Abstract 16968: Troponin I Is an Independent Predictor of Long-Term Coronary Events Following Myocardial Infarction or Unstable Angina: Results from the Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) Trial

Background The role of higher-sensitivity troponins in predicting long-term outcomes in patients with stable CHD is not clearly defined. Objective: To assess the value of a higher sensitivity troponin I (TnI) assay to predict outcomes during median follow-up of 6 years and to assess the effect of pravastatin on TnI levels and outcomes. Methods Among 9014 patients in LIPID with cholesterol levels 4.0-7.0 mmol/L randomized to placebo or pravastatin after MI or unstable angina 3-36 months previously, TnI levels (Siemens ultra, level of detection 0.006 ng/mL, 99th percentile with CV 10% 0.04 ng/mL) were measured at randomization and at 1 year. Baseline TnI levels (ng/ml) were assessed in 3 groups: not detectable (38%), 0.006-0.018 (31%), and ≥0.018 (31%), and change over 1 year defined as a change in group. Results Patients with the highest TnI levels were older, more likely to have previous MI, and to be on ACE inhibitors but less likely to be on beta-blockers. Levels of TnI at 1 year had decreased in 25%, were unchanged (51%) or increased (23%), but pravastatin had no effect on TnI levels. In a multivariable Cox regression for CHD death or nonfatal MI, HR was 2.02 (95% CI 1.66-2.45), P <0.001, for levels of TnI above the reference 99th percentile (0.04 ng/mL), vs undetectable levels, adjusted for baseline risk factors. In multivariable landmark analysis of 6544 patients event-free at 12 months, baseline TnI levels and changes in TnI were both independent predictors of subsequent CHD events ( P <0.001), even after adjustment for 23 traditional risk factors, including treatment. The effect of pravastatin in reducing CHD events remained highly significant in each model ( P <0.02) and was independent of TnI levels. Conclusions Baseline and change to 1 year in TnI levels, additional to traditional risk factors, were independent predictors of CHD death and MI. TnI was more powerful for predicting fatal than nonfatal events (table), and the benefits of pravastatin were independent of TnI levels.