Patented biomarker for cardiac injury. 

Patented biomarker for cardiac injury. 

Tag: AMI

Incorporating cMyBP-C and hs-cTnT - effectively rules out AMI, showing non-inferiority to hs-cTnT-only-based rapid rule-out algorithms and offers a promising alternative, potentially enhancing clinical decision-making in emergency settings.
The study brings new evidence supporting the role of MyBP-C as a comprehensive biomarker in AHF. While NT-proBNP remains the gold standard biomarker in AHF, MyBPC has been shown to have an impressive diagnostic performance with high sensitivity and specificity, providing complementary information. MyBP-C may serve as a valuable adjunctive tool in enhancing diagnostic accuracy and guiding clinical decisions in AHF. In addition, MyBP-C has a promising role as a prognostic biomarker in AHF, being able to complement existing markers, and thus achieve better risk stratification and the prediction of short-term outcomes.
We have previously shown that significant circadian oscillations exist for cardiac troponin T (cTnT) but not for cardiac troponin I (cTnI). Cardiac myosin-binding protein C (cMyC) is a novel protein biomarker of myocardial injury with a promising role in the diagnosis and risk stratification of acute myocardial injury. In this study, we examine and compare the diurnal variation of cMyC with cTnT/I.
Phosphorylation and fragmentation pattern of cMyC are dependent on the type of myocardial injury and might aid the differentiation between Type-1 and non-Type-1 AMI.
The cMyC 0/1h-algorithm provided excellent safety and identified a greater proportion of patients suitable for direct rule-out or rule-in based on a single measurement than the ESC 0/1h-algorithm using hs-cTnT/I.
Cardiac myosin-binding protein C (cMyBP-C, MYBPC3, cMyC; UniProtKB—Q14896) is a 140 kDa sarcomeric protein that is loosely associated with both myosin and actin. It was identified in the coronary effluent from ischaemic myocardium about 10 years ago and after systematic screening of monoclonal antibodies a sensitive sandwich immunoassay was formulated. Using this assay, cMyC has been measured in a variety of patient groups and directly compared to cardiac troponin T (cTnT) and cardiac troponin I (cTnI) measured in the same blood samples using high-sensitivity assays.
Webinar held by the ESC 27th of October 2021. ACVC Biomarker Talk Series - A new diagnostic marker on the horizon - cMyC
cMyC concentrations, which may quantify cardiomyocyte injury even more accurately than hs-cTnT or hs-cTnI levels, were lower in T2MI vs T1MI and provided modest diagnostic accuracy, comparable with that provided by hs-cTnT and hs-cTnI.
cMyC is mentioned in the 2020 ESC Guidelines for the management of acute coronary syndromes in NSTEMI patients as an alternative to troponin.
cMyC is superior to hs-cTnT to rule-out chest pain patients with final AMI diagnose with blood-samples done at time of ambulance pickup.
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.
King's College London researchers are developing a point-of-care blood test to diagnose heart attacks that uses cardiac myosin-binding protein C as an alternative biomarker to high-sensitivity troponin used in laboratory testing.
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.
The cMyC test correctly excluded a heart attack in 32 per cent of patients. It could mean thousands of patients are given the all-clear and sent home within quarter of an hour of arriving at A&E. Resulting in cost savings for healthcare.
Switching to cMyC from hs-cTn at King's College London, would yearly save the hospital £800,000 through reduced admissions.
Research related to heart attacks shows that the cMyC test has the potential to reassure many thousands more patients with a single test, freeing up valuable hospital beds in ED / A&E.
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.
cMyC release following cardiac surgical interventions shows a similar time release pattern as Troponins but rises faster to detectable levels.
Discovery of cMyC in the coronary effluent after myocardial infarction.