Key result
Exercise-induced cMyC changes moderately correlate with hs-cTnI dynamics in HFrEF.
Why the study?
It is currently unclear how cardiac myosin binding protein C relates to cardiac troponins in patients with chronic heart failure undergoing exercise training.
Does a structured 12-week exercise training programme affect cMyC levels and how do they correlate with hs-cTnI in patients with symptomatic chronic HFrEF?
RCT (n=205)
randomized to one of three arms
Yes
Does a structured 12-week exercise training programme affect cMyC levels and how do they correlate with hs-cTnI in patients with symptomatic chronic HFrEF?
Changes in the novel biomarker cMyC correlate significantly with hs-cTnI in HFrEF patients undergoing exercise training, suggesting its potential as a marker of subclinical myocardial damage.
cMyC may track myocardial stress during exercise in HFrEF; leaves open its incremental value over hs-cTnI in prospective studies.
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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Riveland et al. (2025) conducted an RCT in symptomatic chronic HFrEF (n=205). Exercise training (high-intensity interval or moderate continuous) vs. Recommendation of regular exercise was evaluated on Correlation between change in log hs-cTnI and change in log cMyC (R 0.52, 95% CI 0.37-0.66, p=<0.001). Changes in cMyC levels during a 12-week exercise training program in patients with HFrEF were significantly correlated with changes in hs-cTnI (R=0.52; 95% CI 0.37-0.66; P<0.001).
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