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Updated Chest Pain Pathway: Incorporating High-Sensitivity Troponin

Drew Kalnow, DO, Andy Little, DO, and Cameron Berg, MD

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The summary below is from an episode of ERcast: Clinical Perspectives

High-sensitivity troponin changes ED chest pain evaluation because it detects myocardial injury far more often than older assays, and an elevated value is not the same as acute coronary syndrome. Safe use depends on assay-specific cutoffs, timed delta testing, and ECG-guided clinical context.

High-Sensitivity Troponin in Chest Pain

  • Assay-specific interpretation matters: High-sensitivity troponin I is not interchangeable with conventional troponin or with other manufacturers’ assays, so reference ranges, units, and delta rules must match the exact test your lab uses.
  • Elevation is not ACS: Most elevated hs-TnI results are not occlusive MI; roughly 80% reflect myocardial injury from causes like renal dysfunction, heart failure, systemic illness, or severe hypertension.
  • Timed delta drives disposition: A single hs-TnI rarely settles the question in intermediate results because the pathway depends on repeat testing at defined intervals and whether the value is rising, flat, or falling. We walk through that timing logic in the episode.
  • ECG plus troponin framing: A nonischemic ECG with a normal hs-TnI supports discharge, while a clearly elevated hs-TnI generally warrants admission for further workup even though it does not by itself diagnose AMI.
  • Sex-specific cutoffs matter: Intermediate hs-TnI ranges are sex-specific, and using the correct female thresholds can identify myocardial infarction that older pathways were more likely to miss.
  • Order it when it matters: Because hs-TnI is much more likely to return abnormal than prior-generation troponin, indiscriminate testing can increase admissions without helping care unless the result will change management or disposition.

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 References:

  1. Sandoval Y, et al. Myocardial Infarction Risk Stratification With a Single Measurement of High-Sensitivity Troponin I. J Am Coll Cardiol. 2019;74(3):271-282. PMID: 31319909
  2. Christenson RH, et al. Pivotal findings for a high-sensitivity cardiac troponin assay: Results of the HIGH-US study. Clin Biochem. 2020;78:32-39. PMID: 31669511
  3. Nowak RM, et al. Performance of Novel High-Sensitivity Cardiac Troponin I Assays for 0/1-Hour and 0/2- to 3-Hour Evaluations for Acute Myocardial Infarction: Results From the HIGH-US Study. Ann Emerg Med. 2020;76(1):1-13. PMID: 32046869
  4. Sandoval Y, et al. Single High-Sensitivity Cardiac Troponin I to Rule Out Acute Myocardial Infarction. Am J Med. 2017;130(9):1076-1083.e1. PMID: 28344141
  5. Sandoval Y, et al. Clinical Features and Outcomes of Emergency Department Patients With High-Sensitivity Cardiac Troponin I Concentrations Within Sex-Specific Reference Intervals. Circulation. 2019;139(14):1753-1755. PMID: 30933618
  6. Sandoval Y, et al. Type 1 and 2 Myocardial Infarction and Myocardial Injury: Clinical Transition to High-Sensitivity Cardiac Troponin I. Am J Med. 2017;130(12):1431-1439.e4. PMID: 28739197
  7. Writing Committee, Kontos MC, et al. 2022 ACC Expert Consensus Decision Pathway on the Evaluation and Disposition of Acute Chest Pain in the Emergency Department: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022;80(20):1925-1960. PMID: 36241466

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