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Short- and long-term biological variation of cardiac troponin I in healthy individuals, and patients with end-stage renal failure requiring haemodialysis or cardiomyopathy

  • Nick S. R. Lan , Lan T. Nguyen , Samuel D. Vasikaran , Catherine Wilson , Jacqueline Jonsson , James M. Rankin and Damon A. Bell EMAIL logo
Published/Copyright: June 29, 2020

Abstract

Objectives

High-sensitivity (hs) cardiac troponin (cTn) assays can quantitate small fluctuations in cTn concentration. Determining biological variation allows calculation of reference change values (RCV), to define significant changes. We assessed the short- and long-term biological variation of cardiac troponin I (cTnI) in healthy individuals and patients with renal failure requiring haemodialysis or cardiomyopathy.

Methods

Plasma samples were collected hourly for 4 h and weekly for seven further weeks from 20 healthy individuals, 9 renal failure patients and 20 cardiomyopathy patients. Pre- and post-haemodialysis samples were collected weekly for 7 weeks. Samples were analysed using a hs-cTnI assay (Abbott Alinity ci-series). Within-subject biological variation (CVI), analytical variation (CVA) and between-subject biological variation (CVG) was used to calculate RCVs and index of individuality (II).

Results

For healthy individuals, CVI, CVA, CVG, RCV and II values were 8.8, 14.0, 43.1, 45.8% and 0.38 respectively for short-term, and 41.4, 14.0, 25.8, 121.0% and 1.69 for long-term. For renal failure patients, these were 2.6, 5.8, 50.5, 17.6% and 0.30 respectively for short-term, and 19.1, 5.8, 11.2, 55.2% and 1.78 for long-term. For cardiomyopathy patients, these were 4.2, 10.0, 65.9, 30.0% and 0.16 respectively for short-term, and 17.5, 10.0, 63.1, 55.8% and 0.32 for long-term. Mean cTnI concentration was lower post-haemodialysis (15.2 vs. 17.8 ng/L, p < 0.0001), with a 16.9% mean relative change.

Conclusions

The biological variation of cTnI is similar between end-stage renal failure and cardiomyopathy patients, but proportionately greater in well-selected healthy individuals with very low baseline cTnI concentrations.


Corresponding author: A/Prof. Damon A. Bell, Department of Clinical Biochemistry, PathWest Laboratory Medicine, Fiona Stanley Hospital, 11 Robin Warren Drive, Murdoch, Western Australia, 6150, Australia; Medical School, The University of Western Australia, Perth, Western Australia, Australia; Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Fiona Stanley Hospital, Perth, Western Australia, Australia; Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth Hospital, Perth, Western Australia, Australia; Department of Cardiology, Lipid Disorders Clinic, Royal Perth Hospital, Perth, Western Australia, Australia; and Department of Clinical Biochemistry, Clinipath Pathology, Perth, Western Australia, Australia, E-mail:

Acknowledgments

We acknowledge all participants for providing plasma samples and staff from the phlebotomy service, the dialysis unit and the PathWest Laboratory, who assisted in the study conduct. Furthermore, we acknowledge Abbott Diagnostics, who provided the cardiac troponin kits, but did not have any role in the study design, collection, analysis, and interpretation of data, nor in writing the report or the decision to submit the report for publication.

  1. Research funding: None declared.

  2. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  3. Competing interests: Abbott Diagnostics provided the cardiac troponin kits, but did not have any role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication. Authors state no conflict of interest.

  4. Informed consent: Informed consent was obtained from all individuals included in this study.

  5. Ethical approval: Ethical approval was obtained from the Human Research Ethics Committee (number: EMHS-2016-110).

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Received: 2020-01-15
Accepted: 2020-05-20
Published Online: 2020-06-29
Published in Print: 2020-10-25

© 2020 Walter de Gruyter GmbH, Berlin/Boston

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