Open AccessDiagnostic Performance of Copeptin in Patients With Acute Nontraumatic Chest Pain: BWH‐TIMI ED Chest Pain Study
Author(s) -
Sukul Devraj,
Bonaca Marc P.,
Ruff Christian T.,
Kosowsky Joshua,
Conrad Michael,
Murphy Sabina A.,
Sabatine Marc S.,
Jarolim Petr,
Morrow David A.
Publication year - 2014
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.22244
Subject(s) - copeptin , medicine , chest pain , cardiology , myocardial infarction , emergency department , troponin , troponin i , area under the curve , receiver operating characteristic , timi , anesthesia , vasopressin , psychiatry , thrombolysis
Background Arginine‐vasopressin ( AVP ) is an acute marker of physiologic stress. Copeptin is the C‐terminal fragment of vasopressin precursor hormone that is more easily measured than AVP . Studies assessing the utility of copeptin in the diagnosis of myocardial infarction ( MI ) have demonstrated mixed results. Hypothesis The aim of this study was to test the hypothesis that copeptin improves diagnostic performance when added to troponin for detecting MI in patients presenting to the emergency department with nontraumatic chest pain. Methods We measured copeptin, local cardiac troponin I (local cTnI ), and a contemporary sensitive cardiac troponin I (sensitive cTnI ) at presentation and serially in patients who presented with acute chest pain. A copeptin cutoff of 14 pmol/L was utilized. Results MI was diagnosed in 25.7% of patients. Noncoronary acute cardiopulmonary causes of chest pain occurred in 12.8%. Patients with MI had significantly higher copeptin levels than patients with noncardiac chest pain ( P < 0.001). The area under the receiver operating characteristic curve ( AUC ) for copeptin was 0.60 (95% confidence interval: 0.54‐0.66), significantly less than the AUC for local cTnI (0.92) or sensitive cTnI (0.96). The combination of copeptin with either the local or sensitive troponin assay (c‐statistics 0.92 and 0.95, respectively) did not significantly improve the AUC as compared to either troponin assay alone. This finding persisted in the subgroup of early presenters (≤6 hours from symptom onset). Conclusions Copeptin did not improve the diagnostic performance for detecting MI when used alone or in combination with a contemporary sensitive cTnI assay, though our cohort had relatively few early presenters.