Clinical chemistry · 2015
Temporal release pattern of copeptin and troponin T in patients with suspected acute coronary syndrome and spontaneous acute myocardial infarction.
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Slagman Anna, Searle Julia, Müller Christian, Möckel Martin
Аннотация
BACKGROUND: The release pattern of copeptin during the initial 36 h of spontaneous acute myocardial infarction (AMI) has received relatively little investigation but may provide important information on optimal timing of diagnostic measurements.
METHODS: We investigated the release pattern of copeptin and cardiac troponin T in patients with suspected acute coronary syndrome (ACS). Blood samples were collected in the ambulance, at admission, and after 2, 4, 6, and 12-36 h. Copeptin and high-sensitivity cardiac troponin T (hs-cTnT) were measured in heparin plasma samples.
RESULTS: Of 93 patients studied, 37 (39.8%) had ST-elevation myocardial infarction (STEMI), 20 (21.5%) non-STEMI, 20 (21.5%) unstable angina pectoris (UAP), and 16 (17.2%) non-ACS diagnoses. Peak copeptin concentrations were detected during ambulance transport for NSTEMI patients [median 94.0 pmol/L, interquartile range (IQR) 53.3-302.1 pmol/L] and at admission for patients with STEMI (70.0 pmol/L, 22.0-144.8 pmol/L). In patients with AMI, copeptin decreased significantly over time (P < 0.0001). This was true for patients with STEMI (P = 0.005) and non-STEMI (P = 0.021). The diagnostic performance during ambulance transport was similar for hs-cTnT (area under the ROC curve 0.75, 95% CI 0.62-0.88) and copeptin (0.81, 0.69-0.92). In early presenters (n = 52), no patient with AMI was initially (in ambulance or at admission) negative for copeptin, resulting in an area under the ROC curve of 0.963 for ambulance values and a negative predictive value of 100%. In late presenters, the negative predictive value of copeptin was 50% in ambulance and at admission.
CONCLUSIONS: Our analysis is the first to show a consistent early increase in copeptin at first medical contact in the ambulance and a decrease to routine values within 12-36 h in patients presenting early with spontaneous AMI.
METHODS: We investigated the release pattern of copeptin and cardiac troponin T in patients with suspected acute coronary syndrome (ACS). Blood samples were collected in the ambulance, at admission, and after 2, 4, 6, and 12-36 h. Copeptin and high-sensitivity cardiac troponin T (hs-cTnT) were measured in heparin plasma samples.
RESULTS: Of 93 patients studied, 37 (39.8%) had ST-elevation myocardial infarction (STEMI), 20 (21.5%) non-STEMI, 20 (21.5%) unstable angina pectoris (UAP), and 16 (17.2%) non-ACS diagnoses. Peak copeptin concentrations were detected during ambulance transport for NSTEMI patients [median 94.0 pmol/L, interquartile range (IQR) 53.3-302.1 pmol/L] and at admission for patients with STEMI (70.0 pmol/L, 22.0-144.8 pmol/L). In patients with AMI, copeptin decreased significantly over time (P < 0.0001). This was true for patients with STEMI (P = 0.005) and non-STEMI (P = 0.021). The diagnostic performance during ambulance transport was similar for hs-cTnT (area under the ROC curve 0.75, 95% CI 0.62-0.88) and copeptin (0.81, 0.69-0.92). In early presenters (n = 52), no patient with AMI was initially (in ambulance or at admission) negative for copeptin, resulting in an area under the ROC curve of 0.963 for ambulance values and a negative predictive value of 100%. In late presenters, the negative predictive value of copeptin was 50% in ambulance and at admission.
CONCLUSIONS: Our analysis is the first to show a consistent early increase in copeptin at first medical contact in the ambulance and a decrease to routine values within 12-36 h in patients presenting early with spontaneous AMI.