Iwan Harries1, Giovanni Biglino2, Anna Baritussio1, Estefania De Garate1, Amardeep Dastidar1, Juan Carlos Plana3, Chiara Bucciarelli-Ducci4. 1. Bristol Heart Institute, Department of Cardiology, University Hospitals Bristol, Bristol, UK. 2. Bristol Medical School, Department of Translational Health Sciences, Bristol Royal Infirmary, Bristol, UK. 3. Baylor College of Medicine, Houston, TX, United States. 4. Bristol Heart Institute, Department of Cardiology, University Hospitals Bristol, Bristol, UK; Bristol Medical School, Department of Translational Health Sciences, Bristol Royal Infirmary, Bristol, UK; NIHR Bristol Biomedical Research Centre, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Bristol, UK. Electronic address: C.Bucciarelli-Ducci@bristol.ac.uk.
Abstract
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 long-term anthracycline cardiomyopathy, the prevalence of myocardial fibrosis and its association with cardiac remodeling, systolic function and clinical outcomes. METHODS AND RESULTS: We undertook contrast-enhanced CMR in 81 cancer survivors at median 5 years after anthracycline (mean dose 279 SD 89 mg/m2). 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 23 ml/m2). 19% of participants exhibited LGE, which was associated with significant adverse left ventricular remodeling and reduced systolic function (iLVEDV: 102 SD 34 vs 83 SD 21 ml/m2, p = 0.03; iLVESV 61 SD 32 vs 43 SD 20 ml/m2, p = 0.03; LVEF: 43 SD 11 vs 50 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 remodeling (iLVEDV: 97 SD 22 vs 74 SD 19 ml/m2, p = 0.002; iLVESV: 56 SD 22 vs 35 SD 15 ml/m2, p = 0.005), reduced systolic function (LVEF 44 SD 13 vs 55 SD 9%, p = 0.01), and hospitalizations for heart failure (38% vs 9%, p = 0.03). Absolute native T1 measurements correlated significantly with iLVEDV (p ≤ 0.001, R2 0.33), iLVESV (p < 0.001, R2 0.36), LVEF (p < 0.001, R2 0.35), LAVi (p = 0.04, R2 0.12) and MAPSE (p = 0.02, R2 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 remodeling and reduced systolic function, and the latter with heart failure hospitalizations.
BACKGROUND:Anthracyclinecardiomyopathy contributes to the morbidity and mortality of cancer survivors but long-term data are lacking. This study sought to describe the phenotype of long-term anthracyclinecardiomyopathy, the prevalence of myocardial fibrosis and its association with cardiac remodeling, systolic function and clinical outcomes. METHODS AND RESULTS: We undertook contrast-enhanced CMR in 81 cancer survivors at median 5 years after anthracycline (mean dose 279 SD 89 mg/m2). 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 23 ml/m2). 19% of participants exhibited LGE, which was associated with significant adverse left ventricular remodeling and reduced systolic function (iLVEDV: 102 SD 34 vs 83 SD 21 ml/m2, p = 0.03; iLVESV 61 SD 32 vs 43 SD 20 ml/m2, p = 0.03; LVEF: 43 SD 11 vs 50 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 remodeling (iLVEDV: 97 SD 22 vs 74 SD 19 ml/m2, p = 0.002; iLVESV: 56 SD 22 vs 35 SD 15 ml/m2, p = 0.005), reduced systolic function (LVEF 44 SD 13 vs 55 SD 9%, p = 0.01), and hospitalizations for heart failure (38% vs 9%, p = 0.03). Absolute native T1 measurements correlated significantly with iLVEDV (p ≤ 0.001, R2 0.33), iLVESV (p < 0.001, R2 0.36), LVEF (p < 0.001, R2 0.35), LAVi (p = 0.04, R2 0.12) and MAPSE (p = 0.02, R2 0.14). CONCLUSIONS: Long-term anthracyclinecardiomyopathy is characterized by pathologically increased iLVESV. Both LGE and elevated native T1 measurements were associated with significant adverse cardiac remodeling and reduced systolic function, and the latter with heart failure hospitalizations.