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Editorial
How do comorbidities influence troponin concentrations?
  1. Johannes Tobias Neumann1,
  2. Raphael Twerenbold2
  1. 1 Department of Cardiology, University Heart and Vascular Center Hamburg, Hamburg, Germany
  2. 2 Department of Cardiology, University Hospital Basel, Basel, Switzerland
  1. Correspondence to Dr Johannes Tobias Neumann, Cardiology, University Heart Center Hamburg, Hamburg 20246, Germany; j.neumann{at}uke.de

https://doi.org/10.1136/heartjnl-2019-316283

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    Cardiac troponin is the most established biomarker for acute cardiac care and recommended for the diagnosis of acute myocardial infarction (MI).1 2 Cardiac troponin concentrations above the 99th percentile are defined as pathological and indicate myocardial injury, not necessarily caused by underlying acute or chronic ischaemia.3 The 99th percentile itself is determined in a healthy population, whereas elevated troponin concentrations above this cut-off are regarded as abnormal. A multitude of comorbidities and conditions other than myocardial ischaemia can influence troponin concentrations in the acute or chronic setting. This includes, among many others, age, sex, renal dysfunction and prevalent cardiovascular diseases.1 4 Such confounders are frequent bystanders in the setting of an acute MI and can complicate the diagnostic evaluation. Peak cardiac troponin concentrations correlate with infarct size in imaging modalities and thereby contain strong prognostic information. How peak cardiac troponin concentrations in patients with MI are influenced by comorbidities has been poorly explored. In their present Heart manuscript, Sundaram and colleagues5 investigated the association of peak cardiac troponin concentrations with various comorbidities in a very large registry data set. Between 2003 and 2013, data from more than 330 000 patients with MI were collected within the UK-wide Myocardial Ischemia National …

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    Footnotes

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    • Contributors Both authors contributed equally to this editorial.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors. Outside the submitted work J.N. has received honoraria from Abbott Diagnostics and Siemens. JN was supported by a grant from the German Research Foundation, the German Heart Foundation/German Foundation of Heart Research, the Else Kröner Fresenius Stiftung and the DZHK; and is recipient of a research fellowship by the Deutsche Forschungsgemeinschaft (NE 2165/1-1). RT reports honoraria from Abbott, Roche, Siemens, Brahms, Singulex and Amgen. He is supported by grants from Swiss National Science Foundation (Grant No P300PB_167803), the Swiss Heart Foundation, the Swiss Society of Cardiology, the University of Basel and the Cardiovascular Research Foundation Basel.

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Patient consent for publication Not required.

    • Provenance and peer review Commissioned; internally peer reviewed.

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