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. 2024 May 14;83(19):1855-1866.
doi: 10.1016/j.jacc.2024.03.365. Epub 2024 Mar 25.

Uniform or Sex-Specific Cardiac Troponin Thresholds to Rule Out Myocardial Infarction at Presentation

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Uniform or Sex-Specific Cardiac Troponin Thresholds to Rule Out Myocardial Infarction at Presentation

Ziwen Li et al. J Am Coll Cardiol. .
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Abstract

Background: Myocardial infarction can be ruled out in patients with a single cardiac troponin measurement. Whether use of a uniform rule-out threshold has resulted in sex differences in care remains unclear.

Objectives: The purpose of this study was to evaluate implementation of a uniform rule-out threshold in females and males with possible myocardial infarction, and to derive and validate sex-specific thresholds.

Methods: The implementation of a uniform rule-out threshold (<5 ng/L) with a high-sensitivity cardiac troponin I assay was evaluated in consecutive patients presenting with possible myocardial infarction. The proportion of low-risk patients discharged from the emergency department and incidence of myocardial infarction or cardiac death at 30 days were determined. Sex-specific thresholds were derived and validated, and proportion of female and male patients were stratified as low-risk compared with uniform threshold.

Results: In 16,792 patients (age 58 ± 17 years; 46% female) care was guided using a uniform threshold. This identified more female than male patients as low risk (73% vs 62%), but a similar proportion of low-risk patients were discharged from the emergency department (81% for both) with fewer than 5 (<0.1%) patients having a subsequent myocardial infarction or cardiac death at 30 days. Compared with a uniform threshold of <5 ng/L, use of sex-specific thresholds would increase the proportion of female (61.8% vs 65.9%) and reduce the proportion of male (54.8% vs 47.8%) patients identified as low risk.

Conclusions: Implementation of a uniform rule-out threshold for myocardial infarction was safe and effective in both sexes. Sex-specific rule-out thresholds should be considered, but their impact on effectiveness and safety may be limited.

Keywords: cardiac troponin; myocardial infarction; sex.

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Conflict of interest statement

Funding Support and Author Disclosures This work was supported by DataLoch, which is funded by the Data Driven Innovation program within the Edinburgh and South East Scotland City Region Deal. Abbott Laboratories provided cardiac troponin assay reagents, calibrators, and controls without charge for the conduct of the High-STEACS trial. The HiSTORIC trial was funded by the British Heart Foundation (grant PG/15/51/31596) with support from British Heart Foundation Research Excellence Awards (awards RE/18/5/34216 and RE/18/6134217). The High-STEACS trial was funded by the British Heart Foundation (SP/12/10/29922). Dr Wereski is supported by Clinical Research Training Fellowship (MR/V007017/1) from the Medical Research Council. Drs Lowry and Doudesis are supported by Medical Research Council (MR/W000598/1; MR/N013166/1). Dr McDermott is supported by the British Heart Foundation Clinical Research Training Fellowship (FS/CRTF/23/24491). Dr Chapman is supported by a British Cardiovascular Interventional Society (BCIS) Advanced Coronary Intervention Fellowship. Dr Lee is supported by an ECAT/SCREDS Clinical Lectureship in Cardiology. Dr Anand is supported by a Clinical Lectureship from the Chief Scientist Office (PCL/18/05). Dr Mills is supported by the British Heart Foundation through a Chair Award (CH/F/21/90010), a Programme Grant (RG/20/10/34966), and a Research Excellence Award (RE/18/5/34216) from the British Heart Foundation. Dr Kimenai is supported by a British Heart Foundation Intermediate Basic Science Research Fellowship (FS/IBSRF/23/25161). The funders played no role in the design, conduct, data collection, analysis, or reporting of the trial. Dr Mills has received honoraria from Abbott Diagnostics, Roche Diagnostics, Siemens Healthineers, LumiraDx, and Psyros Diagnostics; and is employed by the University of Edinburgh, who has received research funding from Abbott Diagnostics, Siemens Healthineers, and Roche Diagnostics unrelated to the current work. Dr Chapman is supported by a BCIS Advanced Coronary Intervention Fellowship, which is in part funded by Abbott Cardiovascular and Edwards Lifesciences. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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