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Vasopressin, measured as copeptin, in elderly individuals with or without unrecognized myocardial infarction. A report from the ICELAND MI Cohort.
KTH, School of Architecture and the Built Environment (ABE), Real Estate and Construction Management, Building and Real Estate Economics. KTH, School of Architecture and the Built Environment (ABE), Centres, Centre for Transport Studies, CTS.
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2017 (English)In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 38, no suppl_1, p. 863-864Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

Background: A subset of patients with myocardial infarction (MI) has minimal or no symptoms, i.e. clinically unrecognized MI (UMI). Copeptin, a marker of vasopressin, predicts cardiovascular events (CVE).

Purpose: To investigate the prognostic implication of copeptin in people with or without MI and to study whether it differs between UMI and recognized MI (RMI).

Methods: Copeptin was measured in 926 participants (age 76.0; male 48.5%) in the observational ICELAND MI study. At baseline 246 patients had hospital/surveillance records supporting a RMI (n=91) or myocardial scars detected by magnetic resonance imaging (UMI, n=155). Cox proportional hazard regression was used to assess the prognostic capability of (log) copeptin, in the multiple model adjusted for prior heart failure, fasting blood glucose, age groups and creatinine. The primary endpoint was CVE (cardiovascular death/MI/stroke/PCI/CABG) and the secondary endpoint was total mortality during 9.1 years of follow-up.

Results: Copeptin levels were significantly higher in participants with compared to those without a MI (8.9 pmol/L vs. 6.4 pmol/L; p<0.01), but did not differ between the subsets with RMI vs. UMI.

In the unadjusted analysis CVE:s were predicted by copeptin in the total cohort (HR 1.60; 95% CI 1.17–2.19; p<0.01) but not after adjustments (HR 1.18; 95% CI 0.84–1.65; p=0.33).

Total mortality in the total cohort was predicted by copeptin in the unadjusted analysis. The same was found in patients with and without MI as well as in the subset with RMI, however, not in those with UMI. In the adjusted model copeptin remained as a predictor in the total cohort (HR 1.77; 95% CI 1.24–2.51; p<0.01), in all patients with MI (HR 2.20; 95% CI 1.25–3.87; p<0.01), and in those with RMI (HR 5.73; 95% CI 2.13–15.36; p<0.01).

Conclusion: Copeptin levels were higher for participants with MI, however no difference was seen for those with RMI or UMI. Copeptin did not remain as a significant predictor for CVE after adjustments while it was an independent predictor for total mortality in patients with MI including the subset with RMI. This implies that copeptin is a general marker of disease rather than a specific marker for cardiovascular disease.

Place, publisher, year, edition, pages
Barcelona, Spain, 2017. Vol. 38, no suppl_1, p. 863-864
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:kth:diva-251053DOI: 10.1093/eurheartj/ehx504.P4236OAI: oai:DiVA.org:kth-251053DiVA, id: diva2:1314455
Conference
European Society of Cardiology, 26-30 August 2017, Barcelona, Spain
Note

QC 20190619

Available from: 2019-05-08 Created: 2019-05-08 Last updated: 2019-06-19Bibliographically approved

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CiteExportLink to record
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