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Aims: Cardiac myosin-binding protein C (cMyC) seems to be even more sensitive in the quantification of cardiomyocyte injury vs. high-sensitivity cardiac troponin, and may therefore have diagnostic and prognostic utility.
Methods And Results: In a prospective multicentre diagnostic study, cMyC, high-sensitivity cardiac troponin T (hs-cTnT), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) plasma concentrations were measured in blinded fashion in patients presenting to the emergency department with acute dyspnoea. Two independent cardiologists centrally adjudicated the final diagnosis. Diagnostic accuracy for acute heart failure (AHF) was quantified by the area under the receiver operating characteristic curve (AUC). All-cause mortality within 360 days was the prognostic endpoint. Among 1083 patients eligible for diagnostic analysis, 51% had AHF. cMyC concentrations at presentation were higher among AHF patients vs. patients with other final diagnoses [72 (interquartile range, IQR 39-156) vs. 22 ng/L (IQR 12-42), P < 0.001)]. cMyC's AUC was high [0.81, 95% confidence interval (CI) 0.78-0.83], higher than hs-cTnT's (0.79, 95% CI 0.76-0.82, P = 0.081) and lower than NT-proBNP's (0.91, 95% CI 0.89-0.93, P < 0.001). Among 794 AHF patients eligible for prognostic analysis, 28% died within 360 days; cMyC plasma concentrations above the median indicated increased risk of death (hazard ratio 2.19, 95% CI 1.66-2.89; P < 0.001). cMyC's prognostic accuracy was comparable with NT-proBNP's and hs-cTnT's. cMyC did not independently predict all-cause mortality when used in validated multivariable regression models. In novel multivariable regression models including medication, age, left ventricular ejection fraction, and discharge creatinine, cMyC remained an independent predictor of death and had no interactions with medical therapies at discharge.
Conclusion: Cardiac myosin-binding protein C may aid physicians in the rapid triage of patients with suspected AHF.
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http://dx.doi.org/10.1002/ejhf.2094 | DOI Listing |
Sci Rep
August 2025
Department of Cardiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, Jiangsu, China.
While cardiac myosin-binding protein-C (cMyBP-C) is a promising biomarker for acute coronary syndrome, its clinical utility in stable coronary artery disease (CAD) remains poorly defined. To investigate the association of cMyBP-C with the presence and angiographic severity of stable CAD, and to evaluate its prognostic value for 1-year major adverse cardiovascular events (MACEs). This study enrolled 367 patients undergoing coronary angiography for suspected CAD.
View Article and Find Full Text PDFRapid Commun Mass Spectrom
December 2025
Leicester van Geest MultiOMICs Facility, University of Leicester, Leicester, UK.
Rationale: Molecular imprinting has emerged as a promising strategy to create custom imprints for precision recognition of proteins. This study proposes using dopamine polymers as a novel approach to enhance the retrieval of proteins from human plasma. Dopamine polymers possess adhesive properties due to their ability to form hydrophobic interactions, π-π, hydrogen bonding and van der Waals forces with various substrates; in this study, we have leveraged these adhesive properties to capture and retrieve proteins from complex biological samples.
View Article and Find Full Text PDFJ Gen Physiol
November 2025
Department of Molecular Physiology and Biophysics, Larner College of Medicine, University of Vermont, Burlington, VT, USA.
Cardiac contractility is driven by shortening of ∼2-μm-long, macromolecular assemblies known as sarcomeres. During contraction, the motor protein myosin binds to, and exerts force upon actin filaments, utilizing energy from the hydrolysis of ATP. When not actively contracting, myosin partition into two subpopulations, distinguished by their basal rates of ATP hydrolysis, known as the "Disordered Relaxed" (DRX) and "Super Relaxed" (SRX) states.
View Article and Find Full Text PDFAnn Med Surg (Lond)
July 2025
Department of Research, Medical Research Circle (MedReC), Goma, DR Congo.
Background: Hypertrophic cardiomyopathy (HCM) is a genetic cardiovascular disorder characterized by unexplained left ventricular hypertrophy, affecting approximately 0.2% of the global population. Around 40% of HCM cases are linked to mutations in sarcomeric protein genes such as β-myosin heavy chain and myosin-binding protein C, which impair calcium signaling and myocardial contractility.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
August 2025
Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110.
Heart failure is a leading cause of death worldwide, and even with current treatments, the 5-y transplant-free survival rate is only ~50 to 70%. As such, there is a need to develop new treatments for patients that improve survival and quality of life. Recently, there have been efforts to develop small molecules for heart failure that directly target components of the sarcomere, including cardiac myosin.
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