The utility of copeptin in the emergency department for non-ST-elevation myocardial infarction rapid rule out: COPED-MIRRO study
aEmergency Department, Short Stay Unit and Hospital at Home Care, Hospital General Universitario de Alicante, Alicante bEmergency Department, Hospital Clínic de Barcelona, Grupo de Investigación 'Urgencias: procesos y patologias', IDIBAPS, Barcelona cEmergency Department, Hospital Universitario Central de Asturias, Oviedo dEmergency Department and Short Stay Unit, Hospital Clínico San Carlos, Madrid eEmergency Department, Hospital Reina Sofía, Murcia, Spain. European Journal of Emergency Medicine
(Impact Factor: 1.58).
06/2013; 21(3). DOI: 10.1097/MEJ.0b013e3283632f8b
To evaluate whether the addition of copeptin measurement to the first troponin determination allows non-ST-elevation acute myocardial infarction to be ruled out in patients consulting the emergency department (ED) for nontraumatic chest pain (NTCP) suggestive of acute coronary syndrome (ACS) whose first electrocardiogram and troponin determination are nondiagnostic, thereby avoiding a second determination of troponin and shortening ED stay.
We carried out a multicentric, prospective, observational, longitudinal, cohort study. Copeptin and troponin determination was performed on arrival of the patient to the ED. We selected consecutive patients with NTCP of less than 12 h of evolution suggestive of ACS with nondiagnostic electrocardiogram and normal troponin values on arrival to the ED. A second troponin determination was performed at 6 h. The negative predictive values and the global discriminative capacity of copeptin were calculated.
We studied 1018 patients (66.4±14.9 years, 62.8% men), 107 (10.5%) having non-ST-elevation acute myocardial infarction. The negative predictive value of copeptin was 94.2% and was significantly greater in patients older than 70 years of age (95.1 vs. 92.6%; P<0.05), without diabetes mellitus (95.4 vs. 90.4%; P=0.01) and arriving at the ED 6 h after the onset of NTCP (97.8 vs. 93.9%; P<0.01). The area under the copeptin receiver operating characteristic curve was 0.71 (95% confidence interval: 0.65-0.76; P<0.001).
The determination of copeptin on arrival to the ED in patients with NTCP suggestive of ACS, in addition to routine troponin determination, does not allow the presence of myocardial infarction to be ruled out quickly and safely and does not avoid ED stay for a second determination of troponin.
Available from: Jonathan Duchenne
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ABSTRACT: To determine whether copeptin-us can rule out diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI) without prolonged monitoring and serial blood sampling in patients with high-sensitive cardiac troponin I (hs-cTnT) below the 99th centile at presentation to the emergency department (ED).
Prospective, non-randomised, individual blinded diagnostic accuracy study.
Two EDs of a rural region of France.
Patients with chest pain suspected of NSTEMI with onset within the last 12 h were considered for enrolment.
Serial clinical, electrographical and biochemical investigations were performed at admission and after 2, 4, 6 and 12 h. Hs-cTnT was measured using an assay with Dimension VISTA, Siemens. Copeptin was measured by the BRAHMS copeptin-us assay on the KRYPTOR Compact Plus system. The follow-up period was 90 days.
Copeptin, troponin, myoglobin and creatine kinase values. Clinical and paraclinical events. The final diagnosis was adjudicated blinded to copeptin result.
During 12 months, 102 patients were analysed. Final diagnosis was NSTEMI for 7.8% (n=8), unstable angina for 3.9% (n=4), cardiac but non-coronary artery disease for 8.8% (n=9), non-cardiac chest pain for 52% (n=53) and unknown for 27.5% (n=28). There was no statistical difference for copeptin values between patients with NSTEMI and others (respectively 5.5 pmol/L IQR (3.1-7.9) and 6.5 pmol/L IQR (3.9-12.1), p=0.49). Only one patient with NSTEMI had a copeptin value above the cut-off of 95th centile at admission.
In this study, copeptin does not add a diagnostic value at admission to ED for patients with suspected acute coronary syndrome without ST-segment elevation and with hs-cTnT below the 99th centile.
Clinicaltrials.gov identifier: NCT01334645.
BMJ Open 03/2014; 4(3):e004449. DOI:10.1136/bmjopen-2013-004449 · 2.27 Impact Factor
Revista Espa de Cardiologia 03/2014; 67(7). DOI:10.1016/j.rec.2013.11.009 · 3.79 Impact Factor
Available from: Johannes von Recum
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ABSTRACT: This randomized controlled trial (RCT) evaluated whether a process with single combined testing of copeptin and troponin at admission in patients with low-to-intermediate risk and suspected acute coronary syndrome (ACS) does not lead to a higher proportion of major adverse cardiac events (MACE) than the current standard process (non-inferiority design).
A total of 902 patients were randomly assigned to either standard care or the copeptin group where patients with negative troponin and copeptin values at admission were eligible for discharge after final clinical assessment. The proportion of MACE (death, survived sudden cardiac death, acute myocardial infarction (AMI), re-hospitalization for ACS, acute unplanned percutaneous coronary intervention, coronary artery bypass grafting, or documented life threatening arrhythmias) was assessed after 30 days. Intention to treat analysis showed a MACE proportion of 5.17% [95% confidence intervals (CI) 3.30-7.65%; 23/445] in the standard group and 5.19% (95% CI 3.32-7.69%; 23/443) in the copeptin group. In the per protocol analysis, the MACE proportion was 5.34% (95% CI 3.38-7.97%) in the standard group, and 3.01% (95% CI 1.51-5.33%) in the copeptin group. These results were also corroborated by sensitivity analyses. In the copeptin group, discharged copeptin negative patients had an event rate of 0.6% (2/362).
After clinical work-up and single combined testing of troponin and copeptin to rule-out AMI, early discharge of low- to intermediate risk patients with suspected ACS seems to be safe and has the potential to shorten length of stay in the ED. However, our results need to be confirmed in larger clinical trials or registries, before a clinical directive can be propagated.
European Heart Journal 04/2014; 36(6). DOI:10.1093/eurheartj/ehu178 · 15.20 Impact Factor
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