Category: Clinical Papers
- E. Riveland, A. Ushakova, T. Valborgland, et al
Changes in levels of the novel biomarker cMyC were significantly associated with hs-cTnI serum levels in patients
with symptomatic chronic HFrEF during a structured 12-week exercise training programme. This may indicate that cMyC
has a role as a future marker of subclinical myocardial damage.
- Hideto Nishimura, Junnichi Ishii, Hiroshi Takahashi, et al
In conclusion, similar to hs-cTnT, cMyC at admission may be a potent, independent predictor of 6-month all-cause mortality in patients without ACS treated at medical CICUs, and their prognostic abilities may be comparable. Combining cMyC or hs-cTnT with NT-proBNP may substantially improve early risk stratification of this population.
- M. Yildirim, C. Salbach, B.R. Milles et al
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.
- E Riveland, A Ushakova, T Valborgland, et al
Changes in levels of the novel biomarker cMyC were significantly associated with hs-cTnI plasma levels in patients with
symptomatic chronic HFrEF during a structured 12-week exercise training program. Being more sensitive may indicate a role as a future
marker of subclinical myocardial damage.
- Adriana Chetran, Minerva Codruta Bădescu, Ionela Lăcrămioara Serban, et al
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.
- Debabrata Dutta, Vu Nguyen, Kenneth S. Campbell, Raúl Padrón & Roger Craig
Here we solve the structure of the main (cMyBP-C-containing) region of the human cardiac filament using cryo-electron microscopy. The reconstruction reveals the architecture of titin and cMyBP-C and shows how myosin’s motor domains (heads) form three different types of motif (providing functional flexibility), which interact with each other and with titin and cMyBP-C to dictate filament architecture and function.
- Tom Gilbey, Liam Couch, Bashir Alaour, et al
When compared with high-sensitivity troponin, cMyC concentrations showed greater interindividual variability and rose to a level that was statistically distinguishable from baseline at the 3 hour timepoint, as opposed to 5 hours for the more established biomarker, high-sensitivity troponin.
- Davide Tamborrini, Zhexin Wang, Thorsten Wagner, et al
The structure demonstrates that MyBP-C bridges thin and thick filaments, with its carboxy-terminal region binding to the myosin tails and directly stabilizing the OFF state of the myosin heads in an unforeseen manner.
- Bashir Alaour, Thomas E Kaier, Rasmus Bo Hasselbalch, et al
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.
- Michael Mallouppas , Robin Chung , Arjun K. Ghosh , Alison Macklin , Derek M. Yellon , and J. Malcolm Walker
cTnT and cMyC significantly increased during anthracycline chemotherapy.
- Bashir Alaour, Yu Jin Chung, Thomas Edward Kaier et al
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.
- Thomas E. Kaier, Raphael Twerenbold, Pedro Lopez-Ayala et al
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.
- Michael S Marber, Nicholas L Mills, David A Morrow, Christian Mueller, et al
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.
- Vincent L. Aengevaeren , Roland R. J. van Kimmenade , Jordi Ordóñez‐Llanos , et al.
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.
- Bashir Alaour, Torbjørn Omland, Janniche Torsvik, et al
cMyC exhibits acceptable RCV and low II suggesting that it could be suitable for disease monitoring, risk stratification and prognostication if measured serially. Analytical quality specifications based on biological variation are similar to those for cardiac troponin and should be achievable at clinically relevant concentrations.
- Thomas Nestelberger, Jasper Boeddinghaus, Pedro Lopez-Ayala, et al
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.
- Nikola Kozhuharov, Desiree Wussler, Thomas Kaier, et al.
cMyC (Cardiac Myosin-Binding Protein C) may aid physicians in the rapid triage of patients with suspected Acute Heart Failure (AHF).
- Jean-Philippe Collet, Holger Thiele, et al.
cMyC is mentioned in the 2020 ESC Guidelines for the management of acute coronary syndromes in NSTEMI patients as an alternative to troponin.
- Thomas E. Kaier, Carsten Stengaard, Jack Marjot, et al.
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.
- Xiang-Jian Chen, Wei Zhang, Zhi-Ping Bian, et al.
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.
- Thomas E. Kaier, Bashir Alaour, Michael Marber.
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.
- T E Kaier, R Twerenbold, B Alaour, et al.
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.
- Thomas E Kaier, Bashir Alaour, Michael Marber.
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.
- Thomas E Kaier, Raphael Twerenbold, Carsten Stengaard, et al.
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.
- Atul Anand, Calvin Chin, Anoop S V Shah, et al.
Serum cMyC concentration is associated with myocardial hypertrophy, fibrosis and an increased risk of mortality in aortic stenosis.
- Thomas E. Kaier, Raphael Twerenbold, Christian Puelacher, et al.
Using cMyC to triage on first blood draw results in fewer patients in grey zone compared with hs-cTnT and hs-cTnI.
- Jack Marjot, Thomas E Kaier, Eva D Martin, et al.
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.
- Thomas E Kaier, Atul Anand, Anoop S V Shah, et al.
In these early presenters, cMyC is relatively higher than cTnI on presentation and then cTnI catches up.
- Jack Marjot, Christoph Liebetrau, Robert J. Goodson, et al.
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).
- James O. Baker, Raymond Tyther, Christoph Liebetrau, et al.
cMyC release following cardiac surgical interventions
shows a similar time release pattern as Troponins but rises faster to detectable levels.
- Sebastien Jacquet, Xiaoke Yin, Pierre Sicard, et al.
Discovery of cMyC in the coronary effluent after myocardial infarction.