Abstract

Background: High copeptin levels are associated with adverse outcome after ST-segment elevation myocardial infarction (STEMI). However, the association between copeptin and myocardial infarct size and function has not been described so far. We therefore investigated the relationship between plasma copeptin concentrations and infarct size, as well as myocardial function at baseline and 4 months after mechanical reperfusion for STEMI. Methods: STEMI patients (n = 54) successfully reperfused by primary angioplasty underwent contrast-enhanced cardiac magnetic resonance imaging within a median of 2 days after the acute event and 4 months thereafter. Infarct size was determined with the use of late gadolinium enhanced images. Left ventricular dimensions and function were measured from cine true-FISP sequences. Adverse remodeling was defined as an increase in end-diastolic volume of ≥ 20% after 4 months. Blood samples were drawn 2 days after the onset of symptoms. Copeptin and N-terminal pro-B-type natriuretic peptide values were determined by an automated immunofluorescent assay. Results: Baseline copeptin concentrations (median: 10.4 pmol/L [IQR: 6.0 - 14.4]) were associated with early and chronic infarct sizes (r = 0.39, p = 0.004 at baseline; r = 0.39, p = 0.011 at follow-up) and inversely related to left ventricular ejection fraction (r = -0.48, p < 0.001 at baseline; r = -0.46, p < 0.001 at follow-up). Patients with adverse remodeling showed higher baseline copeptin levels compared to patients without remodelling (10.3 pmol/L [6.1 - 13.2] vs. 19.2 pmol/L [10.4 - 28.5], p = 0.024). Receiver operating characteristic analysis indicated a cut-off value of 16.7 pmol/L to best identify patients with future adverse remodelling (area under the curve = 0.79, 95% CI 0.59 to 0.98). Compared to copeptin, the area under the curve for N-terminal pro-B-type natriuretic peptide for prediction of remodeling 4 months after STEMI was slightly lower (0.75, 95% CI 0.52 to 0.98). Conclusions: Increased copeptin values at an early stage after STEMI are associated with larger acute and chronic infarct sizes. Moreover, copeptin is a potential predictor of myocardial function and remodeling 4 months after STEMI. These findings highlight the possible role of copeptin as a biomarker predicting adverse outcome after STEMI.

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