Key result
Adding copeptin to hs-cTnI yields no significant gain in AMI sensitivity, while substantially reducing specificity.
Why the study?
Early diagnosis of AMI remains challenging in patients presenting with initially non-elevated hs-cTnI, prompting evaluation of the diagnostic contribution of copeptin alongside endothelin-1 and chemerin as exploratory comparators.
Does adjunctive copeptin testing at presentation improve the early diagnostic sensitivity for acute myocardial infarction in adults presenting with suspected acute coronary syndrome and initially non-elevated hs-cTnI?
Case-Control (n=160)
Blinded adjudication
No
Does adjunctive copeptin testing at presentation improve the early diagnostic sensitivity for acute myocardial infarction in adults presenting with suspected acute coronary syndrome and initially non-elevated hs-cTnI?
Adding copeptin to hs-cTnI at presentation identified 80% of initially troponin-negative NSTEMI cases and increased overall AMI sensitivity from 85.0% to 95.0%, though at the expense of reduced specificity (from 95.0% to 62.5%) and no significant improvement in overall clinical model fit.
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May aid early AMI diagnosis when hs-cTnI is normal; leaves open incremental value pending larger prospective validation.
Early diagnosis of acute myocardial infarction (AMI) remains challenging in patients with initially non-elevated high-sensitivity cardiac troponin I (hs-cTnI). We assessed the diagnostic contribution of copeptin, with endothelin-1 and chemerin as exploratory comparators. This prospective, single-center case–control study included 160 adults with suspected acute coronary syndrome: 40 controls, 40 with unstable angina, 40 with non-ST-elevation myocardial infarction (NSTEMI), and 40 with ST-elevation myocardial infarction (STEMI). Samples were obtained at presentation, and diagnoses were adjudicated blinded to investigational biomarkers. Twelve of the 80 AMI cases had initially non-elevated hs-cTnI (7 STEMI; 5 NSTEMI). Copeptin was positive in 8/12 and the three-marker panel in 9/12. Among the five initially troponin-negative NSTEMI cases, all positive on repeat hs-cTnI testing, copeptin was positive in 4/5 (80.0%; 95% confidence interval, 28.4–99.5%). The hs-cTnI OR copeptin strategy increased sensitivity from 85.0% to 95.0%, while specificity among controls decreased from 95.0% to 62.5%. Adding the biomarkers to a clinical model containing hs-cTnI changed the apparent area under the curve from 0.961 to 0.965, without significantly improving model fit (likelihood-ratio p = 0.718). These findings may support evaluating adjunctive copeptin within contemporary accelerated troponin pathways.
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Sülü et al. (2026) conducted a case-control in Suspected acute coronary syndrome / Acute myocardial infarction (n=160). Copeptin (with endothelin-1 and chemerin as exploratory comparators) added to hs-cTnI vs. hs-cTnI alone was evaluated on Diagnostic sensitivity for acute myocardial infarction (hs-cTnI OR copeptin vs hs-cTnI alone) (p=0.718). Adding copeptin to hs-cTnI increased AMI diagnostic sensitivity from 85.0% to 95.0% (identifying 80.0% of troponin-negative NSTEMIs), though specificity fell from 95.0% to 62.5%.
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