Troponin and Cardiac Events in Stable Ischemic Heart Disease and Diabetes

Abstract

Background: Cardiac troponin concentrations are used to identify patients who would benefit from urgent revascularization for acute coronary syndromes. We hypothesized that they might be used in patients with stable ischemic heart disease to identify those at high risk for cardiovascular events who might also benefit from prompt coronary revascularization.

Methods: We measured the cardiac troponin T concentration at baseline with a high-sensitivity assay in 2285 patients who had both type 2 diabetes and stable ischemic heart disease and were enrolled in the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes trial. We tested for an association between the troponin T concentration and a composite end point of death from cardiovascular causes, myocardial infarction, or stroke; we then evaluated whether random assignment to prompt revascularization reduced the rate of the composite end point in patients with an abnormal troponin T concentration (≥14 ng per liter) as compared with those with a normal troponin T concentration (<14 ng per liter).

Results: Of the 2285 patients, 2277 (99.6%) had detectable (≥3 ng per liter) troponin T concentrations and 897 (39.3%) had abnormal troponin T concentrations at baseline. The 5-year rate of the composite end point was 27.1% among the patients who had had abnormal troponin T concentrations at baseline, as compared with 12.9% among those who had had normal baseline troponin T concentrations. In models that were adjusted for cardiovascular risk factors, severity of diabetes, electrocardiographic abnormalities, and coronary anatomy, the hazard ratio for the composite end point among patients with abnormal troponin T concentrations was 1.85 (95% confidence interval [CI], 1.48 to 2.32; P<0.001). Among patients with abnormal troponin T concentrations, random assignment to prompt revascularization, as compared with medical therapy alone, did not result in a significant reduction in the rate of the composite end point (hazard ratio, 0.96; 95% CI, 0.74 to 1.25).

Conclusions: The cardiac troponin T concentration was an independent predictor of death from cardiovascular causes, myocardial infarction, or stroke in patients who had both type 2 diabetes and stable ischemic heart disease. An abnormal troponin T value of 14 ng per liter or higher did not identify a subgroup of patients who benefited from random assignment to prompt coronary revascularization. (Funded by the National Institutes of Health and Roche Diagnostics; BARI 2D ClinicalTrials.gov number, NCT00006305.).

Figure 1. Unadjusted Kaplan–Meier Estimates of Adverse Outcomes over 5 Years

The primary end point (Panel A) was a composite of death from cardiovascular causes, myocardial infarction, or stroke. Death from any cause (Panel B) was a secondary end point. Data are shown for patients with an abnormal high-sensitivity cardiac troponin T level (≥14 ng per liter) at baseline, as compared with those with a normal level (<14 ng per liter) at baseline, who were enrolled in the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes (BARI 2D) trial.

Figure 2. Hazard Ratios for the Primary Composite End Point and Selected Secondary End Points

Data are shown for the patients who were randomly assigned to either prompt revascularization plus intensive medical therapy (revascularization group) or intensive medical therapy alone (medical-therapy group), stratified according to a normal (<14 ng per liter) or an abnormal (≥14 ng per liter) high-sensitivity cardiac troponin T concentration at baseline. The size of the boxes is proportional to the size of the subgroups.

Figure 3. Unadjusted Kaplan–Meier Estimates

Unadjusted Kaplan–Meier estimates are shown for the rate of the primary composite end point of death from cardiovascular causes, myocardial infarction, or stroke (Panel A) and for the rate of the secondary composite end point of death from any cause, myocardial infarction, stroke, or heart failure (Panel B), according to the change in high-sensitivity cardiac troponin T concentration from baseline to 1-year follow-up. The 4-year event rates are derived from a landmark analysis starting at the time of plasma sample collection at 1 year and continuing to the close of the study 4 years later. I bars indicate 95% confidence intervals. Data on the numbers of events and numbers at risk are for the 1984 patients in the BARI 2D trial who had both baseline and 1-year follow-up troponin T concentrations available.