Key result
Anthracycline-treated childhood leukaemia survivors with normal echocardiography exhibited subclinical cardiovascular changes, including significantly reduced left ventricular ejection fraction (55.0% vs 59.4%, p=0.010) and impaired flow-mediated dilation.
Why the study?
Anthracycline-mediated cardiac injury can remain latent for years, so the authors investigated whether subclinical cardiac and vascular dysfunction could be detected early in healthy, anthracycline-treated survivors of childhood leukaemia.
Does a history of anthracycline chemotherapy cause subclinical cardiac and vascular dysfunction in long-term, asymptomatic childhood leukaemia survivors?
Cross-Sectional (n=44)
Assessor-blind
No
Does a history of anthracycline chemotherapy cause subclinical cardiac and vascular dysfunction in long-term, asymptomatic childhood leukaemia survivors?
Cardiac MRI and flow-mediated dilation can detect subclinical cardiac and vascular dysfunction in asymptomatic childhood leukaemia survivors treated with anthracyclines, even when resting echocardiography appears normal.
Answers are grounded in this paper and cite their sources.
Subclinical dysfunction may be detectable by advanced imaging despite normal echocardiography in anthracycline survivors; leaves open whether this alters outcomes or surveillance.
Cardiovascular disease (CVD) is the leading non-malignant cause of death in childhood cancer survivors. Heightened risk of CVD is often attributable to treatment with anthracycline chemotherapy. Anthracycline-mediated cardiac injury may lie latent for years following cessation of treatment and is therefore often not detected until disease is advanced and aggressive therapy is required. Symptomatic CVD may be preceded by subclinical cardiac and vascular dysfunction. This study aimed to determine whether such dysfunction could be detected in healthy, anthracycline-treated survivors of childhood leukaemia. Cardiac magnetic resonance imaging (cMRI) with late gadolinium enhancement and endothelial function were used to characterise pre-clinical stages of CVD. Twenty-two long-term (>5 years survival; age 21 ± 3 years) childhood leukaemia survivors were assessed. All survivors were asymptomatic and had normal resting echocardiography. To exclude potential confounding effects of radiotherapy, no survivors had received this treatment. Twenty-two similarly aged (25 ± 3 years) gender-matched controls were recruited for comparison. Left ventricular ejection fraction was lower in the survivors (55.0 ± 4.6%) compared to the controls (59.4 ± 6.2%; p = 0.010). Further, five survivors (23%) had clinically reduced (<50%) left ventricular ejection fraction. Normalised left ventricular end systolic volume was augmented in survivors (40.0 ± 9.1 mL·m2 vs. 34.5 ± 7.5 mL·m2; p = 0.038). Cardiac MRI did not show any late gadolinium enhancement. High resolution, ultrasound-derived flow mediated dilation was impaired in survivors (6.7 ± 2.1% vs. 8.60 ± 1.91%, p = 0.005). We detected subclinical changes in cardiovascular structure and function indicative of early disease in anthracycline-treated childhood leukaemia survivors with normal echocardiography. Early detection and characterisation of underlying disease allows for timely intervention and improved outcomes in this at-risk population.
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Long et al. (2019) conducted a cross-sectional in Childhood leukaemia survivors (n=44). Anthracycline chemotherapy vs. Healthy matched controls was evaluated on Left ventricular ejection fraction (p=0.010). Anthracycline-treated childhood leukaemia survivors with normal echocardiography exhibited subclinical cardiovascular changes, including significantly reduced left ventricular ejection fraction (55.0% vs 59.4%, p=0.010) and impaired flow-mediated dilation.
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