Copeptin for the early rule-out of non-ST-elevation myocardial infarction

- Unlike troponin, copeptin levels start high and gradually decrease over time.
- Copeptin may be used in the rule-out of non-ST-elevation myocardial infarction.
- Chest pain patients with < 6 h of symptom onset have higher copeptin levels.
- Combined copeptin and troponin should be used in low- to intermediate-risk patients.
- The dual strategy may be used when high-sensitivity troponin is not available.

Copeptin, a neuropeptide of unknown pathophysiological function that is stoichiometrically secreted with the antidiuretic hormone, is a non-specific marker of endogenous stress which has recently gained interest for its use within a dual-marker strategy in combination with cardiac troponin for the early rule-out of non-ST-elevation myocardial infarction (NSTEMI) in emergency department patients with suspected MI.Based on methodologically strong and consistent evidence from large diagnostic studies and even one randomized intervention study, current European Society of Cardiology Guidelines recommend copeptin and the dual-marker strategy for the early rule-out of MI when high-sensitivity cardiac troponin (hs-cTn) assays are not available. When used with conventional cTn assays, the incremental value of copeptin is large. When used with hs-cTn, the incremental value is very small and does not justify routine clinical use.This review aims to describe the structure, function, and release mechanism of copeptin; as well as to provide an explanation on why this biomarker should be used in the rule-out, and not in the rule-in, of NSTEMI.