Abstracts of the 42nd Annual Meeting ofthe American Society of Hematology, December1 - 5,
`2000, The Moscone Center, San Francisco, CA
`
`[2601] CARDIAC IRON DEPOSITION IS NOT PREDICTED BY CONVENTIONAL
`MARKERSOF IRON OVERLOAD IN HOMOZYGOUS B-THALASSAEMIA.
`Lisa Anderson, John B. Porter, Beatrix Wonke, J. Malcolm Walker, Sally Holden, Bernard A. Davis, Emma
`Prescott, Clare Charrier, DavidN. Firmin, Dudley J. Pennell (Intr. by Rosemary E. Gale}. Cardiac MR Unit,
`Royal Brompton Hospital, London; Departments ofHaematology and Cardiology, University College London
`Hospitals, London; Department ofHaematology, The Whittington Hospital, London.
`Monday, December 4, 2000, 10:00 AM, Hall C, Poster Board Number65
`The managementofiron overload requires the identification of patients at highestrisk of heart failure, the
`commonest cause of death in thalassaemia major. Becauseit has not previously been possible to estimate
`cardiac iron deposition non-invasively and reproducibly, managementhasrelied upon assessment of other
`variables. Thus while wholeliver iron levels >15mg/g dry weight or serum ferritin values consistently
`>2500ng/I have been shownto predictpatients at highest risk of cardiac death,it is not known how these
`variables relate to cardiac iron deposition. We report the relationship between myocardial andliver iron,
`measured by magnetic resonance, in 151 regularly transfused patients with homozygous B-thalassemia. We
`measured T2*,an inherent value of any tissue which is inversely related to iron concentration. This
`measurement gives a high degree of reproducibility in both the liver (coefficient of variation=3.3%) and the
`heart (coefficient of variation=5.0%). Liver T2* correlated with liver iron measured at biopsy (r=0.93,
`p<0.0001, n=13 for non-fibrotic samples and 1=0.81, p<0.0001 and n=30 forall samples), but there was a
`striking discordance between myocardial iron deposition and liver iron or serum ferritin in many patients.
`Althoughthe correlations betweenliver T2* and heart T2* (r=0.19, p=0.02) and serum ferritin and heart T2*
`(r=0.14, p=0.01) achievedstatistical significance in this large cohort, the scatter was great. No significant
`relationship could be demonstrated betweenliver iron andleft ventricular ejection fraction (r=0.11, p=0.19) or
`serum ferritin and left ventricular ejection fraction (r=0.032, p=0.70). There wasalso no significant relationship
`between mean serum ferritin for one year prior to the scan and myocardial T2* (r=0.13, p=0.11) or ejection
`fraction (0.001, p=0.98). The highly variable relationship betweenliver and heart ironis likely to reflect
`differences in chelation history between patients as well as differences in the rates at which iron is taken up and
`removed from hepatocytes and myocytes. We conclude that neither serum ferritin or liver iron measurements
`usefully predict those patients with increased myocardialiron deposition.
`Keywords: B-Thalassemia;Iron overload
`
`Poster Session: Thalassemia & Globin Gene Regulation: Switching/Clinical Studies (10:00 AM-6:30 PM)
`
`Supported by an unrestricted educational grant from AstraZeneca.
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