Letters
High-sensitivity troponin in marathon runners TO THE EDITOR: In 2009, we reported on increases in the level of cardiac troponin (using the TnI-Ultra troponin I assay [Siemens Healthcare Diagnostics]) among runners in the Perth marathon.1 Of the 88 runners enrolled, raised troponin levels were seen in 28 participants (32%). The independent predictors were weight loss and an increase in creatinine levels. Recently, high-sensitivity fifthgeneration troponin assays have become available for evaluation pending United States Food and Drug Administration approval. After obtaining approval from the Royal Perth Hospital ethics committee, stored blood samples were reanalysed to compare with our original results. The assay used was the Architect STAT High Sensitive Troponin-I (Abbott Diagnostics). The sex-specific cut-points supplied by the manufacturer for the assay were 16 ng/L for females and 34 ng/L for males. In repeating our original analysis, we found that 70 (80%) had an elevated troponin level, similar to the findings of another study using the hs-cTnT assay, in which 86% of runners had a raised troponin level.2 Repetition of the statistical model used in our original study revealed no variable that was predictive of an elevated troponin level. A Bland– Altman plot showed that the new assay is identical to the old method,
MJA 199 (3) · 5 August 2013
169
Letters but is more sensitive. This suggested that the cut-points have changed. By recalibrating the old cut-points, we found that cut-points of 80 ng/L for females and 70 ng/L for males resulted in a model that produced the same predictor variables that we reported originally. The area under the receiver operating characteristic curve for this model was 0.79 (95% CI, 0.63–0.84). High-sensitivity troponin assays can detect myocardial damage with increasing sensitivity, but are less specific. Using high-sensitivity troponin assays with a single cut-off to assess possible acute coronary syndrome (ACS) will result in more patients being incorrectly classified as having an ACS, with the associated unnecessary use of resources.3 Recognition of this led to the definition of acute myocardial infarction requiring the detection of a rise and/or fall above the cut-off together with evidence of ischaemia (either as clinical symptoms, electrocardiogram changes or imaging evidence that there is loss of viable myocardium).4 Our results support the call by Scott and colleagues for clarification about the real-world effects of this assay and the need to interpret high-sensitivity troponin assay results with caution.3 Daniel M Fatovich Professor of Emergency Medicine, and Emergency Physician1 Michael R Phillips Biostatistician 2 Kelley M Hubble Emergency Physician 3 Samuel D Vasikaran Head of Clinical Biochemistry, PathWest3 1 Emergency Medicine, Royal Perth Hospital, University of Western Australia, Perth, WA. 2 Western Australian Institute for Medical Research, University of Western Australia, Perth, WA. 3 Royal Perth Hospital, Perth, WA.
[email protected] Competing interests: No relevant disclosures.
doi: 10.5694/mja13.10417 1 Hubble KM, Fatovich DM, Grasko JM, Vasikaran SD.
Cardiac troponin increases among marathon runners in the Perth Marathon: the Troponin in Marathons (TRIM) study. Med J Aust 2009; 190: 91-93. 2 Mingels A, Jacobs L, Michielsen E, et al. Reference population and marathon runner sera assessed by highly sensitive cardiac troponin T and commercial cardiac troponin T and I assays. Clin Chem 2009; 55: 101-108. 3 Scott IA, Cullen L, Tate JR, Parsonage W. Highly sensitive troponin assays — a two-edged sword? Med J Aust 2012; 197: 320-323. 4 Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Eur Heart J 2012; 33: 2551-2567. ❏
170
MJA 199 (3) · 5 August 2013
High-sensitivity troponin in marathon runners TO THE EDITOR: In 2009, we reported on increases in the level of cardiac troponin (using the TnI-Ultra troponin I assay [Siemens Healthcare Diagnostics]) among runners in the Perth marathon.1 Of the 88 runners enrolled, raised troponin levels were seen in 28 participants (32%). The independent predictors were weight loss and an increase in creatinine levels. Recently, high-sensitivity fifthgeneration troponin assays have become available for evaluation pending United States Food and Drug Administration approval. After obtaining approval from the Royal Perth Hospital ethics committee, stored blood samples were reanalysed to compare with our original results. The assay used was the Architect STAT High Sensitive Troponin-I (Abbott Diagnostics). The sex-specific cut-points supplied by the manufacturer for the assay were 16 ng/L for females and 34 ng/L for males. In repeating our original analysis, we found that 70 (80%) had an elevated troponin level, similar to the findings of another study using the hs-cTnT assay, in which 86% of runners had a raised troponin level.2 Repetition of the statistical model used in our original study revealed no variable that was predictive of an elevated troponin level. A Bland– Altman plot showed that the new assay is identical to the old method,
MJA 199 (3) · 5 August 2013
169
Letters but is more sensitive. This suggested that the cut-points have changed. By recalibrating the old cut-points, we found that cut-points of 80 ng/L for females and 70 ng/L for males resulted in a model that produced the same predictor variables that we reported originally. The area under the receiver operating characteristic curve for this model was 0.79 (95% CI, 0.63–0.84). High-sensitivity troponin assays can detect myocardial damage with increasing sensitivity, but are less specific. Using high-sensitivity troponin assays with a single cut-off to assess possible acute coronary syndrome (ACS) will result in more patients being incorrectly classified as having an ACS, with the associated unnecessary use of resources.3 Recognition of this led to the definition of acute myocardial infarction requiring the detection of a rise and/or fall above the cut-off together with evidence of ischaemia (either as clinical symptoms, electrocardiogram changes or imaging evidence that there is loss of viable myocardium).4 Our results support the call by Scott and colleagues for clarification about the real-world effects of this assay and the need to interpret high-sensitivity troponin assay results with caution.3 Daniel M Fatovich Professor of Emergency Medicine, and Emergency Physician1 Michael R Phillips Biostatistician 2 Kelley M Hubble Emergency Physician 3 Samuel D Vasikaran Head of Clinical Biochemistry, PathWest3 1 Emergency Medicine, Royal Perth Hospital, University of Western Australia, Perth, WA. 2 Western Australian Institute for Medical Research, University of Western Australia, Perth, WA. 3 Royal Perth Hospital, Perth, WA.
[email protected] Competing interests: No relevant disclosures.
doi: 10.5694/mja13.10417 1 Hubble KM, Fatovich DM, Grasko JM, Vasikaran SD.
Cardiac troponin increases among marathon runners in the Perth Marathon: the Troponin in Marathons (TRIM) study. Med J Aust 2009; 190: 91-93. 2 Mingels A, Jacobs L, Michielsen E, et al. Reference population and marathon runner sera assessed by highly sensitive cardiac troponin T and commercial cardiac troponin T and I assays. Clin Chem 2009; 55: 101-108. 3 Scott IA, Cullen L, Tate JR, Parsonage W. Highly sensitive troponin assays — a two-edged sword? Med J Aust 2012; 197: 320-323. 4 Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Eur Heart J 2012; 33: 2551-2567. ❏
170
MJA 199 (3) · 5 August 2013
