Long term cardiovascular magnetic resonance phenotyping of anthracycline cardiomyopathy

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.

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).

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.