Troponin concentration may help stratify risk in those with stable ischemic heart disease and diabetes

Cardiac troponin concentration may indicate higher risk for death or other outcomes in patients with stable ischemic heart disease and type 2 diabetes, according to a new study.

Researchers used a high-sensitivity assay to measure cardiac troponin T concentration at baseline in patients with type 2 diabetes and stable ischemic heart disease who were enrolled in the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes (BARI 2D) trial, then analyzed whether it was associated with a composite end point (death from cardiovascular causes, myocardial infarction, or stroke). They also examined whether patients with a high concentration (≥14 ng/L) did better than those with a normal concentration (<14 ng/L) after random assignment to prompt revascularization. The study results appeared in the Aug. 13 New England Journal of Medicine.

A total of 2,285 patients were included in the study. Most patients (2,277 patients, 99.6%), had detectable troponin T concentrations at baseline (≥3 ng/L); in 897 (39.3%), troponin T concentrations were abnormal (≥14 ng/L). Of the 2,285 patients, 1,984 (86.8%) also had troponin T samples available for analysis at 1-year follow-up. Patients with analyzable baseline troponin studies were followed for a median time of 5 years (interquartile range, 4.1 to 6.0 years). During the study period, all patients received intensive standard therapy for traditional cardiovascular risk factors (hypertension, diabetes, dyslipidemia). Patients with abnormal baseline troponin concentrations had a 5-year rate of 27.1% for the composite end point versus a rate of 12.9% among those with normal baseline concentrations. In adjusted models, patients with abnormal concentrations had a hazard ratio of 1.85 (95% CI, 1.48 to 2.32) for the composite end point (P<0.001). Random assignment to prompt revascularization compared with medical therapy did not reduce the rate of the composite end point in patients with abnormal troponin T concentrations (hazard ratio, 0.96; 95% CI, 0.74 to 1.25).

The authors noted that the strengths of the study included randomized assignment to the different management groups and the apparent independence of the observed relationship from the possible confounding effect of traditional cardiovascular risk factors. However, the study lacked adequate power to detect a treatment effect of revascularization in subgroups stratified by baseline troponin level, and results were limited in part because of the lack of follow-up troponin values for 13% of the patients who had values available at baseline. The authors nevertheless concluded that their results support a “strong, consistent association between baseline concentrations of circulating cardiac troponin T and the risk of death from any cause, myocardial infarction, stroke, and heart failure” in this patient population but did not indicate a benefit of prompt coronary revascularization based on troponin values.

The authors of an accompanying editorial said that the study's findings have several implications for management and future treatment and called for additional studies to determine precise risk thresholds for troponin values, as well as their potential usefulness as an “enrichment” factor, which they defined as “a factor that is used to specify inclusion criteria for clinical trials to enhance event rates in a randomized population.” Future trials should also look at whether patients with stable ischemic heart disease and elevated troponin values benefit more from recommended treatments such as antiplatelet therapy and statins.

“The precise way in which a high-sensitivity troponin assay can be used for the assessment of patients with stable ischemic heart disease remains uncertain, but accumulating data suggest that cardiac troponin values may become routinely used for risk stratification across the spectrum of ischemic heart disease,” the editorialists wrote.