High-Sensitivity Cardiac Troponin After Cardiac Stress Test: A Systematic Review and Meta-Analysis

Background The recent introduction of high-sensitivity cardiac troponin (hs-cTn) assays has allowed clinicians to measure hs-cTn before and after cardiac stress testing, but the hs-cTn release pattern and potential utility in identifying inducible myocardial ischemia are unclear. We thus conducted a...

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Veröffentlicht in:Journal of the American Heart Association 2019-03, Vol.8 (6), p.e008626-e008626
Hauptverfasser: Samaha, Eslam, Avila, Audrey, Helwani, Mohammad A, Ben Abdallah, Arbi, Jaffe, Allan S, Scott, Mitchell G, Nagele, Peter
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Sprache:eng
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Zusammenfassung:Background The recent introduction of high-sensitivity cardiac troponin (hs-cTn) assays has allowed clinicians to measure hs-cTn before and after cardiac stress testing, but the hs-cTn release pattern and potential utility in identifying inducible myocardial ischemia are unclear. We thus conducted a systematic review and meta-analysis to improve our understanding of hs-cTn release associated with exercise and pharmacological stress testing. Methods and Results Studies published between January 2008 and July 2016 that reported hs-cTn change values (high-sensitivity cardiac troponin T [hs-cTnT] or high-sensitivity cardiac troponin I [hs-cTnI]) in relation to cardiac stress testing were searched and reviewed by 2 independent screeners. Primary outcomes were pooled estimates of absolute and relative hs-cTn changes after cardiac stress test, stratified by the presence of inducible myocardial ischemia. This meta-analysis included 11 studies (n=2432 patients). After exercise stress testing, hs-cTnT increased by 0.5 ng/L or 11% (6 studies, n=406) and hs-cTnI by 2.4 ng/L or 41% (4 studies, n=365) in patients with inducible myocardial ischemia versus hs-cTnT by 1.1 ng/L or 18% (8 studies, n=629; P=0.29) and hs-cTnI by 1.8 ng/L or 72% (4 studies, n=831; P=0.61) in patients who did not develop inducible myocardial ischemia. After pharmacological stress test, hs-cTnT changed by -0.1 ng/L or -0.4% (6 studies, n=251) and hs-cTnI by 2.4 ng/L or 32% (2 studies, n=108) in patients with inducible myocardial ischemia versus hs-cTnT by 0.7 ng/L or 11% (5 studies, n=443, P=0.44) and hs-cTnI by 1.7 ng/L or 38% (2 studies, n=116; P=0.62) in patients who did not develop inducible myocardial ischemia. Conclusions hs-cTn rising patterns after exercise and pharmacological stress testing appear inconsistent and comparably small, and do not appear to be correlated with inducible myocardial ischemia.
ISSN:2047-9980
2047-9980
DOI:10.1161/jaha.118.008626