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High-Sensitivity Cardiac Troponin and the Universal Definition of Myocardial Infarction.

Chapman, AR; Adamson, PD; Shah, ASV; Anand, A; Strachan, FE; Ferry, AV; Lee, KK; Berry, C; Findlay, I; Cruickshank, A; et al. Chapman, AR; Adamson, PD; Shah, ASV; Anand, A; Strachan, FE; Ferry, AV; Lee, KK; Berry, C; Findlay, I; Cruickshank, A; Reid, A; Gray, A; Collinson, PO; Apple, F; McAllister, DA; Maguire, D; Fox, KAA; Vallejos, CA; Keerie, C; Weir, CJ; Newby, DE; Mills, NL; High-STEACS Investigators (2020) High-Sensitivity Cardiac Troponin and the Universal Definition of Myocardial Infarction. Circulation, 141 (3). pp. 161-171. ISSN 1524-4539 https://doi.org/10.1161/CIRCULATIONAHA.119.042960
SGUL Authors: Collinson, Paul

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Abstract

Background: The introduction of more sensitive cardiac troponin assays has led to increased recognition of myocardial injury in acute illnesses other than acute coronary syndrome. The Universal Definition of Myocardial Infarction recommends high-sensitivity cardiac troponin (hs-cTn) testing and classification of patients with myocardial injury based on aetiology, but the clinical implications of implementing this guideline are not well understood. Methods: In a stepped-wedge cluster randomized controlled trial, we implemented a hs-cTn assay and the recommendations of the Universal Definition in 48,282 consecutive patients with suspected acute coronary syndrome. In a pre-specified secondary analysis, we compared the primary outcome of myocardial infarction or cardiovascular death and secondary outcome of non-cardiovascular death at one year across diagnostic categories. Results: Implementation increased the diagnosis of type 1 myocardial infarction by 11% (510/4,471), type 2 myocardial infarction by 22% (205/916), and acute and chronic myocardial injury by 36% (443/1,233) and 43% (389/898), respectively. Compared to those without myocardial injury, the rate of the primary outcome was highest in those with type 1 myocardial infarction (cause-specific hazard ratio [csHR] 5.64, 95% confidence interval [CI] 5.12 to 6.22), but was similar across diagnostic categories, whereas non-cardiovascular deaths were highest in those with acute myocardial injury (csHR 2.65, 95%CI 2.33 to 3.01). Despite modest increases in anti-platelet therapy and coronary revascularization after implementation in patients with type 1 myocardial infarction, the primary outcome was unchanged (csHR 1.00, 95%CI 0.82 to 1.21). Increased recognition of type 2 myocardial infarction and myocardial injury did not lead to changes in investigation, treatment or outcomes. Conclusions: Implementation of high-sensitivity cardiac troponin and the recommendations of the Universal Definition of Myocardial Infarction identified patients at high-risk of cardiovascular and non-cardiovascular events, but was not associated with consistent increases in treatment or improved outcomes. Trials of secondary prevention are urgently required to determine whether this risk is modifiable in patients without type 1 myocardial infarction. Clinical Trial Registration: URL: https://clinicaltrials.gov Unique Identifier: NCT0185212.

Item Type: Article
Additional Information: © 2019 The Authors. Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.
Keywords: myocardial injury, universal definition, High-STEACS Investigators, myocardial injury, universal definition, Cardiovascular System & Hematology, 1103 Clinical Sciences, 1102 Cardiorespiratory Medicine and Haematology, 1117 Public Health and Health Services
SGUL Research Institute / Research Centre: Academic Structure > Molecular and Clinical Sciences Research Institute (MCS)
Journal or Publication Title: Circulation
ISSN: 1524-4539
Language: eng
Dates:
DateEvent
21 January 2020Published
7 October 2019Published Online
18 September 2019Accepted
Publisher License: Creative Commons: Attribution 4.0
Projects:
Project IDFunderFunder ID
SP/12/10/29922British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
BCDSA/100003British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
RE/18/5/34216British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
RE/18/6/3421British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
FS/16/75/32533British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
FS/16/14/32023British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
CH/09/002British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
SGL021\1075Academy of Medical Scienceshttp://dx.doi.org/10.13039/501100000691
PubMed ID: 31587565
Go to PubMed abstract
URI: http://openaccess.sgul.ac.uk/id/eprint/111345
Publisher's version: https://doi.org/10.1161/CIRCULATIONAHA.119.042960

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