Relation of High-sensitivity Cardiac Troponin I Elevation With Exercise to Major Adverse Cardiovascular Events in
Bruno B Lima1, Muhammad Hammadah1, Jeong Hwan Kim2
1Emory Clinical Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia; Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia.
Insights
Elevated cardiac troponin I (hs-cTnI) after exercise stress testing predicts major adverse cardiac events in stable coronary artery disease (CAD) patients. Changes in hs-cTnI offer prognostic value beyond traditional risk factors.
Area of Science:
- Cardiology
- Biomarkers
- Clinical Risk Stratification
Background:
- High-sensitive cardiac troponin I (hs-cTnI) levels increase with inducible myocardial ischemia in patients with coronary artery disease (CAD).
- The prognostic significance of hs-cTnI changes during exercise stress testing for major adverse cardiac events (MACE) in stable CAD remains to be fully elucidated.
Purpose of the Study:
- To assess the association between exercise-induced changes in hs-cTnI levels and the occurrence of MACE in patients with stable CAD.
- To determine if hs-cTnI dynamics improve risk prediction beyond traditional factors and inducible ischemia.
Main Methods:
- A cohort of 365 stable CAD patients underwent treadmill exercise stress testing with myocardial perfusion imaging.
- Plasma hs-cTnI levels were measured at rest and 45 minutes post-stress.
- Multivariable Fine & Gray's subdistribution hazards models analyzed the association between hs-cTnI changes and MACE (cardiovascular death, myocardial infarction, unstable angina requiring revascularization) over a median 3-year follow-up.
Main Results:
- 39 patients (11%) experienced MACE.
- Each two-fold increment in hs-cTnI with stress was associated with a 2.2-fold increase in MACE hazard.
- High resting hs-cTnI and ≥20% stress-induced elevation showed the highest MACE incidence (SHR 4.6).
- Adding hs-cTnI levels (resting and change) significantly improved risk model discrimination (C-statistic 0.67 to 0.71).
Conclusions:
- Higher resting hs-cTnI levels and exercise-induced elevation predict adverse cardiovascular outcomes in stable CAD.
- hs-cTnI dynamics provide prognostic information beyond traditional risk factors and inducible ischemia detected by SPECT.
- hs-cTnI measurements during stress testing can enhance risk stratification in stable CAD patients.
Abstract:
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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