Cardiac myosin-binding protein C in ST-elevation myocardial infarction
File(s)
Published version (corrected proof)
Author(s)
Type
Journal Article
Abstract
Aims
Cardiac myosin-binding protein C (cMyC) is a novel biomarker of myocardial injury, rising and falling more rapidly than cardiac troponins in myocardial infarction (MI), potentially enabling earlier diagnosis. Its performance has not been assessed in reperfused acute ST-segment elevation myocardial infarction (STEMI), against gold-standard biochemical (high-sensitivity cardiac troponin I, hs-cTnI) or imaging (cardiovascular magnetic resonance, CMR) biomarkers. This study tested the hypotheses that: i) cMyC correlates with acute and final MI size by late gadolinium enhancement (LGE) CMR and ii) cMyC is related to the presence of acute microvascular obstruction (MVO) by CMR.
Methods and results
Blood samples were obtained at 6 ± 2 hourly intervals for 24 hours (hrs) for measurement of hs-cTnI and cMyC concentrations in patients with reperfused acute STEMI. Patients underwent 3T LGE-CMR at ∼3–5 days (n = 69) and ∼4 months (n = 65) after reperfusion. Acute cMyC at all timepoints significantly correlated with acute and final MI size on LGE-CMR, most strongly at 6-hrs post reperfusion (r = 0.7, P < 0.001). cMyC at 6-, 12-, 18− and 24-hrs demonstrated significant discriminatory power in identifying patients with acute MVO, with the 6-hr level having the highest discriminative power. Hs-cTnI correlated more strongly with acute and final MI size compared with cMyC and had significantly higher discriminatory ability in identifying MVO at 12−, 18− and 24-hrs.
Conclusion
cMyC is a quantitative biochemical biomarker of myocardial injury in reperfused STEMI. Further studies, using optimised high-sensitivity assays, are warranted to evaluate its potential as a novel biomarker after acute MI.
Cardiac myosin-binding protein C (cMyC) is a novel biomarker of myocardial injury, rising and falling more rapidly than cardiac troponins in myocardial infarction (MI), potentially enabling earlier diagnosis. Its performance has not been assessed in reperfused acute ST-segment elevation myocardial infarction (STEMI), against gold-standard biochemical (high-sensitivity cardiac troponin I, hs-cTnI) or imaging (cardiovascular magnetic resonance, CMR) biomarkers. This study tested the hypotheses that: i) cMyC correlates with acute and final MI size by late gadolinium enhancement (LGE) CMR and ii) cMyC is related to the presence of acute microvascular obstruction (MVO) by CMR.
Methods and results
Blood samples were obtained at 6 ± 2 hourly intervals for 24 hours (hrs) for measurement of hs-cTnI and cMyC concentrations in patients with reperfused acute STEMI. Patients underwent 3T LGE-CMR at ∼3–5 days (n = 69) and ∼4 months (n = 65) after reperfusion. Acute cMyC at all timepoints significantly correlated with acute and final MI size on LGE-CMR, most strongly at 6-hrs post reperfusion (r = 0.7, P < 0.001). cMyC at 6-, 12-, 18− and 24-hrs demonstrated significant discriminatory power in identifying patients with acute MVO, with the 6-hr level having the highest discriminative power. Hs-cTnI correlated more strongly with acute and final MI size compared with cMyC and had significantly higher discriminatory ability in identifying MVO at 12−, 18− and 24-hrs.
Conclusion
cMyC is a quantitative biochemical biomarker of myocardial injury in reperfused STEMI. Further studies, using optimised high-sensitivity assays, are warranted to evaluate its potential as a novel biomarker after acute MI.
Date Issued
2026-03-25
Date Acceptance
2026-02-21
Citation
European Heart Journal: Acute Cardiovascular Care, 2026
ISSN
2048-8726
Publisher
Oxford University Press
Journal / Book Title
European Heart Journal: Acute Cardiovascular Care
Copyright Statement
© The Author(s) 2026. Published by Oxford University Press on behalf of the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
License URL
Identifier
10.1093/ehjacc/zuag032
Publication Status
Published online
Article Number
zuag032
Date Publish Online
2026-03-25