Abstract

The Fourth Universal Definition of Myocardial Infarction (MI) differentiates MI from myocardial injury. We characterised the temporal course of cardiac and non-cardiac outcomes associated with MI, acute and chronic myocardial injury. We included all patients presenting to public emergency departments in South Australia between June 2011-Sept 2019. Episodes of care (EOCs) were classified into 5 groups based on high-sensitivity troponin-T (hs-cTnT) and diagnostic codes: 1) Acute MI [rise/fall in hs-cTnT and primary diagnosis of acute coronary syndrome], 2) Acute myocardial injury with coronary artery disease (CAD) [rise/fall in hs-cTnT and diagnosis of CAD], 3) Acute myocardial injury without CAD [rise/fall in hs-cTnT without diagnosis of CAD], 4) Chronic myocardial injury [elevated hs-cTnT without rise/fall], and 5) No myocardial injury. Multivariable flexible parametric models were used to characterize the temporal hazard of death, MI, heart failure (HF), and ventricular arrhythmia. 372,310 EOCs (218,878 individuals) were included: acute MI (19,052 [5.12%]), acute myocardial injury with CAD (6,928 [1.86%]), acute myocardial injury without CAD (32,231 [8.66%]), chronic myocardial injury (55,056 [14.79%]), and no myocardial injury (259,043 [69.58%]). We observed an early hazard of MI and HF after acute MI and acute myocardial injury with CAD. In contrast, subsequent MI risk was lower and more constant in patients with acute injury without CAD or chronic injury. All patterns of myocardial injury were associated with significantly higher risk of all-cause mortality and ventricular arrhythmia. Different patterns of myocardial injury were associated with divergent profiles of subsequent cardiac and non-cardiac risk. The therapeutic approach and modifiability of such excess risks require further research.

Highlights

  • Cardiac troponin is a highly sensitive biomarker for myocardial injury that plays an essential role in the diagnosis and risk-stratification of acute myocardial infarction (MI) [1, 2]

  • Episodes of care (EOCs) were classified into 5 groups based on high-sensitivity troponin-T and diagnostic codes: 1) Acute Myocardial Infarction (MI) [rise/fall in high-sensitivity cardiac troponin-T (hs-cTnT) and primary diagnosis of acute coronary syndrome], 2) Acute myocardial injury with coronary artery disease (CAD) [rise/fall in hs-cTnT and diagnosis of Coronary artery disease (CAD)], 3) Acute myocardial injury without CAD [rise/fall in hs-cTnT without diagnosis of CAD], 4) Chronic myocardial injury [elevated hs-cTnT without rise/fall], and 5) No myocardial injury

  • We identified consecutive patients presenting to public hospital emergency departments (EDs) in South Australia between July 2011 to September 2019 who had at least one high-sensitivity cardiac troponin-T measured during their Emergency department (ED) stay

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Summary

Introduction

Cardiac troponin is a highly sensitive biomarker for myocardial injury that plays an essential role in the diagnosis and risk-stratification of acute myocardial infarction (MI) [1, 2]. The improved analytical sensitivity of the new high-sensitivity cardiac troponin (hs-cTn) assays facilitates early diagnosis of MI These assays come with new challenges including increased identification of troponin elevations above the conventional reference threshold (>99th percentile upper reference limit) in patients without objective evidence of myocardial ischemia (e.g. on echocardiography or ECG) [3,4,5]. The Fourth Universal Definition of MI is the first guideline to formally define this syndrome as myocardial injury and distinguish it from MI. It outlines three main patterns of troponin elevation—acute MI, acute myocardial injury and chronic myocardial injury [2]. We characterised the temporal course of cardiac and non-cardiac outcomes associated with MI, acute and chronic myocardial injury

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