Key result
ΔQTc ≥30.5 ms within 24 h of cyclophosphamide administration predicts CY-induced cardiomyopathy in children with 100% sensitivity and 89.1% specificity.
Why the study?
Cyclophosphamide can cause potentially fatal cardiotoxicity, but no electrocardiographic indices have been established for early detection of cyclophosphamide-induced cardiomyopathy in pediatric patients.
Does QTc prolongation within 24 hours of high-dose cyclophosphamide administration predict the early onset of cyclophosphamide-induced cardiomyopathy in pediatric hematology and oncology patients?
Does QTc prolongation within 24 hours of high-dose cyclophosphamide administration predict the early onset of cyclophosphamide-induced cardiomyopathy in pediatric hematology and oncology patients?
An increase in QTc interval (ΔQTc ≥30.5 ms) within 24 hours of high-dose cyclophosphamide administration is a highly sensitive and specific early noninvasive marker for predicting potentially fatal cyclophosphamide-induced cardiomyopathy in pediatric patients.
May support early QTc monitoring post-cyclophosphamide; hypothesis-generating and requires prospective validation before adoption.
Background Cyclophosphamide (CY) is associated with potentially fatal cardiotoxicity, yet no electrocardiographic indices have been established for early detection of CY‐induced cardiomyopathy. This study aimed to determine whether corrected QT interval (QTc) prolongation can predict early onset of CY‐related cardiac dysfunction in pediatric patients. Methods We retrospectively analyzed 62 children who received high‐dose CY therapy (≥100 mg/kg) for hematologic or oncologic diseases between 2010 and 2025. CY‐induced cardiomyopathy was defined as a ≥10% reduction in the left ventricular ejection fraction to less than 50% or elevated brain natriuretic peptide/ N ‐terminal pro‐brain natriuretic peptide levels, according to the 2021 International Cardio‐Oncology Society criteria. Resting 12‐lead ECGs were obtained before and within 24 h of CY administration. QTc was calculated using the Fridericia and Bazett formulas, and ΔQTc (post–pre) was evaluated using logistic regression and receiver operating characteristic (ROC) analyses. Results Seven (11.3%) patients developed CY‐induced cardiomyopathy. QTc after CY administration and ΔQTc were significantly greater in the cardiomyopathy group ( p < 0.001). In multivariate analysis, ΔQTc was independently associated with cardiomyopathy (odds ratio 2.21, 95% confidence interval [CI]: 1.26–3.90, p = 0.0060). ROC analysis revealed excellent predictive accuracy (area under the curve = 0.96), with a ΔQTc ≥30.5 ms yielding 100% sensitivity and 89.1% specificity. Progressive QTc prolongation was also observed from pre‐ to post‐CY and at diagnosis in the affected patients. Conclusions QTc prolongation within 24 h of CY administration suggests subsequent CY‐induced cardiomyopathy in children. ΔQTc may serve as an early, noninvasive marker for timely detection and intervention in CY‐induced cardiotoxicity.
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Kawamura et al. (2026) studied this question. ΔQTc ≥30.5 ms within 24 h of cyclophosphamide administration predicts CY-induced cardiomyopathy in children with 100% sensitivity and 89.1% specificity.
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