Cardiac myosin-binding protein C is a novel marker of myocardial injury and fibrosis in aortic stenosis

Figures

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  Figure 1. Relationships between cMyC and markers of disease severity in the mechanism cohort. β values (95% CI) represent change in the progression variable for each log unit change in cMyC concentration after adjustment in multivariate modelling. Markers of disease severity are: (A) indexed LV mass (g/m2) determined by MRI; (B) fibrosis volume (g) by MRI; (C) AVmax (m/s) determined by echocardiography; (D) diastolic function from echocardiographic measures of E/e′ ratio. *Adjusted for age, sex, glomerular filtration rate, AVmax, cardiac troponin, history of ischaemic heart disease, diabetes and hypertension. +As above plus body surface area. ‡As above excluding AVmax. AV, aortic valve; cMyC, cardiac myosin-binding protein C; LV, left ventricle.

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  Figure 2. cMyC and late gadolinium enhancement. (A) Receiver operating characteristic (ROC) curve analysis for outcome of LGE. Addition of cMyC improves the prediction of age and gender for LGE, P=0.002 (DeLong’s method with bootstrapping). (B) Logistic regression modelling for the predicted probability of LGE with serum cMyC concentration (adjusted for age and sex). Shaded area represents 95% CI. AUC, area under the curve; cMyC, cardiac myosin-binding protein C; LGE, late gadolinium enhancement.

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  Figure 3. Patterns of myocyte death in patients with aortic stenosis. Images showing differing patterns of oncosis and autophagy visualised using a 3,3′-diaminobenzidine-based detection kit in individuals with aortic stenosis. (A) Oncosis and (B) autophagy in a patient with a low (9.4 ng/L) cMyC concentration. (C) Oncosis and (D) autophagy in a patient with a high (87.2 ng/L) cMyC concentration. There is a marked difference in staining intensity by cMyC concentration for both oncosis and autophagy. cMyC, cardiac myosin-binding protein C.

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  Figure 4. Survival by tertiles of cMyC in the outcome cohort. cMyC, cardiac myosin-binding protein C.