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Long term cardiovascular magnetic resonance phenotyping of anthracycline cardiomyopathy

Research output: Contribution to journalArticle

Original languageEnglish
Number of pages5
JournalInternational Journal of Cardiology
Early online date10 Apr 2019
DOIs
DateAccepted/In press - 8 Apr 2019
DateE-pub ahead of print (current) - 10 Apr 2019

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.

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  • Full-text PDF (accepted author manuscript)

    Rights statement: This is the author accepted manuscript (AAM). The final published version (version of record) is available online via Elsevier at https://www.sciencedirect.com/science/article/pii/S0167527319302931 . Please refer to any applicable terms of use of the publisher.

    Accepted author manuscript, 478 KB, PDF-document

    Embargo ends: 10/04/20

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    Licence: CC BY-NC-ND

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