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Education in Heart
Systemic disorders in heart disease
Analytically false or true positive elevations of high sensitivity cardiac troponin: a systematic approach
  1. Mehrshad Vafaie1,
  2. Moritz Biener1,
  3. Matthias Mueller1,
  4. Philipp A Schnabel2,
  5. Florian André1,
  6. Henning Steen1,
  7. Markus Zorn3,
  8. Melanie Schueler1,
  9. Stefan Blankenberg4,
  10. Hugo A Katus1,
  11. Evangelos Giannitsis1
  1. 1Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, Heidelberg, Germany
  2. 2Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany
  3. 3Central Laboratory, University Hospital Heidelberg, Heidelberg, Germany
  4. 4Clinic for General and Interventional Cardiology, University Heart Center Hamburg, Hamburg, Germany
  1. Correspondence to Professor Evangelos Giannitsis, Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, Medizinische Klinik III, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany; evangelos_giannitsis{at}med.uni-heidelberg.de

https://doi.org/10.1136/heartjnl-2012-303202

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    Keywords

    Cardiac troponin (cTn) is a regulatory protein of the myofibrillar thin filament of striated muscle regulating excitation–contraction coupling in the heart.w1 Among the three subunits (T, I, and C), only cardiac troponin T (cTnT) and I (cTnI) are expressed in cardiac muscle and released into blood following myocardial cell death. Several distinct pathobiological mechanisms leading to elevated troponin values have been suggested, not all of which involve myocyte necrosis.w2

    cTnT or cTnI are routinely used in emergency units as the preferred biomarkers for the diagnosis of acute myocardial infarction (MI). According to joint criteria for the diagnosis of acute MI by the European Society of Cardiology/American College of Cardiology/American Heart Association/World Heart Federation Task Force, an acute MI should be diagnosed in patients with symptoms of myocardial ischaemia and detection of a rise and/or fall of cardiac biomarkers (preferentially troponins) with at least one value above the 99th percentile of the upper reference limit.1

    Use of high sensitivity troponin assays allows more accurate and earlier detection of MI.2 w3 Higher analytical sensitivity increases the number of patients with analytically true positive cTn results due to non-ST elevation MI (NSTEMI) but also due to numerous acute or chronic diseases in the absence of overt ischaemic heart disease (box 1).3 w4

    Box 1

    Elevations of cardiac troponin values because of myocardial injury

    Injury related to primary myocardial ischaemia

    Plaque rupture

    Intraluminal coronary artery thrombus formation

    Injury related to supply/demand imbalance of myocardial ischaemia

    Tachy-/bradyarrhythmias

    Aortic dissection or severe aortic valve disease

    Hypertrophic cardiomyopathy

    Cardiogenic, hypovolaemic, or septic shock

    Severe respiratory failure

    Severe anaemia

    Hypertension with or without left ventricular hypertrophy

    Coronary spasm

    Coronary embolism or vasculitis

    Coronary endothelial dysfunction without significant coronary artery disease

    Injury not related to myocardial ischaemia

    Cardiac contusion, surgery, ablation, pacing, or …

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    Footnotes

    • Contributors MV and EG were involved in the conception, design and drafting of this manuscript. MV, MB, MM, PAS, FA, HS, MZ, MS, SB, HAK and EG critically revised the draft manuscript. FA and HS prepared and interpreted the sections on MRI. All the authors read and approved the final manuscript.

    • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. EG is a consultant to Roche Diagnostics and Brahms Biomarkers and has received speakers’ honoraria from Roche Diagnostics, Siemens Healthcare, Brahms Biomarkers, and Mitsubishi Chemicals. HAK has developed the cardiac troponin T assay and holds a patent jointly with Roche Diagnostics. He has received grants and research support from several companies, and has received honoraria for lectures from Roche Diagnostics. SB reported receiving lecture fees from and consulting for Brahms Thermo Fisher and receiving lecture fees from Abbott Diagnostics and Siemens. MV has been reimbursed for travel expenses and fees associated with attending seminars and conferences by Octapharma, Lilly Germany, GlaxoSmithKline, Roche Diagnostics, Brahms, Leo Pharma, and Abbott. All other authors declared no competing interests.

    • Provenance and peer review Commissioned; externally peer reviewed.