Abstract 1790: Prospective Evaluation of the Prognostic Implications of Low Level Elevation of Cardiac Troponin Using a New Highly-sensitive Assay for Cardiac Troponin I: Results from the MERLIN-TIMI 36 Trial
Myocardial infarction (MI) is defined using a cut-point for troponin at the 99th %ile of a control population. The availability of new highly sensitive assays has raised questions as to the clinical relevance of very low-level increases.
METHODS: We measured cardiac troponin I (cTnI) using a new generation assay (TnI-Ultra, Siemens Medical Solutions Diagnostics) at baseline in 4,513 pts with non-ST elevation acute coronary syndromes (NSTE-ACS) randomized to ranolazine or placebo in the MERLIN-TIMI 36 trial. We stratified pts using decision limits at the 99th %ile (0.04 μg/L), the cut-point of the predecessor assay (0.1 μg/L), and one quivalent to elevation of CK-MB (1.5 ng/ml).
RESULTS: Pts with baseline cTnI >=0.04 μg/L (N = 2924) were at higher risk of death/MI at 30 days than pts with a negative cTnI (6.1 vs 2.0%, p<0.001). After adjusting for elements of the TIMI Risk Score for NSTE-ACS, cTnI >=0.04 μg/L was associated with a 3.0 fold (95% CI 2.0 – 4.4, p<0.001) higher risk of death/MI at 30 days. Moreover, pts with very low level increases detectable with the newer assay, cTnI (0.04 - <0.1 μg/L), were at significantly higher risk of death/MI at 30 days than those without (5.0 vs 2.0%, p=0.001), only modestly lower than those with cTnI >=0.1 μg/L (6.2%). This persisted at 1 yr (Figure⇓). There was no heterogeneity in the effect of ranolazine compared with placebo between pts with and without elevation of cTnI.
CONCLUSIONS: Low-level increases in cTnI using a highly sensitive assay identify pts at increased risk of death or MI. These findings support evolution of AHA/ACC recommendations defining MI, and the incremental value of new more sensitive assays in identifying high risk pts with NSTE-ACS.