Background: Some posit that any amount of myocardial ischemia can be detected by high-sensitivity cardiac troponin assays. We hypothesized that patients with myocardial ischemia induced by exercise stress would have significantly higher increases in high-sensitivity cardiac troponin T (hs-cTnT) concentrations than patients without ischemia.
Methods: We prospectively recruited for a biorepository 317 adult patients who presented to an academic hospital emergency department for evaluation possible ischemic symptoms and who were scheduled for exercise echocardiography. Blood samples were obtained before stress testing and 2-h post-testing. For this study, plasma hs-cTnT (Roche Diagnostics) concentrations were determined in a core laboratory blinded to clinical status. Absolute and relative changes between baseline and 2-h post-stress measurements were compared between patients with and without ischemia induced by stress testing.
Results: The median age was 51 (44.0, 60.0) years, 45.9% were male, and 37.8% were African American. In total, 26 patients (8.1%) had myocardial ischemia induced by exercise. Median baseline, 2-h post-stress, and absolute δ concentrations were, respectively, 6.0, 8.0, and 0.2 ng/L for patients with evidence of ischemia; 3.8, 4.6, and 0.0 ng/L for those without; and 3.9, 4.9, and 0.0 ng/L overall. Baseline and 2-h hs-cTnT concentrations were higher among patients with abnormal stress tests (all P ≤0.05), but absolute and relative changes in hs-cTnT concentrations were not significantly different between individuals with ischemia and individuals without.
Conclusions: There was no evidence of change in hs-cTnT values in response to exercise stress testing, regardless of the presence of myocardial ischemia.
Authors' Disclosures or Potential Conflicts of Interest: Upon manuscript submission, all authors completed the author disclosure form.
Employment or Leadership: R.H. Christenson, Roche Diagnostics.
Consultant or Advisory Role: A.T. Limkakeng, Biomerieux and ZS Pharma; R.H. Christenson, Siemens Healthcare Diagnostics, Roche Diagnostics, and Philips; L.K. Newby, Roche Diagnostics, and Philips.
Stock Ownership: None declared.
Honoraria: R.H. Christenson, Roche Diagnostics, Siemens Healthcare Diagnostics, and Philips.
Research Funding: A.T. Limkakeng, Roche Diagnostics, Abbott Laboratories, and Siemens Healthcare Diagnostics to the institution(s); Y. Lokhnygina, Roche Diagnostics to the institution; R.H. Christenson, Roche Diagnostics. Support from the Duke Office of Clinical Research was made possible by grant UL1 RR024128-01 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research.
Expert Testimony: None declared.
Patents: None declared.
Role of Sponsor: The funding organizations played no role in the design of study, choice of enrolled patients, review and interpretation of data, or preparation or approval of manuscript.
- Received August 26, 2016.
- Accepted November 1, 2016.
- © 2016 American Association for Clinical Chemistry