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Article

Copeptin Levels Are Independent from Mild Therapeutic Hypothermia but Do Not Predict Infarct Size in Patients Presenting with ST-Segment Elevation Myocardial Infarction

1
Department of Emergency Medicine, Medical University of Vienna, 1090 Vienna, Austria
2
Division of Cardiovascular and Interventional Radiology, Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, 1090 Vienna, Austria
3
Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, 1090 Vienna, Austria
4
Department of Laboratory Medicine, Medical University of Vienna, 1090 Vienna, Austria
*
Author to whom correspondence should be addressed.
J. Cardiovasc. Dev. Dis. 2021, 8(10), 131; https://doi.org/10.3390/jcdd8100131
Received: 17 September 2021 / Revised: 8 October 2021 / Accepted: 11 October 2021 / Published: 14 October 2021
Background: Mild therapeutic hypothermia (MTH) is a treatment adjunct in ST-segment elevation myocardial infarction (STEMI) that deserves investigation. Copeptin―a surrogate marker for vasopressin―is an early biomarker in STEMI. Data from cardiac arrest patients suggest a reduction of copeptin levels through MTH; however, copeptin levels have not been investigated in MTH during STEMI. Methods: We analyzed patients treated with MTH during STEMI in a sub-study of the STATIM trial (Testori, Heart 2019). Patients were randomized to normothermia or MTH with out-of-hospital initiation. Seven copeptin samples were collected from each patient. Primary endpoint was the difference in copeptin levels between the groups. As secondary endpoints, we defined differences in the kinetics between the sampling timepoints and the correlation between copeptin and the infarct size in relation to left ventricular myocardium. Results: We included 99 patients (MTH n = 47, control n = 52) in our intention to treat analysis. No differences in copeptin values at first medical contact between the MTH and normothermia groups were found. MTH showed no effect on copeptin levels, neither during cooling phase nor through the course. Copeptin peaked at first medical contact and hospital admission in both groups. No differences in kinetics between the timepoints were found. Copeptin showed no correlation with infarct size, neither at first medical contact nor hospital admission. Conclusions: Copeptin levels were not influenced by MTH in STEMI, suggesting the use of this biomarker also during temperature management. Furthermore, copeptin levels were not usable as a surrogate marker for infarct size at any timepoint. View Full-Text
Keywords: copeptin; arginine vasopressin; acute myocardial infarction; targeted temperature management; mild therapeutic hypothermia copeptin; arginine vasopressin; acute myocardial infarction; targeted temperature management; mild therapeutic hypothermia
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MDPI and ACS Style

Mueller, M.; Beitzke, D.; Scherz, T.; Loewe, C.; Mangold, A.; Marculescu, R.; Poppe, M.; Sterz, F.; Herkner, H.; Lang, I.; Testori, C.; Weiser, C. Copeptin Levels Are Independent from Mild Therapeutic Hypothermia but Do Not Predict Infarct Size in Patients Presenting with ST-Segment Elevation Myocardial Infarction. J. Cardiovasc. Dev. Dis. 2021, 8, 131. https://doi.org/10.3390/jcdd8100131

AMA Style

Mueller M, Beitzke D, Scherz T, Loewe C, Mangold A, Marculescu R, Poppe M, Sterz F, Herkner H, Lang I, Testori C, Weiser C. Copeptin Levels Are Independent from Mild Therapeutic Hypothermia but Do Not Predict Infarct Size in Patients Presenting with ST-Segment Elevation Myocardial Infarction. Journal of Cardiovascular Development and Disease. 2021; 8(10):131. https://doi.org/10.3390/jcdd8100131

Chicago/Turabian Style

Mueller, Matthias, Dietrich Beitzke, Thomas Scherz, Christian Loewe, Andreas Mangold, Rodrig Marculescu, Michael Poppe, Fritz Sterz, Harald Herkner, Irene Lang, Christoph Testori, and Christoph Weiser. 2021. "Copeptin Levels Are Independent from Mild Therapeutic Hypothermia but Do Not Predict Infarct Size in Patients Presenting with ST-Segment Elevation Myocardial Infarction" Journal of Cardiovascular Development and Disease 8, no. 10: 131. https://doi.org/10.3390/jcdd8100131

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