PLoS ONE (Jan 2022)

Diagnostic and prognostic performance of the ratio between high-sensitivity cardiac troponin I and troponin T in patients with chest pain

  • Kai M. Eggers,
  • Ola Hammarsten,
  • Sally J. Aldous,
  • Louise Cullen,
  • Jaimi H. Greenslade,
  • Bertil Lindahl,
  • William A. Parsonage,
  • Christopher J. Pemberton,
  • John W. Pickering,
  • A. Mark Richards,
  • Richard W. Troughton,
  • Martin P. Than

Journal volume & issue
Vol. 17, no. 11

Abstract

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Background Elevations of high-sensitivity cardiac troponin (hs-cTn) concentrations not related to type 1 myocardial infarction are common in chest pain patients presenting to emergency departments. The discrimination of these patients from those with type 1 myocardial infarction (MI) is challenging and resource-consuming. We aimed to investigate whether the hs-cTn I/T ratio might provide diagnostic and prognostic increment in this context. Methods We calculated the hs-cTn I/T ratio in 888 chest pain patients having hs-cTnI (Abbott Laboratories) or hs-cTnT (Roche Diagnostics) concentrations above the respective 99th percentile at 2 hours from presentation. All patients were followed for one year regarding mortality. Results The median hs-cTn I/T ratio was 3.45 (25th, 75th percentiles 1.80–6.59) in type 1 MI patients (n = 408 ☯46.0%]), 1.18 (0.81–1.90) in type 2 MI patients (n = 56 ☯6.3%]) and 0.67 (0.39–1.12) in patients without MI. The hs-cTn I/T ratio provided good discrimination of type 1 MI from no type 1 MI (area under the receiver-operator characteristic curve 0.89 ☯95% confidence interval 0.86–0.91]), of type 1 MI from type 2 MI (area under the curve 0.81 ☯95% confidence interval 0.74–0.87]), and was associated with type 1 MI in adjusted analyses. The hs-cTn I/T ratio provided no consistent prognostic value. Conclusions The hs-cTn I/T ratio appears to be useful for early diagnosis of type 1 MI and its discrimination from type 2 MI in chest pain patients presenting with elevated hs-cTn. Differences in hs-cTn I/T ratio values may reflect variations in hs-cTn release mechanisms in response to different types of myocardial injury.