Background-Anthracycline cardiomyopathy contributes to the morbidity and mortality of cancer survivors, but long-term data are lacking. This study sought to describe the phenotype of anthracycline cardiomyopathy, the prevalence of myocardial fibrosis and its association with cardiac remodelling, systolic function and clinical outcomes in the long-term. Methods and Results We undertook contrast-enhanced CMR in 81 cancer survivors at median 5 years after anthracycline (mean dose 279 SD 89mg/m 2). Participants were aged 55 SD 14 years; 68% were female. Mean LVEF was impaired (49 SD 12%), driven by a pathological increase in iLVESV (47 SD 23ml/m 2). 19% of participants exhibited LGE, which was associated with significant adverse left ventricular remodelling and reduced systolic function (iLVEDV: 102 SD 34vs83 SD 21ml/m2, p=0.03; iLVESV 61 SD 32vs43 SD 20ml/m 2 , p=0.03; LVEF: 43 SD 11vs50 SD 12%, p=0.03). In subgroup analysis of 36 patients, 36% had elevated native T1 measurements, which was associated with significant adverse left ventricular remodelling (iLVEDV: 97 SD 22vs74 SD 19ml/m 2 , p=0.002; iLVESV: 56 SD 22vs35 SD15ml/m 2 , p=0.005), reduced systolic function (LVEF 44 SD 13 vs 55 SD 9%, p=0.01), and hospitalizations for heart failure (38%vs9%, p=0.03). Absolute native T1 measurements correlated significantly with iLVEDV (p =<0.001, R 2 0.33), iLVESV (p<0.001, R 2 0.36), LVEF (p<0.001, R 2 0.35), LAVi (p=0.04, R 2 0.12) and MAPSE (p =0.02, R 2 0.14). Conclusions-Long-term anthracycline cardiomyopathy is characterized by pathologically increased iLVESV. Both LGE and elevated native T1 measurements were associated with significant adverse cardiac remodelling and reduced systolic function, and the latter with heart failure hospitalizations.