Discrimination of Patients With Type 2 Myocardial Infarction

Johannes Tobias Neumann; Nils Arne Sörensen; Nicole Rübsamen; Francisco Ojeda; Thomas Renné; Vazhma Qaderi; Elena Teltrop; Solveig Kramer; Laura Quantius; Tanja Zeller; Mahir Karakas; Stefan Blankenberg; Dirk Westermann

Disclosures

Eur Heart J. 2017;38(47):3514-3520. 

In This Article

Methods

Study Population

Data from the Biomarkers in Acute Cardiac Care (BACC) study were used for the analyses. An earlier version of this study population has been published before.[13,14] In the present analyses, we had data of 1641 patients who presented with suspected MI to the ED of the University Heart Center Hamburg. The enrolment took place between 19 July 2013 and 10 April 2016. Patients were not included when the age was below 18 years or the patient was not able or willing to provide written informed consent. Patients with ST-elevation MI (n = 75) and with non-ST-elevation MI type 4 (n = 2) were excluded from the analyses. Sixteen patients were excluded due to missing hs-TnI values. The BACC study was approved by the local Ethics Committee and registered at www.clinicaltrials.gov (NCT02355457). The study design complied with the Declaration of Helsinki.

Study Design

All patients with suspected MI were treated according to the current ESC Guidelines, including electrocardiogram (ECG), monitoring, serial measurement of high-sensitivity troponin T (hs-TnT, Elecsys®, Roche diagnostics) at admission and after 3 h as well as further imaging.[2,15] Depending on the individual results, each patient was discharged or admitted for further treatment. Independently from clinical routine, hs-TnI was measured using the Architect immunoassay (Abbott Diagnostics, ARCHITECT i1000SR) at admission, after 1 and 3 h. This assay had a limit of detection at a concentration of 1.9 ng/L and a 10% coefficient of variation at a concentration of 5.2 ng/L.[16] In the general population, the 99th percentile has been reported at 27 ng/L.[17]

An ECG was performed immediately after presentation to the ED and directly interpreted by the ED physician. The ECG interpretation and the clinical assessment are described in the Supplementary material online.

Adjudication of Myocardial Infarction Diagnosis

The final diagnosis of each patient was determined by two physicians (J.T.N. and N.A.S.) separately. In cases of disagreement, a third cardiologist (D.W.) reviewed the case. The final diagnosis was based on all available clinical and imaging results, ECG and standard laboratory testing, including hs-TnT and creatinine. Adjudication was performed according to the ESC guidelines at least 30 days after the index admission.[2,15] The diagnosis of MI was adjudicated, when evidence of myocardial necrosis and a clinical setting of myocardial ischaemia were present. Myocardial necrosis was defined by a hs-TnT concentration above the 99th percentile in combination with a significant change within 3 h (according to the ESC working group[18]). The differentiation between T1MI and T2MI based on the 2012 universal definition of MI:[3] Patients with acute plaque disruption (observed via angiography or clinically highly suspected) were classified as T1MI. Patients with other causes of symptoms (e.g. arrhythmias, severe hypertension, or acute decompensated heart failure) were classified as T2MI.

Outcome

All patients were followed after the index presentation. Overall 1638 of 1641 patients (99.8%) completed the follow-up. The follow-up was performed up to 2 years after admission and completed on the 31 of August 2016. The median follow-up time for death was 450 days. The assessment and definition of follow-up events are provided in the Supplementary material online.

Statistical Analysis

Continuous variables were described as quartiles; categorical variables as absolute numbers and percentages. The Wilcoxon rank-sum (for continuous variables) or the χ 2 (for categorical variables) test were employed for between-group comparisons.

Outcome. Survival curves for the non-MI, T1MI, and T2MI patients were produced using the Kaplan–Meier method. Survival curve differences were tested with the log-rank test. Hazard ratios for each adverse event (adjusted for age, sex, and CAD) were estimated using Cox regression.

Score development. The detailed score development is described in the Supplementary material online.

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