Bonaca M., Scirica B., Sabatine M., Dalby A., Spinar J., Murphy S.A., Jarolim P., Braunwald E., Morrow D.A.
TIMI Study Group, Brigham and Women's Hospital, Boston, MA, United States; Department of Pathology, Brigham and Women's Hospital, Boston, MA, United States; South African Cardiology Clinical Trials Group, Johannesburg, South Africa; University Hospital St. Ann, Pekarska, Czech Republic
Bonaca, M., TIMI Study Group, Brigham and Women's Hospital, Boston, MA, United States; Scirica, B., TIMI Study Group, Brigham and Women's Hospital, Boston, MA, United States; Sabatine, M., TIMI Study Group, Brigham and Women's Hospital, Boston, MA, United States; Dalby, A., South African Cardiology Clinical Trials Group, Johannesburg, South Africa; Spinar, J., University Hospital St. Ann, Pekarska, Czech Republic; Murphy, S.A., TIMI Study Group, Brigham and Women's Hospital, Boston, MA, United States; Jarolim, P., Department of Pathology, Brigham and Women's Hospital, Boston, MA, United States; Braunwald, E., TIMI Study Group, Brigham and Women's Hospital, Boston, MA, United States; Morrow, D.A., TIMI Study Group, Brigham and Women's Hospital, Boston, MA, United States
Objectives: The purpose of this study was to investigate the prognostic implications of low-level increases in cardiac troponin I (cTnI) using a current-generation sensitive assay in patients with suspected acute coronary syndrome (ACS). Background: Recent enhancements in troponin assays have enabled resolution of the 99th percentile reference limit at progressively lower concentrations. However, the clinical significance of low-level increases with sensitive assays is still debated. Methods: We measured cTnI using a sensitive assay (TnI-Ultra, Siemens Healthcare Diagnostics, Deerfield, Illinois) at baseline in 4,513 patients with non-ST-segment elevation ACS randomly assigned to ranolazine or placebo. We applied decision limits at the 99th percentile reference limit (0.04 μg/l), the cut point of the predecessor assay (0.1 μg/l), and 1 equivalent to elevation of creatine kinase-myocardial band (1.5 ng/ml). Results: Patients with baseline cTnI ≥0.04 μg/l (n = 2,924) were at higher risk of death/myocardial infarction (MI) at 30 days than were patients with a negative cTnI (6.1% vs. 2.0%, p < 0.001). After adjusting for the TIMI (Thrombolysis In Myocardial Infarction) risk score, cTnI ≥0.04 μg/l was associated with a 3-fold (95% confidence interval: 2.0 to 4.4, p < 0.001) higher risk of death/MI at 30 days. Moreover, patients with low-level increases (0.04 μg/l to <0.1 μg/l), were at significantly higher risk of death/MI at 30 days (5.0% vs. 2.0%, p = 0.001) and death at 12 months (6.4% vs. 2.4%, p = 0.005) than were patients with cTnI <0.04 μg/l. Conclusions: Low-level increases in cTnI using a sensitive assay identify patients at higher risk of death or MI. These findings support current American College of Cardiology/American Heart Association recommendations defining MI, and the incremental value of newer, more sensitive assays in identifying high-risk patients with ACS. © 2010 American College of Cardiology Foundation.