TY - JOUR
T1 - Relation of High-sensitivity Cardiac Troponin I Elevation With Exercise to Major Adverse Cardiovascular Events in Patients With Coronary Artery Disease
AU - Lima, Bruno B.
AU - Hammadah, Muhammad
AU - Kim, Jeong Hwan
AU - Uphoff, Irina
AU - Shah, Amit
AU - Levantsevych, Oleksiy
AU - Almuwaqqat, Zakaria
AU - Moazzami, Kasra
AU - Sullivan, Samaah
AU - Ward, Laura
AU - Sun, Yan
AU - Kutner, Michael
AU - Ko, Yi An
AU - Sheps, David S.
AU - Beshiri, Agim
AU - Murtagh, Gillian
AU - Bremner, J. Douglas
AU - Vaccarino, Viola
AU - Quyyumi, Arshed A.
N1 - Funding Information:
This work was supported by the NIH through the following grants: P01 HL101398, R01 HL109413, R01HL109413-02S1, R01HL125246, K24HL077506, K24 MH076955, UL1TR000454, KL2TR000455, K23HL127251, and T32HL130025A. High-sensitivity troponin I assays were kindly provided by Abbott Laboratories. Disclosures: The authors A.B. and G.M. are full-time employees at Abbott. Otherwise, the authors report no biomedical financial interests or potential conflicts of interest. The sponsors of this study had no role in the study design or in the collection, analysis, or interpretation of the data, the writing of the manuscript, or the decision to submit the manuscript for publication.
Funding Information:
This work was supported by the NIH through the following grants: P01 HL101398 , R01 HL109413 , R01HL109413-02S1 , R01HL125246 , K24HL077506 , K24 MH076955 , UL1TR000454 , KL2TR000455 , K23HL127251 , and T32HL130025A . High-sensitivity troponin I assays were kindly provided by Abbott Laboratories.
Publisher Copyright:
© 2020 Elsevier Inc.
PY - 2020/12/1
Y1 - 2020/12/1
N2 - High sensitive cardiac troponin I (hs-cTnI) increases with inducible myocardial ischemia in patients with coronary artery disease (CAD). We aimed to assess if the change in hs-cTnI levels with exercise stress testing is associated with major adverse cardiac events (MACE). A cohort of 365 (age 62 ± 9 years, 77% men) patients with stable CAD underwent 99mTc sestamibi myocardial perfusion imaging with treadmill testing. Plasma hs-cTnI level was measured at rest and at 45 min after stress. Multivariable Fine & Gray's subdistribution hazards models were used to determine the association between the change in hs-cTnI and MACE, a composite end point of cardiovascular death, myocardial infarction, and unstable angina requiring revascularization. During a median follow-up of 3 years, 39 (11%) patients experienced MACE. After adjustment, for each two-fold increment in hs-cTnI with stress, there was a 2.2 (95% confidence interval 1.3-3.6)-fold increase in the hazard for MACE. Presence of both a high resting hs-cTnI level (>median) and ≥ 20% stress-induced hs-cTnI elevation was associated with the highest incidence of MACE (subdistribution hazards models 4.6, 95% confidence interval 1.6 to 13.0) compared with low levels of both. Risk discrimination statistics significantly improved after addition of resting and change in hs-cTnI levels to a model including traditional risk factors and inducible ischemia (0.67 to 0.71). Conversely, adding inducible ischemia by SPECT did not significantly improve the C-statistic from a model including traditional risk factors, baseline and change in hs-cTnI (0.70 to 0.71). In stable CAD patients, higher resting levels and elevation of hs-cTnI with exercise are predictors of adverse cardiovascular outcomes beyond traditional cardiovascular risk factors and presence of inducible ischemia.
AB - High sensitive cardiac troponin I (hs-cTnI) increases with inducible myocardial ischemia in patients with coronary artery disease (CAD). We aimed to assess if the change in hs-cTnI levels with exercise stress testing is associated with major adverse cardiac events (MACE). A cohort of 365 (age 62 ± 9 years, 77% men) patients with stable CAD underwent 99mTc sestamibi myocardial perfusion imaging with treadmill testing. Plasma hs-cTnI level was measured at rest and at 45 min after stress. Multivariable Fine & Gray's subdistribution hazards models were used to determine the association between the change in hs-cTnI and MACE, a composite end point of cardiovascular death, myocardial infarction, and unstable angina requiring revascularization. During a median follow-up of 3 years, 39 (11%) patients experienced MACE. After adjustment, for each two-fold increment in hs-cTnI with stress, there was a 2.2 (95% confidence interval 1.3-3.6)-fold increase in the hazard for MACE. Presence of both a high resting hs-cTnI level (>median) and ≥ 20% stress-induced hs-cTnI elevation was associated with the highest incidence of MACE (subdistribution hazards models 4.6, 95% confidence interval 1.6 to 13.0) compared with low levels of both. Risk discrimination statistics significantly improved after addition of resting and change in hs-cTnI levels to a model including traditional risk factors and inducible ischemia (0.67 to 0.71). Conversely, adding inducible ischemia by SPECT did not significantly improve the C-statistic from a model including traditional risk factors, baseline and change in hs-cTnI (0.70 to 0.71). In stable CAD patients, higher resting levels and elevation of hs-cTnI with exercise are predictors of adverse cardiovascular outcomes beyond traditional cardiovascular risk factors and presence of inducible ischemia.
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U2 - 10.1016/j.amjcard.2020.09.019
DO - 10.1016/j.amjcard.2020.09.019
M3 - Article
C2 - 32941818
AN - SCOPUS:85091799397
SN - 0002-9149
VL - 136
SP - 1
EP - 8
JO - American Journal of Cardiology
JF - American Journal of Cardiology
ER -