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Review article: Biomedical intelligence

Vol. 141 No. 1920 (2011)

High-sensitive cardiac troponin: friend or foe?

  • Raphael Twerenbold
  • Tobias Reichlina
  • Miriam Reiter
  • Christian Mueller
DOI
https://doi.org/10.4414/smw.2011.13202
Cite this as:
Swiss Med Wkly. 2011;141:w13202
Published
09.05.2011

Summary

Cardiac troponin I and T (cTn) are structural proteins unique to the heart. Detection of cTn in peripheral blood indicates cardiomyocyte necrosis. As acute myocardial infarction (AMI) is the most important cause of cardiomyocyte necrosis, cTns have become an integral part in the diagnosis of AMI. In this indication, cTns are superior to all other biomarkers indicating cardiomyocyte necrosis such as CK-MB and myoglobin, and are therefore considered the preferred marker in the diagnosis of AMI. It is important to highlight that cTn indicates and quantifies cardiomyocyte necrosis irrespective of its cause? The major limitation of contemporary cTn assays is a sensitivity deficit in the first few hours of AMI due to a delayed increase of circulating levels. Recent advances in assay technology have lead to a refinement in cardiac troponin (cTn) assays that have had a profound impact on clinical practice. High-sensitive cTn assays have two differentiating features from contemporary cTn assays: 1) detection of cTn in healthy persons and 2) a precise definition of what is “normal” (= the 99th percentile). Recent multicentre studies have shown that high-sensitive cTn assays improve the early diagnosis of AMI. To achieve the best clinical use, cTn has to be interpreted as a quantitative variable. Rising and/or falling levels differentiate acute from chronic cardiomyocyte necrosis. The term “troponin-positive” should therefore be avoided. “Detectable” levels will become the norm and have to be clearly differentiated from “elevated” levels. The differential diagnosis of a small amount of cardiomyocyte necrosis and therefore mild elevation of cTn is broad and includes acute and chronic cardiac disorders. The differential diagnosis of a large amount of cardiomyocyte necrosis and therefore substantial elevation of cTn is much smaller and largely restricted to AMI, myocarditis and tako-tsubo cardiomyopathy.

Recent advances in assay technology have lead to a refinement in cardiac troponin I and T (cTn) assays and therefore the clinical ability to detect and quantify cardiomyocyte necrosis [1–3].

Cardiac troponins (cTn) are structural proteins unique to the heart. Detection of cTn in peripheral blood indicates cardiomyocyte necrosis [1]. As acute myocardial infarction (AMI) is the most important cause of cardiomyocyte necrosis, the use of high-sensitive cTn assays is expected to lead to an important improvement in the diagnosis of AMI [4]. This review will highlight the most relevant aspects from a clinical perspective and provide suggestions on how to clinically apply high-sensitive cTn assays most effectively.

As with any other innovation, it is key to start with the question: what is the unmet clinical need?

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