Key result
Cardiac myosin-binding protein C serves as a quantitative biomarker of myocardial injury in reperfused STEMI.
Why the study?
Does Cardiac myosin-binding protein C (cMyC) correlate with MI size and microvascular obstruction in patients with reperfused acute STEMI?
Observational (n=69)
Does Cardiac myosin-binding protein C (cMyC) correlate with MI size and microvascular obstruction in patients with reperfused acute STEMI?
Effect estimate: r = 0.7
p-value: p=<0.001
cMyC is a quantitative biochemical biomarker of myocardial injury in reperfused STEMI that correlates with MI size and microvascular obstruction, though hs-cTnI demonstrated stronger correlation and discriminatory ability.
May allow better quantification of myocardial injury in reperfused STEMI; leaves open routine adoption pending high-sensitivity assay validation.
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.
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Rajakulasingam et al. (2026) conducted an observational in Reperfused acute ST-segment elevation myocardial infarction (STEMI) (n=69). Cardiac myosin-binding protein C (cMyC) vs. High-sensitivity cardiac troponin I (hs-cTnI) was evaluated on Correlation with acute and final MI size by LGE-CMR (r = 0.7, p=<0.001).
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