Key result
NT-proBNP >200 pg/mL identified severe systolic dysfunction in Duchenne muscular dystrophy with 90.5% sensitivity and 90.9% specificity (AUC 0.96; 95% CI 0.88-1.00).
Why the study?
Cardiomyopathy is a major cause of morbidity and mortality in Duchenne muscular dystrophy, motivating evaluation of whether NT-proBNP identifies severe systolic dysfunction.
Does NT-proBNP measurement identify severe systolic dysfunction and predict mortality in male patients with Duchenne muscular dystrophy and established cardiomyopathy?
Cohort
Does NT-proBNP measurement identify severe systolic dysfunction and predict mortality in male patients with Duchenne muscular dystrophy and established cardiomyopathy?
NT-proBNP >200 pg/mL accurately discriminates severe systolic dysfunction in Duchenne muscular dystrophy patients and is associated with mortality, suggesting its utility as a complementary diagnostic biomarker.
Hypothesis-generating for NT-proBNP in DMD cardiomyopathy; prospective validation required before clinical adoption.
Background: Cardiomyopathy is a major cause of morbidity and mortality in Duchenne muscular dystrophy (DMD). We evaluated whether N-terminal pro–brain natriuretic peptide (NT-proBNP) identifies severe systolic dysfunction and assessed its diagnostic performance. Methods: Male patients with genetically confirmed DMD and established cardiomyopathy were included if NT-proBNP measurement and echocardiographic ejection fraction (EF) were available within one month. Severe systolic dysfunction was defined as EF < 40%. Clinical, cardiac, and respiratory variables were analysed. ROC analysis with bootstrap validation and exploratory logistic regressions was performed. Results: NT-proBNP levels were significantly higher in patients with EF < 40% (median 843 vs. 81 pg/mL). A cut-off >200 pg/mL identified severe systolic dysfunction with 90.5% sensitivity and 90.9% specificity (AUC 0.96, 95% CI 0.88–1.00). During 24 months of follow-up, five deaths occurred. NT-proBNP showed moderate discrimination for mortality (AUC 0.79) and was associated with mortality in exploratory analysis. Conclusions: NT-proBNP was associated with severe systolic dysfunction in Duchenne cardiomyopathy and may complement imaging. Prospective validation is warranted.
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Marcì et al. (2026) conducted a cohort in Duchenne muscular dystrophy with cardiomyopathy. NT-proBNP was evaluated on Severe systolic dysfunction (EF < 40%) (AUC 0.96, 95% CI 0.88-1.00). NT-proBNP >200 pg/mL identified severe systolic dysfunction in Duchenne muscular dystrophy with 90.5% sensitivity and 90.9% specificity (AUC 0.96; 95% CI 0.88-1.00).
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