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

Author:

Chapman Andrew R.1,Adamson Philip D.12,Shah Anoop S.V.1,Anand Atul1,Strachan Fiona E.1,Ferry Amy V.1,Ken Lee Kuan1,Berry Colin3,Findlay Iain4,Cruikshank Anne5,Reid Alan5,Gray Alasdair6,Collinson Paul O.7,Apple Fred8,McAllister David A.9,Maguire Donogh10,Fox Keith A.A.1,Vallejos Catalina A.1112,Keerie Catriona1314,Weir Christopher J.1314,Newby David E.1,Mills Nicholas L.114,Tuck Christopher,Bularga Anda,Wereski Ryan,Sandeman Dennis,Stables Catherine L.,Tsanasis Athanasios,Marshall Lucy,Stewart Stacey D.,Fujisawa Takeshi,Hautvast Mischa,McPherson Jean,McKinlay Lynn,Walker Simon,Ford Ian,Walker Simon,Amoils Shannon,Stevens Jennifer,Norrie John,Andrews Jack,Adamson Phil,Moss Alastair,Anwar Mohamed,Hung John,Walker Simon,Malo Jonathan,Fischbacher Colin,Croal Bernard,Leslie Stephen J.,Parker Richard,Walker Allan,Harkess Ronnie,Tuck Chris,Wackett Tony,Armstrong Roma,Flood Marion,Stirling Laura,MacDonald Claire,Sadat Imran,Finlay Frank,Charles Heather,Linksted Pamela,Young Stephen,Alexander Bill,Duncan Chris

Affiliation:

1. BHF Centre for Cardiovascular Science (A.R.C., P.D.A., A.S.V.S., A.A., F.E.S., A.V.F., K.K.L., K.A.A.F., D.E.N., N.L.M.), University of Edinburgh, United Kingdom.

2. Christchurch Heart Institute, University of Otago, New Zealand (P.D.A.).

3. Institute of Cardiovascular and Medical Sciences (C.B.), University of Glasgow, United Kingdom.

4. Department of Cardiology, Royal Alexandra Hospital, Paisley, United Kingdom (I.F.).

5. Department of Biochemistry, Queen Elizabeth University Hospital, Glasgow, United Kingdom (A.C., A.R.).

6. Emergency Medicine Research Group Edinburgh, Royal Infirmary of Edinburgh, United Kingdom (A.G.).

7. Departments of Clinical Blood Sciences and Cardiology, St George’s, University Hospitals NHS Trust and St George’s University of London, United Kingdom (P.O.C.).

8. Department of Laboratory Medicine and Pathology, Hennepin Healthcare/Hennepin County Medical Center & University of Minnesota, Minneapolis (F.A.).

9. Institute of Health and Wellbeing (D.A.McA.), University of Glasgow, United Kingdom.

10. Emergency Medicine Department, Glasgow Royal Infirmary, United Kingdom (D.M).

11. MRC Human Genetics Unit (C.A.V.), University of Edinburgh, United Kingdom.

12. The Alan Turing Institute, London, United Kingdom (C.A.V.).

13. Edinburgh Clinical Trials Unit (C.K., C.J.W.), University of Edinburgh, United Kingdom.

14. Usher Institute of Population Health Sciences and Informatics (C.K., C.J.W., N.L.M.), University of Edinburgh, United Kingdom.

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 testing and classification of patients with myocardial injury based on pathogenesis, but the clinical implications of implementing this guideline are not well understood. Methods: In a stepped-wedge cluster randomized, controlled trial, we implemented a high-sensitivity cardiac troponin assay and the recommendations of the Universal Definition in 48 282 consecutive patients with suspected acute coronary syndrome. In a prespecified secondary analysis, we compared the primary outcome of myocardial infarction or cardiovascular death and secondary outcome of noncardiovascular death at 1 year across diagnostic categories. Results: Implementation increased the diagnosis of type 1 myocardial infarction by 11% (510/4471), type 2 myocardial infarction by 22% (205/916), and acute and chronic myocardial injury by 36% (443/1233) and 43% (389/898), respectively. Compared with those without myocardial injury, the rate of the primary outcome was highest in those with type 1 myocardial infarction (cause-specific hazard ratio [HR] 5.64 [95% CI, 5.12–6.22]), but was similar across diagnostic categories, whereas noncardiovascular deaths were highest in those with acute myocardial injury (cause specific HR 2.65 [95% CI, 2.33–3.01]). Despite modest increases in antiplatelet therapy and coronary revascularization after implementation in patients with type 1 myocardial infarction, the primary outcome was unchanged (cause specific HR 1.00 [95% CI, 0.82–1.21]). 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 assays and the recommendations of the Universal Definition of Myocardial Infarction identified patients at high-risk of cardiovascular and noncardiovascular 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: https://www.clinicaltrials.gov . Unique identifier: NCT01852123.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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