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Search: WFRF:(Smaradottir M. I.)

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  • Smaradottir, M. I., et al. (author)
  • Copeptin in patients with acute myocardial infarction and newly detected glucose abnormalities - A marker of increased stress susceptibility? : A report from the Glucose in Acute Myocardial Infarction cohort
  • 2017
  • In: Diabetes & Vascular Disease Research. - : Sage Publications. - 1479-1641 .- 1752-8984. ; 14:2, s. 69-76
  • Journal article (peer-reviewed)abstract
    • Objective: To characterize copeptin levels and to explore its prognostic importance in patients with acute myocardial infarction with newly detected glucose abnormalities. Methods: Copeptin was measured in 166 patients with acute myocardial infarction without known diabetes and in 168 age- and gender-matched controls. Participants were classified as having normal glucose tolerance or abnormal glucose tolerance (impaired glucose tolerance + type 2 diabetes mellitus) by oral glucose tolerance test. Study participants were followed over a decade for major cardiovascular event (acute myocardial infarction/stroke/congestive heart failure/cardiovascular death), cardiovascular and total death. Results: Median copeptin level was higher in patients (10.5 pmol/L) than controls (5.9 pmol/L; p < 0.01). Patients with abnormal glucose tolerance had higher copeptin (12.2 pmol/L) than those with normal glucose tolerance (7.9 pmol/L; p < 0.01) but levels of copeptin did not differ in controls with abnormal glucose tolerance or normal glucose tolerance. Copeptin predicted major cardiovascular events [n = 64; hazard ratio = 1.15 (1.01-1.32; p = 0.04)], cardiovascular mortality [n = 29; hazard ratio = 1.24 (1.06-1.46; p = 0.01)] and total death [n = 51; hazard ratio = 1.21 (1.05-1.40; p = 0.01)] in unadjusted Cox regression analyses in the patient cohort. In controls, copeptin predicted major cardiovascular events [n = 26; hazard ratio = 1.17 (1.01-1.36; p = 0.03)]. Conclusion: Copeptin levels are highest among acute myocardial infarction patients with glucose disturbances and predict an adverse prognosis in unadjusted analyses. These findings imply that raised copeptin reflects stress rather than acting as a pathogenic factor for glucose abnormalities.
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  • Smaradottir, M. I., et al. (author)
  • Copeptin is associated with mortality in elderly people
  • 2021
  • In: European Journal of Clinical Investigation. - : John Wiley and Sons Inc. - 0014-2972 .- 1365-2362. ; 51:7
  • Journal article (peer-reviewed)abstract
    • Background: Elevated copeptin, a marker for vasopressin release, has been associated with impaired prognosis in acute myocardial infarction (MI). The aim was to investigate whether this association extends beyond the acute phase and whether it is related to markers of stress (cortisol) and heart failure (NTproBNP). Methods: Copeptin, cortisol and NTproBNP were measured in 926 participants (age: 76.0; male: 48.5%) in the ICELAND MI study whereof 246 had a previous MI (91 recognizable (RMI) and 155 previously unrecognizable (UMI) detected by cardiac magnetic resonance imaging). The primary endpoint was cardiovascular events (CVEs), and secondary endpoints were total mortality, heart failure and MI (median follow-up was 9.1 years). The relation between copeptin and prognosis was assessed with the Cox proportional hazard regression (unadjusted, adjusted for cortisol and NTproBNP, respectively, and a multiple model: copeptin, cortisol, NTproBNP, age, sex, serum creatinine, heart failure). Results: Copeptin was higher in participants with MI (8.9 vs. 6.4 pmol/L; P <.01), with no difference between RMI vs. UMI. Increased copeptin correlated with evening cortisol (r =.11; P <.01) and NTproBNP (r =.07; P =.04). Copeptin was associated with CVE and total mortality after adjusting for cortisol and NTproBNP separately, and remained significantly associated with total mortality in the multiple model. Conclusions: Copeptin was higher in subjects with previous MI regardless whether previously recognized or not. Copeptin correlated weakly with cortisol and NTproBNP, and was independently associated with total mortality. This indicates that the prognostic implications of copeptin are not only mediated by heart failure or stress, supporting the assumption that copeptin is a marker of general vulnerability. 
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4.
  • Smaradottir, M I, et al. (author)
  • Vasopressin, measured as copeptin, in elderly individuals with or without unrecognized myocardial infarction. A report from the ICELAND MI Cohort.
  • 2017
  • In: European Heart Journal. - Barcelona, Spain. - 0195-668X .- 1522-9645. ; 38:suppl_1, s. 863-864
  • Journal article (other academic/artistic)abstract
    • 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.
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