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Sensitive cardiac troponins and N-terminal pro-B-type natriuretic peptide in stable coronary artery disease: correlation with left ventricular function as assessed by myocardial strain

  • Marit Kristine Smedsrud
  • Jørgen Gravning
  • Torbjørn Omland
  • Christian Eek
  • Lars Mørkrid
  • Helge Skulstad
  • Lars Aaberge
  • Bjørn Bendz
  • John Kjekshus
  • Thor EdvardsenEmail author
Original Paper

Abstract

N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponins (cTns) measured with sensitive assays provide strong prognostic information in patients with stable coronary artery disease. However, the relationship between these biomarkers and myocardial contractile function, as well as infarct size, in this patient group, remains to be defined. The study population consisted of 160 patients referred to a follow-up echocardiography scheduled 1 year after coronary revascularization. Concentrations of NT-proBNP, high-sensitive cTnT (hs-cTnT) and sensitive cTnI assays were assessed. Left ventricular function was measured as global peak systolic longitudinal strain by speckle tracking echocardiography and infarct size was assessed by late-enhancement MRI. NT-proBNP and sensitive cTnI levels were significantly associated with left ventricular function by peak systolic strain (R-values 0.243 and 0.228, p = 0.002 and 0.004) as well as infarct size (R-values 0.343 and 0.366, p = 0.014 and p = 0.008). In contrast, hs-cTnT did not correlate with left ventricular function (R = 0.095, p = 0.231) and only marginally with infarct size (R = 0.237, p = 0.094). NT-proBNP and sensitive cTnI levels correlate with left ventricular function and infarct size in patients with stable coronary artery disease after revascularization. As opposed to hs-cTnT, NT-proBNP and cTnI seem to be indicators of incipient myocardial dysfunction and the extent of myocardial necrosis.

Keywords

Coronary artery disease Troponin I Troponin T B-type natriuretic peptide Echocardiography Speckle tracking 

Notes

Conflict of interest

Jørgen Gravning has received lecture fees from Siemens. Torbjørn Omland has received speaker honoraria and research support from Roche Diagnostics.

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Copyright information

© Springer Science+Business Media Dordrecht 2015

Authors and Affiliations

  • Marit Kristine Smedsrud
    • 1
    • 2
    • 3
  • Jørgen Gravning
    • 4
  • Torbjørn Omland
    • 3
    • 4
  • Christian Eek
    • 1
  • Lars Mørkrid
    • 3
    • 5
  • Helge Skulstad
    • 1
  • Lars Aaberge
    • 1
  • Bjørn Bendz
    • 1
  • John Kjekshus
    • 1
  • Thor Edvardsen
    • 1
    • 2
    • 3
    Email author
  1. 1.Department of CardiologyOslo University Hospital, RikshospitaletOsloNorway
  2. 2.Institute for Surgical ResearchOslo University Hospital, RikshospitaletOsloNorway
  3. 3.University of OsloOsloNorway
  4. 4.Division of MedicineAkershus University HospitalLørenskogNorway
  5. 5.Department of Medical BiochemistryOslo University HospitalOsloNorway

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