Predictors of Stress-Delta High-Sensitivity Troponin T in Emergency Department Patients Undergoing Stress Testing

Cureus. 2022 Sep 26;14(9):e29601. doi: 10.7759/cureus.29601. eCollection 2022 Sep.

Abstract

Background and objective Elevations in high-sensitivity troponin T (hs-TnT) are frequently observed following extreme physical exercise. In light of this, we sought to determine whether specific clinical characteristics are associated with this phenomenon in patients undergoing cardiac exercise tolerance testing (ETT). Methods We conducted a retrospective analysis of a prospectively collected biospecimen repository of 257 patients undergoing a stress echocardiogram for possible acute coronary syndrome (ACS). Ischemic electrocardiogram (ECG) changes during ETT and the presence or absence of ischemia on imaging were determined by a board-licensed cardiologist. N-terminal pro-brain natriuretic peptide (NT-proBNP) and hs-TnT assays were obtained immediately before and two hours following ETT. We developed linear regression models including several clinical characteristics to predict two-hour stress-delta hs-TnT. Variable selection was performed using the least absolute shrinkage and selection operator (LASSO). Results The mean age of the patients was 52 years [standard deviation (SD): 11.4]; 125 (48.6%) of them were men, and 88 (34.2%) were African-American. Twenty-two patients (8.6%) had ischemia evident on echocardiography, and 31 (12.1%) had ischemic ECG changes during exercise. The mean baseline hs-TnT was 5.6 ng/L (SD: 6.4) and the mean two-hour hs-TnT was 7.1 ng/L (SD: 10.2). Age and ischemic ECG changes were associated with two-hour stress-delta hs-TnT values. Conclusions Based on our findings, ischemic changes in stress ECG and age were associated with an increase in hs-TnT levels following exercise during a stress echo.

Keywords: acs risk stratification; biomarkers; high-sensitivity troponin t; myocardial ischemia; stress test.

Grants and funding

We would like to acknowledge Roche Diagnostics International AG for their financial support for this project via an investigator-initiated grant. Financial support was not dependent on the results of the study. Roche Diagnostics International AG provided salary support for investigators to our institution and materials for testing samples. The investigators retained control of the data throughout the entire study and the decision of whether to publish the results. The Duke Office of Clinical Research’s support of this project was made possible by funding from the National Center for Research Resources (NCRR) (grant number 1 UL1 RR024128-01), a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of NCRR or NIH. The study authors retained the rights to data and the decision of whether to publish them