Patented biomarker for cardiac injury. 

Patented biomarker for cardiac injury. 

Tag: cTnI

Because postexercise cTn elevations can be challenging to interpret in the clinical setting because of concentrations exceeding the URL in the absence of signs of myocardial ischemia, a parallel assessment of cMyC might aid in discerning whether cTn elevations are physiological or pathological in endurance athletes.
cMyC is mentioned in the 2020 ESC Guidelines for the management of acute coronary syndromes in NSTEMI patients as an alternative to troponin.
cMyBP-C is the first cardiac-specific protein to be regarded as a promising diagnostic biomarker for acute myocardial injury since Troponin (cTn). Circulating cMyBP-C is a promising novel biomarker for evaluating cardiac surgical trauma in patients undergoing a cardiac operation.
Favourable release kinetics and a higher sensitivity than hs-cTn assays are likely responsible for the better performance in patients presenting early after chest pain onset.
A newly developed cMyC AMI rule-in/rule-out pathway identifies a greater proportion of patients suitable for safe rule-out as compared with the ESC 0/1h-algorithm using hs-cTnI and thus reduces the number of patients in a diagnostic grey zone.
Cardiac myosin-binding protein C (cMyC) is a promising novel biomarker of myocardial injury. 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.
cMyC is more abundant than Troponin and provides discriminatory power comparable to hs-cTnT/I for the diagnosis of AMI in all-comers, and identifies a greater proportion of patients with AMI in very early presenters. A standout feature is cMyC’s ability to more effectively triage patients. This distinction is likely related to the documented greater abundance and more rapid release profile of cMyC. If used on a POCT platform, cMyC could significantly improve the early triage of patients with suspected AMI.
In summary, this is really great work. It’s not quite the 15 minute wonder test that the Daily Mail has suggested, but it does have a lot of promise. We’ll look forward to seeing how this progresses.
Using cMyC to triage on first blood draw results in fewer patients in grey zone compared with hs-cTnT and hs-cTnI.
We examined how many myocytes and how much myocardium these concentrations represent. We also examined if dietary troponin can confound the rule-out algorithm. Based on pragmatic assumptions regarding cTn and cMyC release efficiency, circulating species, and volume of distribution, 99th centile concentrations may be exceeded by necrosis of 40 mg of myocardium. This volume is much too small to detect by noninvasive imaging.
In these early presenters, cMyC is relatively higher than cTnI on presentation and then cTnI catches up.
The cMyC assay is very sensitive, cMyC concentration is closely related to hs-cTnT and hs-cTnI and seems perturbed by the same sorts of things (renal dysfunction, age, poor LV function).
cMyC release following cardiac surgical interventions shows a similar time release pattern as Troponins but rises faster to detectable levels.