Cardiac myosin-binding protein C in ST-elevation myocardial infarction
Ramyah Rajakulasingam1,2, Bashir Alaour3, Sam McGrath3
1National Heart and Lung Institute, Imperial College London, Sydney Street, London SW3 6NP,UK.
Insights
Cardiac myosin-binding protein C (cMyC) shows potential as an early biomarker for myocardial injury in ST-elevation myocardial infarction (STEMI). While it correlates with infarct size, cardiac troponins demonstrate superior performance in identifying microvascular obstruction.
Area of Science:
- Cardiology
- Biomarker Discovery
- Myocardial Infarction Research
Background:
- Cardiac myosin-binding protein C (cMyC) is a novel biomarker for myocardial injury.
- cMyC kinetics are faster than cardiac troponins, suggesting earlier diagnostic potential.
- Its utility in reperfused ST-segment elevation myocardial infarction (STEMI) requires evaluation against established biomarkers.
Purpose of the Study:
- To assess the correlation of cMyC with acute and final myocardial infarction (MI) size using late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR).
- To determine if cMyC levels are associated with acute microvascular obstruction (MVO) detected by CMR.
- To compare cMyC performance against high-sensitivity cardiac troponin I (hs-cTnI) and CMR findings.
Main Methods:
- Blood samples were collected for cMyC and hs-cTnI measurements at 6-hour intervals for 24 hours post-reperfusion in STEMI patients.
- Late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) was performed at approximately 3-5 days and 4 months post-reperfusion.
- Correlation and discriminatory analyses were conducted to compare cMyC and hs-cTnI with MI size and MVO.
Main Results:
- Acute cMyC levels significantly correlated with acute and final MI size, with the strongest correlation at 6 hours post-reperfusion (r=0.7).
- cMyC at 6, 12, 18, and 24 hours showed discriminatory power for acute MVO, with the 6-hour level being most effective.
- Hs-cTnI showed stronger correlations with MI size and superior discriminatory ability for MVO at later time points (12, 18, 24 hours).
Conclusions:
- cMyC serves as a quantitative biomarker of myocardial injury in reperfused STEMI.
- Further research with optimized high-sensitivity assays is needed to fully explore cMyC's potential as a novel post-MI biomarker.
- Hs-cTnI remains a stronger biomarker for assessing MI size and MVO in the early hours post-reperfusion.
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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