Copeptin and high sensitive troponin for a rapid rule out of acute myocardial infarction?

Abstract

Background: Rapid and reliable exclusion of acute myocardial infarction during emergency department triage is an important clinical need. The purpose of this study was to evaluate the potential role of copeptin, a marker of acute endogenous stress, together with high sensitive troponin-I for a rapid and early rule-out of acute myocardial infarction.

Methods: Copeptin and myoglobin were measured in 80 subjects presenting to the emergency department with chest pain and symptoms suggestive of acute myocardial infarction, 46 patients had a negative high sensitive troponin-I concentration at presentation, 3, 6 and 12 hours; whereas 34 patients had negative or very low high sensitive troponin-I at presentation, but rising troponin values at 3, 6 and 12 hours.

Results: Copeptin was significantly higher in patients with evidence of myocardial damage (median 92.2 pmol/L vs 8.5 pmol/L, p < 0.0001). The area under the receiver-operating characteristic curve (AUC) for copeptin at initial presentation was 0.86 (95 % confidence interval, CI: 0.76 to 0.93), which was significantly higher than 0.68 (95% CI: 0.57 to 0.78, p < 0.05) for myoglobin but not significantly different from 0.88 (95% CI: 0.79 to 0.93) for high sensitive troponin-I. The combination of high sensitive troponin-I and copeptin resulted in an AUC of 0.94 (95% CI: 0.86 to 0.98), while the combination of high sensitive troponin-I and myoglobin results in an AUC of 0.89 (95% CI: 0.81 to 0.95).

Conclusions: Copeptin concentrations are more sensitive than myoglobin as an early marker of myocardial damage. Although copeptin provides significant incremental value on top of high sensitivity troponin-I, myoglobin does not.