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

Biochemistry Case report Falsely elevated troponin Macrotroponin

Journal

European heart journal. Case reports
ISSN: 2514-2119
Titre abrégé: Eur Heart J Case Rep
Pays: England
ID NLM: 101730741

Informations de publication

Date de publication:
Jun 2020
Historique:
received: 12 11 2019
revised: 12 12 2019
accepted: 17 03 2020
entrez: 4 7 2020
pubmed: 4 7 2020
medline: 4 7 2020
Statut: epublish

Résumé

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). 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. 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.

Sections du résumé

BACKGROUND 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 METHODS
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 CONCLUSIONS
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.

Identifiants

pubmed: 32617489
doi: 10.1093/ehjcr/ytaa082
pii: ytaa082
pmc: PMC7319834
doi:

Types de publication

Case Reports

Langues

eng

Pagination

1-5

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.

Références

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Auteurs

Zaki Akhtar (Z)

Department of Cardiology, St George's University Hospital, Blackshaw Road, London SW17 0QT, UK.

James Dargan (J)

Department of Cardiology, St George's University Hospital, Blackshaw Road, London SW17 0QT, UK.

David Gaze (D)

Department of Cardiology, St George's University Hospital, Blackshaw Road, London SW17 0QT, UK.
School of Life Sciences, University of Westminster, Cavendish Street, London W1W 6UW, UK.

Sami Firoozi (S)

Department of Cardiology, St George's University Hospital, Blackshaw Road, London SW17 0QT, UK.

Paul Collinson (P)

Department of Cardiology, St George's University Hospital, Blackshaw Road, London SW17 0QT, UK.

Nesan Shanmugam (N)

Department of Cardiology, St George's University Hospital, Blackshaw Road, London SW17 0QT, UK.

Classifications MeSH