Background: Cardiac myosin binding protein C (cMyC) is an emerging new biomarker of myocardial injury rising earlier and cleared faster than cardiac troponins. It has discriminatory power similar to high-sensitive troponins in diagnosing myocardial infarction in patients presenting with chest pain. It is also associated with outcome in patients with acute heart failure. It is currently unclear how it relates to cardiac troponins in patients with chronic heart failure undergoing exercise training.

Methods And Results: This is a post hoc analysis of symptomatic heart failure patients in the multicentre randomized SMARTEX trial. Patients were randomized to one of three arms: high-intensity interval training, moderate continuous training and recommendation of regular exercise serving as control group (CG) for 12 weeks. As the training load in the two intervention arms was similar, these patients were merged and constituted the intervention group (IG). Clinical data and measurements were obtained at baseline and at 12 weeks. In 205 patients, serum was available for cMyC testing and in 196 patients, serum was available for hs-cTni testing. Due to non-normal distribution, cMyC and hs-cTnI measurements were log-transformed. A Bland-Altman plot was employed to evaluate the agreement of cMyC with hs-cTnI measurements. Lastly, a linear regression model was applied. No significant differences were observed in the change of cMyC levels between the groups throughout the intervention period (∆ cMyC IG: -0.5 [IQR: -3.4; 2.1] vs. ∆ cMyC CG: -0.7 [IQR: -2.7; 2.6]). The change in log hs-cTnI was significantly correlated with the change in log cMyC during the 12-week intervention period, with a Pearson correlation coefficient of R = 0.52 (95% CI 0.37-0.66, P < 0.001). For every 10% increase in cMyC levels, hs-cTnI levels rose by approximately 5%.

Conclusions: 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.

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http://dx.doi.org/10.1002/ehf2.15222DOI Listing

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