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Association of Contemporary Sensitive Troponin I Levels at Baseline and Change at 1 Year With Long-Term Coronary Events Following Myocardial Infarction or Unstable Angina: Results From the LIPID Study
Study Questions:
Are levels of troponin I (TnI) at baseline and over 1 year of follow-up associated with myocardial infarction (MI) and coronary heart disease (CHD), and what is the impact of pravastatin on TnI levels and these outcomes?
Methods:
This was a prospective analysis of patients in the LIPID (Long-Term Intervention with Pravastatin in Ischemic Disease) secondary prevention study. In the LIPID study, patients with an MI or hospital admission for unstable angina 3-36 months preceding enrollment with qualifying lipid parameters (total cholesterol 155-271 mg/dl, and fasting triglycerides <445 mg/dl) were randomized to pravastatin 40 mg daily or matching placebo. In this study, TnI was measured at randomization and at 1 year by a contemporary sensitive assay. The composite of CHD death and nonfatal MI (CHD events) was the primary endpoint. Data for troponin were split into tertiles (the detection limit of <0.006 ng/ml, 0.006 ng/ml-<0.018 ng/ml, and ≥0.018 ng/ml).
Results:
In analyses adjusted for 23 baseline risk factors and treatment, baseline TnI was strongly related to the primary outcome of CHD death and nonfatal MI (p < 0.001). Levels of TnI between baseline and 1 year decreased by one tertile category in 26%, increased in 23%, and were unchanged in 51% of patients. If TnI levels moved to a higher category, the adjusted hazard ratio for CHD events was 1.31 (95% confidence interval, 1.06-1.62). After adjustment for change in TnI, the effect of pravastatin on cardiovascular disease event reduction remained unchanged (even though pravastatin had a small effect on troponin levels).
Conclusions:
The authors concluded that baseline troponin levels and change at 1 year are independent predictors of CHD death and MI. The impact of pravastatin was not clinically significant.
Perspective:
The limitations of the study aside (including that two thirds of the troponin values analyzed were below the level of guideline-endorsed precision for the assay, as acknowledged by the authors), the analysis demonstrates that baseline troponin levels and change at 1 year are predictors of cardiovascular disease events. Further research should clarify the mechanisms that account for this relationship and how measurement of troponin levels at baseline and over time could impact clinical practice or guide therapy.
Keywords: Myocardial Infarction, Secondary Prevention, Biomarkers, Troponin I, Hydroxymethylglutaryl-CoA Reductase Inhibitors
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