Despite the effectiveness of anthracycline chemotherapy, cardiotoxicity remains a significant long-term secondary effect. The myofibrillar loss and cellular necrosis from anthracycline cardiotoxicity leads to delayed and irreversible myocardial damage, culminating in cardiac dysfunction, cardiomyopathy and heart failure. The aim of this study was to determine the CMR tissue characteristics (myocardial T1, T2 and derived ECV) in subclinical myocardial toxicity and their association with LV function and structure, exercise capacity and chemotherapy dose in childhood and adolescent cancer survivors [
61]. 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, T1 and T2 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. 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. 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.