101 Differentiating Type 1 from Type 2 Acute Myocardial Infarction in the Emergency Department Using the N-terminal Pro B-type Natriuretic Peptide/High-sensitivity Cardiac Troponin T Ratio

Document Type

Conference Proceeding

Publication Date

10-1-2022

Publication Title

Ann Emerg Med

Abstract

Study Objectives: Acute myocardial infarction (AMI) is currently further diagnosed as being a type 1 (T1), caused by coronary artery atherosclerosis with thrombosis or a type 2 (T2), resulting from cardiac oxygen supply and demand imbalance. It is hypothesized that patients with T2 might develop earlier and increased cardiac wall stressing before the development of AMI as compared to those with T1, resulting in higher N- terminal pro B-type natriuretic peptide (NT-proBNP)/high sensitivity cardiac troponin T (hs-cTnT) ratios. Our objective was to determine the differences in NT-proBNP/hs-cTnT ratios measured in emergency department (ED) patients enrolled in a multi-center hs-cTnT trial and having an adjudicated T1 or T2 AMI. Study Design Methods: This study was a pre-planned subgroup analysis of the STOP-CP (High Sensitivity Cardiac Troponin T to Optimize Chest Pain Risk Stratification) trial, which prospectively enrolled patients (≥ 21 years) presenting to the ED (8 medical centers in the United States) with symptoms suspicious for AMI (1/25/2017-9/6/2018). Patients had study blood samples drawn at baseline (< 1 hour from the troponin draw ordered by the treating physician), 1, 2 and 3 hours later with NT-proBNP and hs-cTnT (Roche, Basel, Switzerland) values determined at a central lab. Subjects were independently adjudicated as having a T1 or T2 AMI using all available clinical information during the 30 days after the ED visit. Receiver Operator Curves (ROC) were plotted for the 4 blood samples with optimal cut points (OCP) determined for the NT- proBNP/hs-cTnT ratios for differentiating a T1 from a T2 AMI along with the sensitivities and specificities (confidence intervals) of these values in predicting a T2 AMI diagnosis. Results/Findings: Of the 1462 enrolled patients 172 (11.8 %) had an AMI with 67 (39.0 %) being a T1 and 105 (61.0%) a T2. Clinical characteristics (age, sex, African American race), medical history (hypertension, diabetes, coronary artery disease, AMI) and ECG findings (normal or with ischemic changes) and presenting symptoms (chest pain, arm/shoulder discomfort, lightheaded) were not different (all p >.05) in patients with T1 or T2 AMIs. The median NT-proBNP/hs-cTnT ratios were higher in T2 as compared to T1 AMI at baseline, 1, 2 and 3 hours: 5.3 v 27.5, 4.4 v 28.0, 3.5 v 29.4 and 5.1 v 30.0 (all p <.0001) respectively. The OCP for NT-proBNP/hs-cTnT ratios to differentiate T1 from a T2 AMI at each timepoint were 6.9, 3.3, 14.0 and 13.1. The sensitivities of these values for the diagnosis of a T2 AMI were 75.2, 86.1, 68.5 and 69.0 and the specificities 59.7, 47.0, 70.5 and 65.5 respectively. Conclusion: The NT-proBNP/hs-cTnT ratio values at all ED blood draws for patients having symptoms suspicious for AMI were higher in those with a T2 as compared to T1 AMI. However, the cut points determined at each time point for AMI type differentiation were associated with sensitivities and specificities that would be inadequate for routine clinical diagnostic use. Further analyses of our results to determine alternative NT-proBNP/hs-cTnT ratio cut points with improved specificity for T2 AMI are ongoing. Yes, authors have interests to disclose Disclosure: The STOP-CP multicenter study was funded by Roche Diagnostics Grant Support The STOP-CP multicenter study was funded by Roche Diagnostics

Volume

80

Issue

4

First Page

S50

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