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Original article
Association of copeptin with myocardial infarct size and myocardial function after ST segment elevation myocardial infarction
  1. Sebastian Johannes Reinstadler1,
  2. Gert Klug1,
  3. Hans-Josef Feistritzer1,
  4. Agnes Mayr2,
  5. Bettina Harrasser1,
  6. Johannes Mair1,
  7. Kerstin Bader1,
  8. Katrin Streil1,
  9. Angelika Hammerer-Lercher3,
  10. Regina Esterhammer2,
  11. Bernhard Metzler1
  1. 1University Clinic of Internal Medicine III, Cardiology, Innsbruck Medical University, Innsbruck, Austria
  2. 2Department of Radiology I, Innsbruck Medical University, Innsbruck, Austria
  3. 3Central Institute for Medical Laboratory Diagnostics, Innsbruck Medical University, Innsbruck, Austria
  1. Correspondence to Dr Bernhard Metzler, University Clinic of Internal Medicine III, Cardiology, Innsbruck Medical University, Anichstrasse 35, Innsbruck A-6020, Austria; Bernhard.Metzler{at}uki.at

Abstract

Objective To investigate the relationship between circulating plasma copeptin values and infarct size as well as myocardial function at baseline and 4 months after mechanical reperfusion for ST segment elevation myocardial infarction (STEMI).

Design Prospective observational cohort study.

Setting University Hospital of Innsbruck.

Patients 54 patients with acute STEMI.

Main outcome measures Correlation of plasma copeptin with infarct size as well as left ventricular ejection fraction (LVEF) and remodelling.

Methods Participants underwent contrast enhanced cardiac MRI at baseline and 4 months thereafter. Blood samples were drawn 2 days after the onset of symptoms. Copeptin values were determined by an immunofluorescent assay.

Results Copeptin concentrations (median 10.4 pmol/l, IQR 6.0–14.4) were associated with early and chronic infarct size (r=0.388, p=0.004 at baseline; r=0.385, p=0.011 at follow-up) and inversely related to LVEF at both times (r=−0.484, p<0.001 at baseline; r=−0.461, p<0.001 at follow-up). Patients with adverse remodelling showed higher baseline copeptin values compared to patients without remodelling (p=0.02). Receiver operating characteristic analysis indicated a cut-off value of 16.7 pmol/l for copeptin to best identify patients with future adverse remodelling.

Conclusions Increased copeptin values 2 days after STEMI are associated with larger acute and chronic infarct sizes. Moreover, elevated copeptin concentrations at baseline were associated with myocardial function and remodelling 4 months post-STEMI. These findings strengthen the role of copeptin as a biomarker of adverse outcome after STEMI.

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