Key result
Elevated cTnI in DMD indicates progressive myocardial injury with ~98% of patients showing abnormal CMR.
Why the study?
The study aimed to clarify the developmental processes of myocardial injury and their significance in Duchenne muscular dystrophy to optimize long-term cardiomyopathy management.
Does elevated cTnI predict persistent progressive myocardial injury on CMR in children with Duchenne muscular dystrophy?
Cohort (n=174)
No
Does elevated cTnI predict persistent progressive myocardial injury on CMR in children with Duchenne muscular dystrophy?
Absolute Event Rate: 97.73% vs 60%
p-value: p=<0.001
Regular monitoring of cTnI levels in children with Duchenne muscular dystrophy can help identify persistent progressive myocardial injury at an early stage.
Serial cTnI monitoring may detect evolving myocardial injury in DMD; leaves open its prognostic role and management impact pending larger trials.
We aimed to clarify the different developmental processes of myocardial injury and their significance in Duchenne muscular dystrophy (DMD), and to optimize the long-term management of DMD-associated cardiomyopathy. A prospective, single-center cohort study of children with DMD was conducted between June 2023 and April 2025 at West China Second University Hospital. Clinical symptoms and heart function-related indicators were monitored in children aged > 7 years. Unpaired two-tailed Student’s t-test, Mann–Whitney U test, and chi-squared test were applied according to the data type and normality, and post hoc Bonferroni correction was performed among the intragroup factors. A total of 174 children with DMD were enrolled, 25.29% of whom had high cardiac troponin I (cTnI) levels (cTnI-H group), among whom 75% had cTnI elevations < 10-fold (cTnI-H1 subgroup), 15.91% had cTnI elevations > 10-fold but < 30-fold (cTnI-H2 subgroup), and 9.09% had cTnI elevations > 30-fold (cTnI-H3 subgroup). During follow-up, 15.38% of the children in the normal cTnI level group (cTnI-N group) had newly elevated cTnI levels, whereas the elevated cTnI levels in the cTnI-H group had decreased to normal in 9.09% of the children, exhibited repeated elevations in 33.33% of the children, had continuous elevations in 57.58% of the children. 100% of the children in the cTnI-H3 subgroup had newer or expanded late gadolinium enhancement (LGE) and perfusion defects on cardiac magnetic resonance (CMR). The longest duration of elevated cTnI was 15 months, in which 100% had newer or expanded LGE and perfusion defects on CMR. There might be three different states of myocardial injury in DMD according to the degree of cTnI elevation, and the outcomes of elevated cTnI levels and CMR: transient injury, fluctuating injury, and persistent progressive injury. These three states might alternate and fluctuate with each other. The significant increase and long duration of elevated cTnI levels might be associated with persistent progressive myocardial damage. Regular monitoring (once a month for elevated cTnI levels) of cTnI levels might help identify persistent progressive myocardial damage at an early stage and optimize the long-term management of DMD-associated cardiomyopathy.
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Zhou et al. (2026) conducted a cohort in Duchenne muscular dystrophy (n=174). High cardiac troponin I (cTnI-H) monitoring vs. Normal cardiac troponin I (cTnI-N) was evaluated on Abnormal cardiac magnetic resonance (CMR) (p=<0.001). Elevated cardiac troponin I in Duchenne muscular dystrophy patients indicated progressive myocardial injury, with 97.73% showing abnormal CMR compared to 60.00% in patients with normal levels.
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