Author + information
- Received May 26, 2016
- Revision received November 10, 2016
- Accepted November 17, 2016
- Published online April 2, 2018.
- Muhammad Hammadah, MDa,
- Ibhar Al Mheid, MDa,
- Kobina Wilmot, MDa,
- Ronnie Ramadan, MDa,
- Ayman Alkhoder, MDa,
- Malik Obideen, MDa,
- Naser Abdelhadi, MDa,
- Shuyang Fang, MDa,b,
- Ijeoma Ibeanu, MDb,
- Pratik Pimple, MBBS, MPHb,
- Heval Mohamed Kelli, MDa,
- Amit J. Shah, MDa,b,
- Brad Pearce, PhDb,
- Yan Sun, PhDb,
- Ernest V. Garcia, PhDc,
- Michael Kutner, PhDd,
- Qi Long, PhDb,
- Laura Ward, MPHd,
- J. Douglas Bremner, MDe,
- Fabio Esteves, MDc,
- Paolo Raggi, MDb,c,f,
- David Sheps, MD, MSPHg,
- Viola Vaccarino, MD, PhDa,b and
- Arshed A. Quyyumi, MDa,∗ ()
- aDepartment of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia
- bDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia
- cDepartment of Radiology, Emory University School of Medicine, Atlanta, Georgia
- dDepartment of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, Georgia
- eDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia
- fMazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
- gDepartment of Epidemiology, University of Florida, Gainesville, Florida
- ↵∗Address for correspondence:
Dr. Arshed A. Quyyumi, Emory University, Department of Cardiology, Emory University School of Medicine, 1462 Clifton Road NE, Suite 507, Atlanta, Georgia 30322.
Objectives This study sought to investigate whether patients with mental stress–induced myocardial ischemia will have high resting and post–mental stress high-sensitivity cardiac troponin I (hs-cTnI).
Background Hs-cTnI is a marker of myocardial necrosis, and its elevated levels are associated with adverse outcomes. Hs-cTnI levels may increase with exercise in patients with coronary artery disease. Mental stress–induced myocardial ischemia is also linked to adverse outcomes.
Methods In this study, 587 patients with stable coronary artery disease underwent technetium Tc 99m sestamibi–single-photon emission tomography myocardial perfusion imaging during mental stress testing using a public speaking task and during conventional (pharmacological/exercise) stress testing as a control condition. Ischemia was defined as new/worsening impairment in myocardial perfusion using a 17-segment model.
Results The median hs-cTnI resting level was 4.3 (interquartile range [IQR]: 2.9 to 7.3) pg/ml. Overall, 16% and 34.8% of patients developed myocardial ischemia during mental and conventional stress, respectively. Compared with those without ischemia, median resting hs-cTnI levels were higher in patients who developed ischemia either during mental stress (5.9 [IQR: 3.9 to 8.3] pg/ml vs. 4.1 [IQR: 2.7 to 7.0] pg/ml; p < 0.001) or during conventional stress (5.4 [IQR: 3.9 to 9.3] pg/ml vs. 3.9 [IQR: 2.5 to 6.5] pg/ml; p < 0.001). Patients with high hs-cTnI (cutoff of 4.6 pg/ml for men and 3.9 pg/ml for women) had greater odds of developing mental (odds ratio [OR]: 2.4; 95% confidence interval [CI]: 1.5 to 3.9; p < 0.001) and conventional (OR: 2.4; 95% CI: 1.7 to 3.4; p < 0.001) stress-induced ischemia. Although there was a significant increase in 45-min post–treadmill exercise hs-cTnI levels in those who developed ischemia, there was no significant increase after mental or pharmacological stress test.
Conclusions In patients with coronary artery disease, myocardial ischemia during either mental stress or conventional stress is associated with higher resting levels of hs-cTnI. This suggests that hs-cTnI elevation is an indicator of chronic ischemic burden experienced during everyday life. Whether elevated hs-cTnI levels are an indicator of adverse prognosis beyond inducible ischemia or whether it is amenable to intervention requires further investigation.
This work was supported by the National Institutes of Health (grants P01 HL101398, P20HL113451-01, P01HL086773-06A1, R56HL126558-01, R01 HL109413, R01HL109413-02S1, UL1TR000454, KL2TR000455, K24HL077506, and K24 MH076955). The sponsors of this study had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript. Dr. Garcia has received consulting honoraria from Syntermed; and has received royalties from the sale of Emory Cardiac Toolbox software, which was used for some analyses in this study. Drs. Vaccarino and Quyyumi have received research support from the National Institutes of Health. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received May 26, 2016.
- Revision received November 10, 2016.
- Accepted November 17, 2016.