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7 Sex differences in late chemotherapy-induced cardiomyopathy in adult cancer survivors: a cardiovascular magnetic resonance study
  1. Iwan Harries1,
  2. Giovanni Biglino2,
  3. Amardeep Ghosh Dastidar1,
  4. Anna Baritussio1,
  5. Estefania DeGarate1,
  6. Samantha Kestenbaum1,
  7. Matthew Williams3,
  8. Chitsa Seyani4,
  9. Paul Brady5,
  10. Jason Chai5,
  11. Gavin Richards6,
  12. Jennifer Bracken6,
  13. Victoria North7,
  14. Chiara Bucciarelli-Ducci1
  1. 1NIHR Bristol Cardiovascular Biomedical Research Unit, Cardiac Magnetic Resonance Department, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
  2. 2Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, UK
  3. 3Taunton and Somerset NHS Foundation Trust, Taunton, UK
  4. 4Great Western Hospitals NHS Foundation Trust, Swindon, UK
  5. 5Royal United Hospitals NHS Foundation Trust, Bath, UK
  6. 6Gloucestershire Hospitals NHS Foundation Trust, Gloucester, UK
  7. 7North Bristol NHS Trust, Bristol, UK

Abstract

Introduction Chemotherapy induced cardiomyopathy (CIC) carries significant morbidity and mortality in cancer survivors. Female sex is a recognised risk factor for CIC in paediatric populations but the effect of sex in adult patients has not been established. We investigated sex differences in CIC using cardiovascular magnetic resonance (CMR).

Method 76 patients without abnormal left ventricular function prior to chemotherapy (30 male [59±15 years], and 46 female [58±13 years, p=0.86]) were included. Cumulative anthracycline dose (193±165 vs. 189±119 mg/m2, p=0.91) and follow-up interval (8.75±8.75 years vs. 8.75±9 years, p=0.99) were similar. All patients underwent contrast-enhanced CMR at 1.5T, including long and short axis cine imaging, mitral and tricuspid annular peak systolic excursion (MAPSE and TAPSE, respectively), and late gadolinium enhancement (LGE). Multivariate regression analysis was undertaken.

Results Left (39±13 vs 46±10%; p=0.027) and right ventricular ejection fraction (50±10 vs. 55±8%; p=0.042) were significantly lower in males, largely driven by differences in LV (208±83 vs. 167±42, p=0.02) and RV end diastolic volume (150±44 vs. 120±31, p=0.002). MAPSE and LAVi correlated significantly with LVEF (p<0.001 in both cases), as did TAPSE with RVEF (p=0.02). LGE prevalence did not differ between males and females (37% vs. 20%, respectively, p=0.10).

Conclusions Adult male cancer survivors developed comparably worse late biventricular CIC than their female counterparts despite receiving similar doses of cancer treatment. These findings need confirmation in larger cohort studies, and if confirmed, could inform bespoke monitoring strategies taking sex differences into account.

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