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      False-positive troponin elevation due to an immunoglobulin-G-cardiac troponin T complex: a case report

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          Abstract

          Background

          Troponin is a crucial biomarker for the diagnosis of an acute coronary syndrome (ACS). It rises in response to myocardial injury from significant acute myocardial ischaemia caused by obstructive coronary artery disease [‘classical’ myocardial infarction (MI)]. However, raised levels have also been noted in conditions not recognized as classical ACS. This may include MI with non-obstructed coronary arteries such as takotsubo cardiomyopathy and other acute or chronic conditions such as pulmonary embolus or chronic kidney disease. This is commonly labelled as a ‘falsely elevated’ troponin although there is some myocardial strain to explain the rise, such as an increase in cardiac oxygen demand. True ‘falsely elevated’ troponin, characterized by a persistent elevation in the absence of cardiac injury does occur and thought to be secondary to an immunoglobulin-troponin complex (macrotroponin).

          Case summary

          A 53-year-old gentleman with a background of diabetes, hypertension, hypercholesterolaemia, and hepatitis B was admitted with chest pain and persistently elevated cardiac troponin T (cTnT) levels. Investigations revealed unobstructed coronary arteries and a structurally normal, well-functioning heart. Subsequent biochemical analysis found the persistently elevated cTnT secondary to macrotroponin T.

          Discussion

          Macrotroponin, an immunoglobulin-troponin bound complex should be considered as a differential diagnosis when the biochemistry is not reflective of the clinical picture. Early recognition requires effective collaboration with the biochemistry laboratory for accurate diagnosis.

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          Most cited references7

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          Cardiac Troponin Elevation in Patients Without a Specific Diagnosis

          Cardiac troponin (cTn) elevation is a common finding in acutely admitted patients, even in the absence of acute coronary syndrome. In some of these patients, no etiology of cTn elevation can be identified. The term troponinemia is sometimes used to describe this scenario.
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            Circulating cardiac troponin-I autoantibodies in human plasma and serum.

            We identified IgG reactive with human cardiac troponin-I (cTnI) in plasma and serum samples (N = 1930) from normal blood donors, and in sample cohorts characterized on the basis of clinical biomarkers associated with cardiac, infectious, and autoimmune diseases. cTnI and brain natriuretic peptide were the biomarkers chosen to reflect myocyte damage or left ventricular dysfunction, respectively. The infectious disease cohorts were serologically positive for antibodies to hepatitis B (natural infection), hepatitis C virus, and Chagas (i.e., T.cruzi). The autoimmune cohorts were represented by samples from diagnosed systemic lupus erythematosus (biomarker: dsDNA) and rheumatoid arthritis (biomarker: rheumatoid factor) subjects. The prevalence of IgG autoantibodies reactive with cTnI was high in the normal donor cohort (95/750, 12.7%). The prevalence in the other sample cohorts was not significantly different from that in the normal blood donors, with the exception of a slight increase in the rheumatoid factor cohort (28/137, 20.4%). The presence of anti-cTnI IgG in highly reactive samples was confirmed by inhibition with the antigen and further by screening with a library of peptides derived from the human cTnI amino acid sequence. Our data suggest that these autoantibodies are polyspecific, encompassing epitopes across the entire cTnI sequence, including the cardiac-specific amino terminal region.
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              Type 2 myocardial infarction: the chimaera of cardiology?

              The term type 2 myocardial infarction first appeared as part of the universal definition of myocardial infarction. It was introduced to cover a group of patients who had elevation of cardiac troponin but did not meet the traditional criteria for acute myocardial infarction although they were considered to have an underlying ischaemic aetiology for the myocardial damage observed. Since first inception, the term type 2 myocardial infarction has always been vague. Although attempts have been made to produce a systematic definition of what constitutes a type 2 myocardial infarction, it has been more often characterised by what it is not rather than what it is. Clinical studies that have used type 2 myocardial infarction as a diagnostic criterion have produced disparate incidence figures. The range of associated clinical conditions differs from study to study. Additionally, there are no agreed or evidence-based treatment strategies for type 2 myocardial infarction. The authors believe that the term type 2 myocardial infarction is confusing and not evidence-based. They consider that there is good reason to stop using this term and consider instead the concept of secondary myocardial injury that relates to the underlying pathophysiology of the primary clinical condition.
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                Author and article information

                Contributors
                Role: Handling Editor
                Role: Editor
                Role: Editor
                Role: Editor
                Role: Editor
                Journal
                Eur Heart J Case Rep
                Eur Heart J Case Rep
                ehjcr
                European Heart Journal: Case Reports
                Oxford University Press
                2514-2119
                June 2020
                03 May 2020
                03 May 2020
                : 4
                : 3
                : 1-5
                Affiliations
                [y1 ] Department of Cardiology, St George’s University Hospital , Blackshaw Road, London SW17 0QT, UK
                [y2 ] School of Life Sciences, University of Westminster , Cavendish Street, London W1W 6UW, UK
                Author notes
                Corresponding author. Tel: 0208 672 1255, Email: zakiakhtar@ 123456doctors.org.uk
                Author information
                http://orcid.org/0000-0002-9365-8826
                http://orcid.org/0000-0002-0544-2356
                http://orcid.org/0000-0002-7000-5996
                http://orcid.org/0000-0002-8293-7600
                Article
                ytaa082
                10.1093/ehjcr/ytaa082
                7319834
                32617489
                1a747b98-c4fc-49c6-bea6-294d41e0c153
                © The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 12 November 2019
                : 12 December 2019
                : 17 March 2020
                Page count
                Pages: 5
                Categories
                Case Reports
                Coronary heart disease (incl. Cardiac Intervention)

                case report,macrotroponin,falsely elevated troponin,biochemistry

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