There might be another way
Cardiac myosin-binding protein C (cMyC) is a promising novel biomarker of myocardial injury – originally described as the C-protein by Offer et al. in 1973, its discovery relied on the characterization of ‘impurities’ detected alongside myosin. cMyC has distinctive release kinetics that should enable it to act as a better adjudicator of acute versus chronic myocardial injury than troponin.
We have raised monoclonal antibodies targeting the cardiac isoform of myosin-binding protein C and successfully migrated the assay onto a high-sensitivity platform [12]. Subsequently, we demonstrated up to tenfold greater abundance of cMyC after myocardial injury than two leading hs-cTnT/I assays [20]. In a small study, involving 174 patients presenting within 3 h of chest pain onset and suspected AMI, we demonstrated a more dynamic rise of cMyC in the early stages of AMI than hs-cTnI [21]. This faster rise ought to yield a positive result (for rule-in of AMI), or an earlier reliable negative result (for rule-out of AMI). Furthermore, the relative abundance of cMyC should allow careful calibration of rule-out and rule-in thresholds, with more ‘headroom’ to enable precise quantification at the low concentrations needed for rule-out.
In conclusion, cMyC is a cardiac-restricted protein which rapidly enters the systemic circulation after myocardial injury and is relatively more abundant than troponin. The biomarker performs favourably in the diagnosis of AMI and is particularly well-suited to a point-of-care diagnostic platform – which could transform the way we perform chest pain triage.
We have raised monoclonal antibodies targeting the cardiac isoform of myosin-binding protein C and successfully migrated the assay onto a high-sensitivity platform [12]. Subsequently, we demonstrated up to tenfold greater abundance of cMyC after myocardial injury than two leading hs-cTnT/I assays [20]. In a small study, involving 174 patients presenting within 3 h of chest pain onset and suspected AMI, we demonstrated a more dynamic rise of cMyC in the early stages of AMI than hs-cTnI [21]. This faster rise ought to yield a positive result (for rule-in of AMI), or an earlier reliable negative result (for rule-out of AMI). Furthermore, the relative abundance of cMyC should allow careful calibration of rule-out and rule-in thresholds, with more ‘headroom’ to enable precise quantification at the low concentrations needed for rule-out.
In conclusion, cMyC is a cardiac-restricted protein which rapidly enters the systemic circulation after myocardial injury and is relatively more abundant than troponin. The biomarker performs favourably in the diagnosis of AMI and is particularly well-suited to a point-of-care diagnostic platform – which could transform the way we perform chest pain triage.
