Copeptin Levels Are Independent from Mild Therapeutic Hypothermia but Do Not Predict Infarct Size in Patients Presenting with ST-Segment Elevation Myocardial Infarction.
acute myocardial infarction
arginine vasopressin
copeptin
mild therapeutic hypothermia
targeted temperature management
Journal
Journal of cardiovascular development and disease
ISSN: 2308-3425
Titre abrégé: J Cardiovasc Dev Dis
Pays: Switzerland
ID NLM: 101651414
Informations de publication
Date de publication:
14 Oct 2021
14 Oct 2021
Historique:
received:
17
09
2021
revised:
08
10
2021
accepted:
11
10
2021
entrez:
22
10
2021
pubmed:
23
10
2021
medline:
23
10
2021
Statut:
epublish
Résumé
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. 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. We included 99 patients (MTH 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.
Sections du résumé
BACKGROUND
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
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
RESULTS
We included 99 patients (MTH
CONCLUSIONS
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.
Identifiants
pubmed: 34677200
pii: jcdd8100131
doi: 10.3390/jcdd8100131
pmc: PMC8539262
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : FWF Austrian Science Fund
ID : APKLI209
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