Release Kinetics of Copeptin in Patients Undergoing Transcoronary Ablation of Septal Hypertrophy

Liebetrau, Christoph; Nef, Holger; Szardien, Sebastian; Dörr, Oliver; Willmer, Matthias; Voss, Sandra; Troidl, Christian; Hoffmann, Jedrzej; Rixe, Johannes; Rolf, Andreas; Hamm, Christian W.; Möllmann, Helge

doi:10.1373/clinchem.2012.194001

Cited by 42 publications

(42 citation statements)

References 19 publications

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“…23,24 Copeptin is released rapidly after hemodynamic stress. 13,14 In our patients, we found no influence of the interval from symptom onset to blood sampling on copeptin levels. Although we cannot rule out that copeptin was elevated before the event, this result suggests an immediate secretion, within the first minutes after developing symptoms.…”

Section: Discussioncontrasting

confidence: 45%

“…13 Increased copeptin levels were found in patients with acute myocardial infarction even when troponin T was still negative. 14 In combination with highsensitive troponin T, copeptin has valid properties ruling-out acute myocardial infarction 15 and thereby, helps to identify patients with chest pain who can be discharged home from the emergency department without increased risk for major adverse coronary events.…”

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confidence: 99%

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Copeptin Levels in Patients With Acute Ischemic Stroke and Stroke Mimics

Wendt

Ebinger

Kunz

et al. 2015

Stroke

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Background and Purpose— Copeptin levels are increased in patients diagnosed with stroke and other vascular diseases. Copeptin elevation is associated with adverse outcome, predicts re-events in patients with transient ischemic attack and is used in ruling-out acute myocardial infarction. We evaluated whether copeptin can also be used as a diagnostic marker in the prehospital stroke setting. Methods— We prospectively examined patients with suspected stroke on the Stroke Emergency Mobile—an ambulance that is equipped with computed tomography and point-of-care laboratory. A blood sample was taken from patients immediately after arrival. We analyzed copeptin levels in patients with final hospital-based diagnosis of stroke or stroke mimics as well as in vascular or nonvascular patients. In addition, we examined the associations of symptom onset with copeptin levels and the prognostic value of copeptin in patients with stroke. Results— Blood samples of 561 patients were analyzed. No significant differences were seen neither between cerebrovascular (n=383) and other neurological (stroke mimic; n=90) patients ( P =0.15) nor between vascular (n=391) and nonvascular patients (n=170; P =0.57). We could not detect a relationship between copeptin levels and time from onset to blood draw. Three-month survival status was available in 159 patients with ischemic stroke. Copeptin levels in nonsurviving patients (n=8: median [interquartile range], 27.4 [20.2–54.7] pmol/L) were significantly higher than in surviving patients (n=151: median [interquartile range], 11.7 [5.2–30.9] pmol/L; P =0.024). Conclusions— In the prehospital setting, copeptin is neither appropriate to discriminate between stroke and stroke mimic patients nor between vascular and nonvascular patients. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT01382862. The Pre-Hospital Acute Neurological Therapy and Optimization of Medical Care in Stroke Patients study (PHANTOM-S) was registered (NCT01382862). This sub-study was observational and not registered separately, therefore.

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Section: Discussioncontrasting

confidence: 45%

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confidence: 99%

Copeptin Levels in Patients With Acute Ischemic Stroke and Stroke Mimics

Wendt

Ebinger

Kunz

et al. 2015

Stroke

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“…Since vasopressin is highly unstable in plasma with a short half-life time of ∼20 min, copeptin, the inactive 39-amino-acid C-terminal fragment of the precursor protein of vasopressin, which is released in equimolar amounts with vasopressin, can be used as a surrogate biomarker with high stability in plasma [6]. Due to its fast release kinetics [7], copeptin emerged as a valuable diagnostic and prognostic biomarker in several acute cardiovascular diseases [8][9][10] and conditions [11] allowing therapeutic decision making at the moment of presentation. In acute pulmonary embolism, copeptin might reflect a novel pathophysiological axis of pulmonary embolism severity by indicating the systemic response to impaired haemodynamics due to RV dysfunction and failure.…”

Section: Introductionmentioning

confidence: 99%

Risk stratification of normotensive pulmonary embolism: prognostic impact of copeptin

et al. 2015

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The prognostic value of copeptin, the C-terminal fragment of the precursor protein of vasopressin which is released upon stress, and hypotension in pulmonary embolism is unknown, especially if combined with biomarkers reflecting different pathophysiological axes such as myocardial injury (highsensitivity troponin T (hsTnT)) and stretch (N-terminal pro-brain natriuretic peptide (NT-proBNP)).We prospectively studied 268 normotensive pulmonary embolism patients included in a single-centre cohort study.Patients with an adverse 30-day outcome (5.6%) had higher copeptin levels than patients with a favourable course (median (interquartile range) 51.8 (21.6-90.8) versus 13.2 (5.9-39.3) pmol·L −1 ; p=0.020). Patients with copeptin levels above the calculated optimal cut-off value of 24 pmol·L −1 had a 5.4-fold increased risk for an adverse outcome (95% CI 1.68-17.58; p=0.005). We developed a strategy for risk stratification based on biomarkers. None of 141 patients (52.6%) with hsTnT <14 pg·mL −1 or NT-proBNP <600 pg·mL −1 had an adverse outcome (low risk). Copeptin ⩾24 pmol·L −1 stratified patients with elevated hsTnT and NT-proBNP as intermediate-low and intermediate-high risk (5.6% and 20.0% adverse outcome, respectively). Compared to the algorithm proposed by the 2014 European Society of Cardiology guideline, more patients were classified as low risk (52.8% versus 17.5%, p<0.001) and more patients in the intermediate-high risk group had an adverse outcome (20.0% versus 11.6%).Copeptin might be helpful for risk stratification of normotensive patients with pulmonary embolism, especially if integrated into a biomarker-based algorithm. @ERSpublications Copeptin may improve risk stratification of normotensive pulmonary embolism by reflecting a new pathophysiological axis http://ow.ly/R9nOV

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“…The plausibility of these results is supported by a study in patients with TASH, in whom copeptin was increased as early as 30 min after induction of ischemia (13 ), with the limitation that TASH patients have no coronary artery disease. Thus, our study provides proof of concept for ACS patients.…”

Section: Discussionmentioning

confidence: 90%

“…Copeptin, in contrast to cardiac troponins, increases early after symptom onset in patients with ST-elevation myocardial infarction (STEMI) and decreases rapidly within 6 -12 h (6, 12 ). Liebetrau et al reported the temporal release pattern of copeptin after septal occlusion in transcoronary ablation of septal hypertrophy (TASH) (13 ). Copeptin increased immediately and peaked 90 min after induction of ischemia.…”

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confidence: 99%

Temporal Release Pattern of Copeptin and Troponin T in Patients with Suspected Acute Coronary Syndrome and Spontaneous Acute Myocardial Infarction

Slagman¹,

Searle²,

Müller

et al. 2015

Clinical Chemistry

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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.

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Release Kinetics of Copeptin in Patients Undergoing Transcoronary Ablation of Septal Hypertrophy

Cited by 42 publications

References 19 publications

Copeptin Levels in Patients With Acute Ischemic Stroke and Stroke Mimics

Copeptin Levels in Patients With Acute Ischemic Stroke and Stroke Mimics

Risk stratification of normotensive pulmonary embolism: prognostic impact of copeptin

Temporal Release Pattern of Copeptin and Troponin T in Patients with Suspected Acute Coronary Syndrome and Spontaneous Acute Myocardial Infarction

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