In asymptomatic childhood cancer survivors, increased myocardial extracellular volume fraction significantly correlated with lower peak VO2 (r = -0.52), higher cumulative anthracycline dose (r = 0.40), and ventricular wall thinning.
Cross-Sectional (n=30)
No
Do CMR-derived myocardial T1 and ECV correlate with exercise capacity, cumulative anthracycline dose, and ventricular remodeling in childhood cancer survivors?
Myocardial T1 mapping and ECV identify early subclinical diffuse fibrosis and ventricular remodeling in childhood cancer survivors with normal ejection fraction post-anthracycline therapy.
Effect estimate: r = -0.52
p-value: p=0.005
BACKGROUND: The late cardiotoxic effects of anthracycline chemotherapy influence morbidity and mortality in the growing population of childhood cancer survivors. Even with lower anthracycline doses, evidence of adverse cardiac remodeling and reduced exercise capacity exist. We aim to examine the relationship between cardiac structure, function and cardiovascular magnetic resonance (CMR) tissue characteristics with chemotherapy dose and exercise capacity in childhood cancer survivors. METHODS: Thirty patients (15 ± 3 years), at least 2 years following anthracycline treatment, underwent CMR, echocardiography, and cardiopulmonary exercise testing (peak VO(2)). CMR measured ventricular function, mass, T(1) and T(2) values, and myocardial extracellular volume fraction, ECV, a measure of diffuse fibrosis based on changes in myocardial T1 values pre- and post-gadolinium. Cardiac function was also assessed with conventional and speckle tracking echocardiography. RESULTS: Patients had normal LVEF (59 ± 7%) but peak VO(2) was 17% lower than age-predicted normal values and were correlated with anthracycline dose (r = -0.49). Increased ECV correlated with decreased mass/volume ratio (r = -0.64), decreased LV wall thickness/height ratio (r = -0.72), lower peak VO(2)(r = -0.52), and higher cumulative dose (r = 0.40). Echocardiographic measures of systolic and diastolic function were reduced compared to normal values (p < 0.01), but had no relation to ECV, peak VO(2) or cumulative dose. CONCLUSIONS: Myocardial T1 and ECV were found to be early tissue markers of ventricular remodeling that may represent diffuse fibrosis in children with normal ejection fraction post anthracycline therapy, and are related to cumulative dose, exercise capacity and myocardial wall thinning.
Tham et al. (2013) conducted a cross-sectional in Subclinical anthracycline cardiotoxicity in childhood cancer survivors (n=30). Anthracycline therapy was evaluated on Correlation between myocardial extracellular volume fraction (ECV) and peak VO2 (r = -0.52, p=0.005). In asymptomatic childhood cancer survivors, increased myocardial extracellular volume fraction significantly correlated with lower peak VO2 (r = -0.52), higher cumulative anthracycline dose (r = 0.40), and ventricular wall thinning.