three indepe ndently developed cTnI assays at a threshold of 0.1 mu g/L for the predicti on of adverse clinical outcomes among patients with non-ST-elevation acute coronary syndromes. (C) 2000 American Association for Clinical Chemistry.